FREE Sample of ZAMboost Immune Support Supplement

UPDATED AS OF 10:20 a.m. AUGUST 21, 2013 
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FREE Sample of ZAMboost Immune Support Supplement

UPDATED AS OF 10:20 a.m. AUGUST 21, 2013 
We’re thrilled you want to give your immune system a fighting chance by trying ZAMboost! Due to overwhelming response, we are currently unable to process any additional sample requests. When we resume processing samples, we’ll let you know via Facebook, Twitter, and our blog.  So “like” or follow us then check back often to get the scoop on deals, giveaways, coupons, and immunity-boosting tips!

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FREE Sample of ZAMboost Immune Support Supplement

UPDATED AS OF 10:20 a.m. AUGUST 21, 2013 
We’re thrilled you want to give your immune system a fighting chance by trying ZAMboost! Due to overwhelming response, we are currently unable to process any additional sample requests. When we resume processing samples, we’ll let you know via Facebook, Twitter, and our blog.  So “like” or follow us then check back often to get the scoop on deals, giveaways, coupons, and immunity-boosting tips!

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Cancer-fighting immune activity boosted by dialing back Treg cell function in animal model

Main Category: Cancer / Oncology
Also Included In: Immune System / Vaccines
Article Date: 20 Aug 2013 - 0:00 PDT Current ratings for:
Cancer-fighting immune activity boosted by dialing back Treg cell function in animal model

By carefully adjusting the function of crucial immune cells, scientists may have developed a completely new type of cancer immunotherapy - harnessing the body's immune system to attack tumors. To accomplish this, they had to thread a needle in immune function, shrinking tumors without triggering unwanted autoimmune responses.

The new research, performed in animals, is not ready for clinical use in humans. However, the approach, making use of a key protein to control immune function, lends itself to further study using candidate drugs that employ the same mechanisms.

"This preclinical study demonstrates proof of principle that using a drug to regulate the function of a special, immunosuppressive subset of so-called T-regulatory (Treg) cells safely controls tumor growth," said study leader Wayne W. Hancock, M.D., Ph.D., of the Division of Transplant Immunology at The Children's Hospital of Philadelphia (CHOP). "It really moves the field along towards a potentially major, new cancer immunotherapy."

Hancock and colleagues published the study in Nature Medicine.

"There's a basic paradox in immunology: why doesn't the immune system prevent cancer in the first place?" said Hancock. The answer is complicated, he adds, but much of it involves a delicate balancing act among elements of the immune system: while immunity protects us against disease, an overly aggressive immune response may trigger dangerous, even life-threatening, autoimmune reactions in which the body attacks itself.

In the current study, Hancock focused on a subtype of immune cells called Foxp3+ Tregs, for short. Tregs were already known to limit autoimmunity, but often at the cost of curtailing immune responses against tumors. "We needed to find a way to reduce Treg function in a way that permits antitumor activity without allowing autoimmune reactions," he said.

Hancock's group showed that inhibiting the enzyme p300 can affect the functions of another protein, Foxp3, which plays a key role in controlling the biology of Tregs. By deleting the gene that expresses p300, the researchers safely reduced Treg function and limited tumor growth in mice. Notably, they also achieved the same effects on p300 and Tregs in mice by using a drug that inhibits p300 in normal mice.

Hancock will pursue further investigations into targeting p300 in immunotherapy. The preclinical findings offer encouraging potential for being translated into the clinic, said Hancock, who added that pharmaceutical companies have expressed interest in researching this approach as a possible cancer therapy.

The antitumor study, down-regulating Treg function, is the flip side of another part of Hancock's Treg research. In a 2007 animal study, also in Nature Medicine, he increased Treg function with the goal of suppressing the immune response to allow the body to better tolerate organ transplants. In the current study, decreasing Treg activity permitted the immune system to attack an unwelcome visitor - a tumor. In both cases, he relied on epigenetic processes - using groups of chemicals called acetyl groups to modify key proteins - but in opposite directions. "This is the yin and yang of immune function," he added.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our cancer / oncology section for the latest news on this subject.

The National Institutes of Health (grants AI073489, AI095353, and CA158941, all to Hancock) supported this research. In addition to his CHOP position, Hancock is on the faculty of the Perelman School of Medicine at the University of Pennsylvania.

Yujie Liu et al., "Inhibition of p300 impairs Foxp3+ T regulatory cell function and promotes antitumor immunity," Nature Medicine, published online Aug. 18, 2013. doi:10.1038/nm.3286

Children's Hospital of Philadelphia

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Bypassing immune rejection in stem-cell-based therapies

Main Category: Transplants / Organ Donations
Also Included In: Stem Cell Research;  Immune System / Vaccines
Article Date: 20 Aug 2013 - 1:00 PDT Current ratings for:
Bypassing immune rejection in stem-cell-based therapies

The scientific community has held tremendous hope for the eventual emergence of stem cell transplantation as a broadly applicable and highly effective therapeutic strategy. However, the realization of this hope has been plagued by the indomitable immune response to the transplantation of human embryonic stem cell (hESC) derivatives, which prevents the engraftment and long-term survival necessary for functional recovery or preservation of the host tissue.

In an article featured in the latest issue of STEM CELLS, a research group from Stanford University describes a novel regimen for quashing this immunologic barrier - a short-course treatment with two costimlation-adhesion blockade agents, allowing engraftment of transplanted differentiated stem cells and their prolonged survival in tissue.

"Inducing immune tolerance to human embryonic stem cell graft is critical for the clinical success of regenerative medicine," commented Dr. Joseph Wu, M.D., Professor of Medicine and Radiology at the Stanford University School of Medicine. "We have realized, however, that traditional immunosuppressive therapies used to prevent solid organ rejection, such as calcineurin inhibitors and corticosteroids, are insufficient to prevent human embryonic stem cell rejection following transplantation."

In the study, hESCs were made to express enhanced green fluorescent protein (eGFP), differentiated to endothelial cells and cardiomyocytes, and transplanted into mouse hindlimbs as well as into both healthy and ischemic mouse myocardia. A novel costimulation-adhesion blockade method was then used alongside a more traditional therapy involving cyclosporine to induce immunosuppression. Detection of eGFP in the tissues allowed the team to track the engraftment and longevity of the transplanted cells over time. The costimulation-adhesion method yielded vastly superior results to the cyclosporine treatment, not only showing significantly improved engraftment and survival of the cells in the tissues but ultimately showing the effective preservation of cardiac function following stem cell transplantation in an induced myocardial infarction model, as shown through MRI.

"Here we demonstrate that a short-course, dual-agent regimen that prevents optimal T cell activation is sufficient to promote the robust and long-term survival of embryonic stem cell derivatives in both healthy and injured tissues in mouse models," Dr. Wu explained. The authors indicate that the superior response of the transplanted cells to the costimulation-adhesion therapy may be attributed to its repression of both adaptive and innate immunity, which is likely to aid in mitigating the tissues' rejection of these characteristically immunogenic cells. The researchers' method led to both local and systemic upregulation of T cell immunoglobulin and mucin domain 3 (TIM3), a Th-1-specific cell surface protein, in addition to an overall reduction of pro-inflammatory cytokines.

"Application of hESC and iPSC-derived cells holds great promise for cell replacement therapies in man, with clinical trials already ongoing in USA/Europe and soon in Japan," noted Majlinda Lako, Ph.D., Associate Editor for STEM CELLS and Professor of Stem Cell Science at the Institute of Genetic Medicine, Newcastle University. "This current study brings us a step closer to overcoming immunological barriers that have hampered these clinical promises and addresses important issues that must be tackled before successful realization of pluripotent stem cell therapies can take place in humans."

Speaking on behalf of his research team, Dr. Wu stated, "We are excited by these findings and about their implications for the field. This work demonstrates a simple, effective approach to overcome the immunologic barrier of using human embryonic stem cell derivatives that is far superior to conventional agents currently in use clinically."

Article adapted by Medical News Today from original press release. Source:

AlphaMed Press

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Malaria DNA vaccine demonstrates robust immune responses in animal models

Main Category: Tropical Diseases
Also Included In: Immune System / Vaccines
Article Date: 16 Aug 2013 - 2:00 PDT Current ratings for:
Malaria DNA vaccine demonstrates robust immune responses in animal models

Inovio Pharmaceuticals, Inc. have announced that its SynCon® DNA vaccine containing multiple malaria antigens delivered via its CELLECTRA® electroporation device demonstrated strong and durable antibody and T-cell immune responses in small animals and non-human primates. With these strong preclinical results, Inovio plans to initiate a phase I/IIa clinical trial next year.

These results appear in the American Society for Microbiology's peer-reviewed journal, Infection & Immunity, in a paper entitled: "Inducing humoral and cellular responses to multiple sporozoite and liver-stage malaria antigens using pDNA," authored by Inovio researchers and collaborators.

The World Health Organization estimated that in 2010 there were more than 200 million cases of malaria and almost 700,000 deaths due to malaria infection, the majority affecting young children in Africa. To date, the most advanced malaria vaccine candidate RTS,S, an adjuvanted recombinant protein vaccine, has not shown substantial protection in the key trial age group of infants. Scientists believe that a more effective malaria vaccine should generate both strong antibody and potent T-cell immune responses.

In this study, Inovio researchers and collaborators designed a highly optimized DNA vaccine composed of four sporozoite and liver-stage malaria antigens using Inovio's SynCon technology. These antigens were chosen because of their important role in the control or elimination of malaria infection. Delivered using Inovio's CELLECTRA delivery system, this malaria vaccine generated robust and long-lasting T-cell responses in both mice and non-human primates. Moreover, these vaccine-produced T-cells exhibited the functional ability to kill and eliminate malaria-infected cells. Researchers also found vaccine-induced CD8+, or "killer T-cells," in the liver, which is essential for rapid elimination of liver-stage malaria parasites. The Inovio DNA/electroporation platform has demonstrated in prior preclinical and human studies the ability to induce potent immune responses to multiple antigens; in this study, robust and sustained antibody responses to all four malaria antigens were observed, a strong indication for a preventive response in humans.

Inovio plans to initiate a phase I/IIa clinical trial in 2014 to test Inovio's DNA vaccine and electroporation technology in approximately 30 individuals as part of a "challenge trial" involving controlled human malaria infection. Volunteers will be administered Inovio's vaccine, then exposed to the malaria parasite through the bite of infected mosquitoes to see whether this approach prevents infection. If deemed successful, this trial would provide valuable information that may further the development of a vaccine against malaria and lead to larger efficacy studies in the field.

Dr. J. Joseph Kim, President and CEO of Inovio, said, "Published data from two clinical studies has demonstrated that Inovio's products generated best-in-class T-cell immune responses. Using the same synthetic vaccine technology that produced clinical candidates against HPV, HIV, and influenza and achieved potent antibody and T-cell immune responses against these targets, we have now generated strong immunology data with our malaria vaccine in non-human primates. We are excited to advance toward the very important healthcare goal of conquering malaria."

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our tropical diseases section for the latest news on this subject.

"Inducing humoral and cellular responses to multiple sporozoite and liver stage malaria antigens using pDNA" Infection & Immunity, Published ahead of print 29 July 2013, doi: 10.1128/IAI.00180-13

About Inovio Pharmaceuticals, Inc.

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Where in the body immune cells reach maturity is important for their later function

Main Category: Immune System / Vaccines
Article Date: 16 Aug 2013 - 0:00 PDT Current ratings for:
Where in the body immune cells reach maturity is important for their later function

Regulatory T cells (or "Tregs" for short) play a central role in the human immune system: They guide all of the other immune cells and make sure they are tolerant of the body's own cells and harmless foreign substances. How Tregs become Tregs in the first place has been only incompletely understood - until now. Scientists at the Helmholtz Centre for Infection Research (HZI) in Braunschweig, Germany, along with their colleagues at the Hannover Medical School (MHH) have recently gleaned important new insights into the workings of these cells. As it turns out, origin is key - greater numbers of Tregs are produced within certain lymph nodes than in others. The researchers are now publishing their insights in the scientific journal Mucosal Immunology.

Without regulatory T cells, the human defence system would not work properly. Defender cells would be fiercely fighting off even harmless foreign substances like the parts of certain kinds of food, for example, as the immune system would simply not be "tolerant" towards these harmless substances. This tolerance is mediated through the Tregs - they are "tolerogenic."

They instruct other immune cells as to which intruders really do need to be fought off and which ones do not pose a threat. However, even regulatory T cells have to first acquire this unique skill. What we have known for some time now is that they receive their "training" inside lymph nodes. "Lymph nodes are basically the immune system's meeting points if you will," says Prof. Jochen Hühn, Head of Experimental Immunology at the HZI. "Here, different types of immune cells meet up and also encounter antigen." An antigen is a structure the immune system is able to recognize like component parts of pathogens or foods.

The researchers compared the development of murine T cells obtained from lymph nodes from various locations in the body, like the liver, intestine, and skin. In the process, they learned that more Tregs capable of teaching other cells to be tolerant of food antigens are made inside lymph nodes of the liver and intestine - a property the lymph nodes maintained even when they were transplanted to the skin. Conversely, skin lymph nodes did not become more tolerogenic if transplanted to the intestine. The HZI scientists made these discoveries together with their colleagues from Prof. Oliver Papst's team at the MHH Institute of Immunology.

Based on their observations, the scientists deduced that lymph node location influences the maturation process of the cells they contain. "The cells retained their original skills for weeks following the transplant," says Dr. Sascha Cording, one of the study's first authors. "You might say lymph nodes have something like a location-specific memory."

And this in spite of the fact that all the various types of blood cells within a lymph node, including the immune cells, are constantly replaced, which means the lymph nodes' location memory must be encoded somewhere in its stroma.

Additional experiments allowed the scientists to probe just how lymph nodes obtain their memory: Following birth, both the supply of vitamin A and the intestinal bacterial microflora figure prominently into this process. Without these two influencing factors, the lymph nodes simply forget about their origin and lose their tolerogenic properties.

These findings about lymph node imprinting apply to humans as well: An inadequate supply of vitamin A after birth or meddling with the baby's developing microflora through administration of antibiotics can interfere with the lymph nodes' long-term memory. "At what age this process happens in humans we cannot as of yet pinpoint with any certainty," says Hühn. "Whether we're talking about the first few days, weeks, or months even, is difficult to surmise." The next step will be identifying the potential repercussions interfering with early imprinting of the immune system. Down the line, things like food allergies or autoimmune diseases might be the result.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our immune system / vaccines section for the latest news on this subject.

The intestinal micro-environment imprints stromal cells to promote efficient Treg induction in gut-draining lymph nodes

Sascha Cording, Benjamin Wahl, Devesha Kulkarni, Himprya Chopra, Jörn Pezoldt, Manuela Buettner, Annegret Dummer, Usri Hadis, Markus Heimesaat, Stefan Bereswill, Christine Falk, Ulrike Bode, Alf Hamann, Diana Fleissner, Jochen Huehn, Oliver Pabst

Mucosal Immunology, 2013, DOI: 10.1038/mi.2013.54

Helmholtz Centre for Infection Research

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Premature aging of immune cells present in joints of kids with chronic arthritis, Pitt/Children's Hospital team says

Main Category: Arthritis / Rheumatology
Also Included In: Immune System / Vaccines;  Pediatrics / Children's Health;  Seniors / Aging
Article Date: 31 Jul 2013 - 1:00 PDT Current ratings for:
Premature aging of immune cells present in joints of kids with chronic arthritis, Pitt/Children's Hospital team says

The joints of children with the most common form of chronic inflammatory arthritis contain immune cells that resemble those of 90-year-olds, according to a new study led by researchers at Children's Hospital of Pittsburgh of UPMC and the University of Pittsburgh School of Medicine. The findings, published in the August issue of Arthritis and Rheumatism, suggest that innovative treatment approaches could aim to prevent premature aging of immune cells.

Juvenile idiopathic arthritis, or JIA, is the most prevalent rheumatic condition in the world and affects one of every 1,000 children in the U.S., said senior researcher Abbe de Vallejo, Ph.D., associate professor of pediatrics and immunology, Pitt School of Medicine. It usually starts with a swollen ankle, knee or wrist that parents often assume is due to a minor injury sustained while playing.

"Untreated JIA has devastating consequences," Dr. de Vallejo said. "It can slow growth and, in extreme cases, the child can be physically disfigured. It's a degenerative disease that eats up the joints."

Doctors have long thought of JIA as an autoimmune disease, meaning the body attacks itself. But previous studies by Dr. de Vallejo of young adults with rheumatoid arthritis indicated that a certain population of cells present in the joint synovial fluid and blood displayed telltale signs of abnormal cell division and premature aging. His current team at Children's wanted to see if that was true in pediatric arthritis.

They examined immune cells called T-cells in the synovial fluid and blood from 98 children ages 1 to 17 and known to have JIA, as well as 46 blood samples from children who didn't have the disease. T-cells are the army of immune cells that eradicate infection, tumors and other dangerous agents to which people may be exposed.

The research team found about one-third of the T-cells of children with JIA had shortened telomeres and had reduced, or in some cases lost, the capacity to proliferate. Telomeres are the ends of chromosomes that don't code for proteins and, because they are not fully copied by enzyme mechanisms, are trimmed slightly during each DNA replication cycle. It is thought that aging occurs when the telomeres become too short for DNA replication and cell division to proceed normally.

"The T-cells of the children with JIA had very short telomeres, about the length we see in a 90-year-old or a young adult with rheumatoid arthritis. Those same T-cells express unusually high levels of several classic protein markers of cell aging and exhaustion," Dr. de Vallejo said. "These kids haven't lived long enough to have cells that look that old. This is the first indication that premature aging in occurring in this childhood condition."

In addition, the T-cells had become dysregulated, and their immune activity could be stimulated through atypical cell surface receptors. Much more must be learned about the unusual cells and about genetic mechanisms that might contribute to the development of JIA, Dr. de Vallejo said, but these findings could point the way to new therapies.

"JIA is typically treated with broad-spectrum drugs such as steroids and biologics that essentially paralyze the entire immune system, but only a third of the cells are affected and their abnormality seems to be premature aging, rather than autoimmune activity," he noted. "This study suggests cell-targeted treatments could be developed to prevent this premature immune aging."

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our arthritis / rheumatology section for the latest news on this subject.

Co-authors of the paper include other researchers from Children’s Hospital of Pittsburgh of UPMC; Pitt School of Medicine; and the Mayo Clinic. The project was funded by the Nancy E. Taylor Foundation for Chronic Diseases, the Arthritis Foundation, and National Institutes of Health grant AR052282.

Children’s Hospital of Pittsburgh of UPMC & University of Pittsburgh Schools of the Health Sciences

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Premature aging of immune cells present in joints of kids with chronic arthritis, Pitt/Children's Hospital team says

Main Category: Arthritis / Rheumatology
Also Included In: Immune System / Vaccines;  Pediatrics / Children's Health;  Seniors / Aging
Article Date: 31 Jul 2013 - 1:00 PDT Current ratings for:
Premature aging of immune cells present in joints of kids with chronic arthritis, Pitt/Children's Hospital team says

The joints of children with the most common form of chronic inflammatory arthritis contain immune cells that resemble those of 90-year-olds, according to a new study led by researchers at Children's Hospital of Pittsburgh of UPMC and the University of Pittsburgh School of Medicine. The findings, published in the August issue of Arthritis and Rheumatism, suggest that innovative treatment approaches could aim to prevent premature aging of immune cells.

Juvenile idiopathic arthritis, or JIA, is the most prevalent rheumatic condition in the world and affects one of every 1,000 children in the U.S., said senior researcher Abbe de Vallejo, Ph.D., associate professor of pediatrics and immunology, Pitt School of Medicine. It usually starts with a swollen ankle, knee or wrist that parents often assume is due to a minor injury sustained while playing.

"Untreated JIA has devastating consequences," Dr. de Vallejo said. "It can slow growth and, in extreme cases, the child can be physically disfigured. It's a degenerative disease that eats up the joints."

Doctors have long thought of JIA as an autoimmune disease, meaning the body attacks itself. But previous studies by Dr. de Vallejo of young adults with rheumatoid arthritis indicated that a certain population of cells present in the joint synovial fluid and blood displayed telltale signs of abnormal cell division and premature aging. His current team at Children's wanted to see if that was true in pediatric arthritis.

They examined immune cells called T-cells in the synovial fluid and blood from 98 children ages 1 to 17 and known to have JIA, as well as 46 blood samples from children who didn't have the disease. T-cells are the army of immune cells that eradicate infection, tumors and other dangerous agents to which people may be exposed.

The research team found about one-third of the T-cells of children with JIA had shortened telomeres and had reduced, or in some cases lost, the capacity to proliferate. Telomeres are the ends of chromosomes that don't code for proteins and, because they are not fully copied by enzyme mechanisms, are trimmed slightly during each DNA replication cycle. It is thought that aging occurs when the telomeres become too short for DNA replication and cell division to proceed normally.

"The T-cells of the children with JIA had very short telomeres, about the length we see in a 90-year-old or a young adult with rheumatoid arthritis. Those same T-cells express unusually high levels of several classic protein markers of cell aging and exhaustion," Dr. de Vallejo said. "These kids haven't lived long enough to have cells that look that old. This is the first indication that premature aging in occurring in this childhood condition."

In addition, the T-cells had become dysregulated, and their immune activity could be stimulated through atypical cell surface receptors. Much more must be learned about the unusual cells and about genetic mechanisms that might contribute to the development of JIA, Dr. de Vallejo said, but these findings could point the way to new therapies.

"JIA is typically treated with broad-spectrum drugs such as steroids and biologics that essentially paralyze the entire immune system, but only a third of the cells are affected and their abnormality seems to be premature aging, rather than autoimmune activity," he noted. "This study suggests cell-targeted treatments could be developed to prevent this premature immune aging."

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our arthritis / rheumatology section for the latest news on this subject.

Co-authors of the paper include other researchers from Children’s Hospital of Pittsburgh of UPMC; Pitt School of Medicine; and the Mayo Clinic. The project was funded by the Nancy E. Taylor Foundation for Chronic Diseases, the Arthritis Foundation, and National Institutes of Health grant AR052282.

Children’s Hospital of Pittsburgh of UPMC & University of Pittsburgh Schools of the Health Sciences

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University of Pittsburgh Medical Center. (2013, July 31). "Premature aging of immune cells present in joints of kids with chronic arthritis, Pitt/Children's Hospital team says." Medical News Today. Retrieved from
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Clearest ever pictures of immune cells could help treat cancers and HIV

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Main Category: Immune System / Vaccines
Also Included In: Cancer / Oncology;  HIV / AIDS
Article Date: 25 Jul 2013 - 0:00 PDT Current ratings for:
Clearest ever pictures of immune cells could help treat cancers and HIV

Immunity has never looked so good. Scientists in the UK recently released images that provide the clearest snapshot of how white blood immune cells attack viral infections and tumors. They are hopeful that these clearer pictures will provide important insights into how diseases can be treated.

White blood cells are the fighters of the body, tackling infections and cancers on our behalf. But when a research team from the University of Manchester used an improved process to view them, the images revealed how the cells change the way their surface molecules are arranged when a protein involved with cancers and viruses is activated.

And the images are something akin to science fiction. The proteins at the surface of the immune cells do not appear to be evenly distributed, but rather, they cluster, producing an image that resembles stars in a galaxy.

Professor Daniel Davis, director of research at the Manchester Collaborative Centre for Inflammation Research (MCCIR), told Medical News Today that before their breakthrough, normal light microscopes were limited in the images they produced because of the way light travels by bending around obstacles. The new microscopes he and his team used were able to employ computer technology and optics to break that barrier.

The image produced by scientists shows, for the first time, the cluster patterns of proteins on the surface of white blood immune cells. Source: MCCIR

They used super-resolution fluorescence microscopy in order to view the immune cells in their lab, and their results were recently published in Science Signalling.

By studying how the proteins change on immune cell surfaces at a nano scale, Davis and his team are able to gain a better understanding of how our immune systems work. He notes that this could give them ideas for how to develop disease-fighting drugs in the future. He told MNT:

"Rather than study one specific disease here, we investigated how immune cells respond to a particular protein that is found on many types of cancer cells or virus-infected cells. This protein is not found on the surface of normal healthy cells, but when a cell becomes cancerous or gets infected with some types of viruses, this protein gets put up on the surface for immune cells to see that there is a problem."

Davis added that these new imaging improvements are leading to unanticipated medical discoveries. For example, he and his team recently discovered new aspects of how HIV "uses membrane nanotubes to spread."

Though he notes that the road between where they are now with research and where they hope to arrive with new medicine is quite long, he's hopeful about where they're heading.

"We are, for example, trying to apply this new imaging technology to look at human lung samples with a view to understanding respiratory infections, asthma and so on," he said.

We may need to wait for new medicines to be developed as a result of the new images, but we can now marvel at the pictures Davis and his team have produced.

Written by Marie Ellis

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New understanding of how Ebola virus suppresses the human immune system

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Researchers reveal the clearest new pictures of immune cells

Main Category: Immune System / Vaccines
Article Date: 24 Jul 2013 - 14:00 PDT Current ratings for:
Researchers reveal the clearest new pictures of immune cells

Scientists from The University of Manchester have revealed new images which provide the clearest picture yet of how white blood immune cells attack viral infections and tumours.

They show how the cells, which are responsible for fighting infections and cancer in the human body, change the organisation of their surface molecules, when activated by a type of protein found on viral-infected or tumour cells.

Professor Daniel Davis, who has been leading the investigation into the immune cells, known as natural killers, said the work could provide important clues for tackling disease.

The research reveals the proteins at the surface of immune cells are not evenly spaced but grouped in clusters - a bit like stars bunched together in galaxies.

Professor Davis, Director of Research at the Manchester Collaborative Centre for Inflammation Research (MCCIR), a partnership between the University and two pharmaceutical companies GlaxoSmithKline and Astra Zeneca, said: "This is the first time scientists have looked at how these immune cells work at such a high resolution. The surprising thing was that these new pictures revealed that immune cell surfaces alter at this scale - the nano scale - which could perhaps change their ability to be activated in a subsequent encounter with a diseased cell.

"We have shown that immune cells are not evenly distributed as once thought, but instead they are grouped in very small clumps - a bit like if you were an astronomer looking at clusters of stars in the Universe and you would notice that they were grouped in clusters.

"We studied how these clusters or proteins change when the immune cells are switched on - to kill diseased cells. Looking at our cells in this much detail gives us a greater understanding about how the immune system works and could provide useful clues for developing drugs to target disease in the future."

Until now the limitations of light microscopy have prevented a clear understanding of how immune cells detect other cells as being diseased or healthy.

The team used high quality, super-resolution fluorescence microscopy to view the cells in blood samples in their laboratory to create the still images published in the journal Science Signalling this week.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our immune system / vaccines section for the latest news on this subject.

The research is published in the journal Science Signalling this week.

Manchester University

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Signal uncovered that prevents the immune system from spinning out of control

Main Category: Immune System / Vaccines
Also Included In: Allergy
Article Date: 25 Jul 2013 - 0:00 PDT Current ratings for:
Signal uncovered that prevents the immune system from spinning out of control

A team led by a University of Arizona researcher has discovered a previously unknown mechanism that prevents the immune system from going into overdrive, shedding light not only on how our body controls its response to pathogens but on conditions such as autoimmune diseases, allergies and chronic inflammation as well.

The group found a protein previously believed to only play a role in blood clotting acts as a negative feedback signal, telling defense cells to calm down, thereby preventing an immune reaction from spiraling out of control. The results, which could lead to new therapeutics for a variety of disorders caused by a faulty immune response, are published in the scientific journal Immunity.

When pathogens such as viruses or bacteria invade our body, the immune system reacts by producing a flurry of chemical signals, known as chemokines that act as a bugle call recruiting specialized defender cells to the scene, such as macrophages, which devour the intruders. This first line of defense is known as inflammation.

"Inflammation is a necessary defense mechanism - you can't live without it," said Sourav Ghosh, assistant professor in the department of cellular and molecular medicine at the UA College of Medicine and lead author of the study. "On the flip side, if you can't regulate the inflammation, it can damage the body."

To be effective against pathogens, yet prevent collateral damage from the body's own defenses, the immune system has to maintain just the right level of inflammation, explained Ghosh, who is also a member of the University of Arizona Cancer Center and theUA's BIO5 Institute.

"It needs to be not too high and not too low," he said. "The question had always been, how does the immune system maintain that balance? Our discovery explains this."

All organisms, even plants, have some kind of immune system at their disposal that acts as an army fighting against the onslaught of microbes, viruses, parasites and other pathogens in the environment. Vertebrates have evolved the most sophisticated arsenal of "soldiers" and "weapons," relying on two powerful lines of defense: a non-specific, or innate, immune response and the specific, or adaptive, immune response.

In the non-specific response, the immune system throws a first wave of countermeasures at the intruders, consisting of - among other things - aggressive chemicals, destructive enzymes and kamikaze-like neutrophils, specialized white blood cells that destroy the attackers by devouring them, killing themselves in the process.

"First you don't know who the enemy is, so you fire everywhere with your eyes closed," Ghosh explained. "But once you know the enemy, you need to shut off this first response firing and bring in the special ops so to speak."

The special ops come in the form of the specific immunity, capable of targeting pathogens very precisely, taking out the enemy in a sniper-like fashion, while sparing friendly microbes and cells belonging to the body. Most importantly, this portion of the immune system contains cells that remember every attacker trying to conquer an organism throughout its lifetime, allowing the immune system to summon the most effective, specialized task force to counter a pathogen it recognizes from a previous battle.

"The innate immune response is necessary to activate the adaptive response," Ghosh said. "But once activated, there has to be a mechanism that prevents the adaptive response from going into overdrive. From previous studies, we knew there had to be some kind of signal that does this, but we didn't know the nature of that signal. Now we do."

Two kinds of immune cells turned out to be the key players in mediating the immune response: the dendritic cells, so called because of the tree-like branches they grow during their development ("dendron" means "tree" in Greek), which belong to the first wave of defense; and the T-cells, so named because they mature in the thymus gland of the second, which are part of the second wave, the specific immune response.

"The dendritic cells activate the T-cells," Ghosh explained. "Only when they're activated, not when they're resting, do the T-cells produce this protein that we knew only from the blood clotting process, called Protein S."

The T-cells display Protein S on their surface, where it makes contact with a receptor the dendritic cells carry on their surface. This triggers a signal telling the dendritic cell to stop switching on T-cells, causing the immune response to slow down.

"We thought about which cells could be the source of that signal," said Carla Rothlin of the School of Medicine at Yale University, who led the study together with Ghosh. "You don't want to put the brakes on from the very beginning, or otherwise the immune response would never amount to anything. But you want to slow it down once it starts going too fast."

"We figured that once the specific response is underway, you don't really need the unspecific response anymore, so the T-cells appeared to be the best candidates for the source of this signal."

To test their hypothesis, the researchers studied the immune response in mice in which the gene coding for Protein S had been deactivated selectively in their T-cells, rendering them unable to communicate with the dendritic cells.

As expected, these mice were unable to regulate their immune response, resulting in higher levels of inflammation compared to their normal counterparts.

To assess the relevance of their findings to humans, Ghosh and his co-workers then studied blood from patients with inflammatory bowel diseases such as ulcerative colitis and Crohn's disease. Consistent with their previous results, patients suffering from increased inflammation had lower levels of Protein S in their blood stream compared to healthy volunteers.

The findings could help scientists and clinicians develop better treatments for inflammatory diseases, for example by designing drugs that substitute for insufficient Protein S. According to Ghosh, patients with inflammatory bowel disease are 20 times more likely to develop colon cancer, further underlining the significance of this study.

Study co-author Dr. Jonathan Leighton reported anecdotal evidence from the clinical practice that is in line with the dual roles Protein S is believed to play.

"Patients with inflammatory bowel disease can develop blood clots if they have active disease," said Leighton, a UA alumnus who holds the Chair of the Division of Gastroenterology at Mayo Clinic in Scottsdale, Ariz. "From a clinical standpoint, we think that three factors predispose to inflammation in inflammatory bowel disease - genetic, environmental and the immune system. This research is exciting because it focuses on the immune system. No one has found a consistent inflammatory pathway that explains all the clinical manifestations, and it may be that different pathways are affected in different patients. We don't understand how it all relates quite yet, but this study is a step toward a better understanding that will ultimately help us treat patients more effectively."

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our immune system / vaccines section for the latest news on this subject.

The study was funded by the National Institutes of Health (NIH) grants R01 AI077058, R01 AI089824, CA95060 and T32 AI007019); the Crohn's and Colitis Foundation; the American Heart Association; the American Asthma Foundation; the Lupus Research Institute; a CONICET Postdoctoral Fellowship and a Gershon-Trudeau Postdoctoral Fellowship.

University of Arizona

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