Posts tagged immune system
Articles and news from the latest research reports.
Why do we get older? When do we die and why? Is there a life without ageing? For centuries, science has been fascinated by these questions. Now researchers from Kiel (Germany) have examined why the polyp Hydra is immortal – and unexpectedly discovered a link to ageing in humans. The study carried out by Kiel University together with the University Medical Center Schleswig-Holstein (UKSH) will be published this week in the Proceedings of the National Academy of Sciences of the United States of America (PNAS). It was funded by the German Research Foundation DFG.
New MS drug proves effective where others have failed
A drug which ‘reboots’ a person’s immune system has been shown to be an effective treatment for multiple sclerosis (MS) patients who have already failed to respond to the first drug with which they were treated (a ‘first-line’ therapy), as well as affected individuals who were previously untreated. The results of these two phase III clinical trials were published today in the journal The Lancet.
The new studies, sponsored by Genzyme (a Sanofi company) and Bayer Schering Pharma, showed that alemtuzumab significantly reduces the number of attacks (or relapses) experienced by people with MS compared to interferon beta-1a (known commercially as Rebif). This was seen both in patients who had not previously received any treatment (drug-naïve) and those who have continued to show disease activity whilst taking an existing treatment for MS.
Sleep loss links to illness studied
Insomniacs know the pattern all too well. You toss and turn at night, kept awake by the rave down the street, stress from work, the snores of a significant other.
After a stretch of restless evenings, you wake up with a sore throat or a fever. You’re no longer just tired - you’re also sick.
Physicians know this pattern, too. Constant lack of sleep has long been linked with a laundry list of unpleasant conditions: cardiovascular disease, diabetes, weight gain, infectious illnesses and even death.
While it’s common knowledge that a full night of rest helps ward off ailments, what largely remains a mystery is exactly how sleep loss triggers the biological mechanisms that in turn bring about illness - like the common cold.
A 2009 study of 153 men and women, for example, showed that those who slept fewer than seven hours on average per night were about three times more likely to develop a cold than those with at least eight hours of sleep daily.
Even a small difference in sleep quality made a big difference in health, the Carnegie Mellon University study showed. Participants who actually slept less than 92 percent of the time between the time they laid down to sleep and when they woke up were 5.5 times more likely to develop a cold than those who stayed asleep 98 percent or more of the time, according to the researchers.
Study Suggests Immune System Can Boost Nerve Regrowth
Modulating immune response to injury could accelerate the regeneration of severed peripheral nerves, a new study in an animal model has found. By altering activity of the macrophage cells that respond to injuries, researchers dramatically increased the rate at which nerve processes regrew.
Influencing the macrophages immediately after injury may affect the whole cascade of biochemical events that occurs after nerve damage, potentially eliminating the need to directly stimulate the growth of axons using nerve growth factors. If the results of this first-ever study can be applied to humans, they could one day lead to a new strategy for treating peripheral nerve injuries that typically result from trauma, surgical resection of tumors or radical prostectomy.
“Both scar formation and healing are the end results of two different cascades of biological processes that result from injuries,” said Ravi Bellamkonda, Carol Ann and David D. Flanagan professor in the Wallace H. Coulter Department of Biomedical Engineering and member of the Regenerative Engineering and Medicine Center at Georgia Tech and Emory University. “In this study, we show that by manipulating the immune system soon after injury, we can bias the system toward healing, and stimulate the natural repair mechanisms of the body.”
Beyond nerves, researchers believe their technique could also be applied to help regenerate other tissue – such as bone. The research was supported by the National Institutes of Health (NIH), and reported online Sept. 26, 2012, by the journal Biomaterials.
Barrow researchers make breakthrough on immune system and brain tumors
In what could be a breakthrough in the treatment of deadly brain tumors, a team of researchers from Barrow Neurological Institute and Arizona State University has discovered that the immune system reacts differently to different types of brain tissue, shedding light on why cancerous brain tumors are so difficult to treat.
The large, two-part study, led by Barrow research fellow Sergiy Kushchayev, MD under the guidance of Dr. Mark Preul, Director of Neurosurgery Research, was published in the Sept. 14 issue of Cancer Management and Research
The study explores the effects of immunotherapy on malignant gliomas, cancerous brain tumors that typically have a poor prognosis.
What the researchers discovered was that immune cells of the brain and of the blood exhibit massive rearrangements when interacting with a malignant glioma under treatment. Essentially, the study demonstrates that the complex immune system reacts differently in different brain tissues and different regions of the brain, including tumors.
"This is the first time that researchers have conducted a regional tissue study of the brain and a malignant glioma to show that these immune cells do not aggregate or behave in the same way in their respective areas of the brain," says Dr. Preul. "This means that effective treatment in one area of the brain may not be effective in another area. In fact, it could even cause other regions of the tumor to become worse."
The results of the study provide important insight into why clinical trials involving immunotherapies on glioma patients may not be working.
(Source: eurekalert.org)
Unique Genetic Marker Discovery May Help Predict Multiple Sclerosis Relapse
Scientists may be one step closer to predicting the uncertain course of relapsing-remitting multiple sclerosis (MS), a disease that can lay dormant for months or years, thanks to the discovery of a unique genetic marker. The marker, detailed by researchers in the August edition of The Journal of Immunology, is the first of its kind to be directly linked to MS.
The study, supported by funding from both the National Institutes of Health (NIH) and the Ohio State Center for Clinical and Translational Science (CCTS) was conducted by a team of scientists with The Ohio State University using blood samples from patients with MS, as well as mouse models. Researchers uncovered the molecule miR-29, while working to identify a biomarker in the blood that could indicate if a patient had an ongoing inflammatory response, such as MS.
“Our research was inspired by the knowledge gap that existed between microRNA and MS, as well as the unpredictable nature of MS,” said Kristen Smith, Ph.D., principal investigator, who received a “mentorship grant” to conduct the study alongside senior scientists at The Ohio State University Wexner Medical Center. “By identifying a unique marker associated with MS, we hope to inspire a relatively noninvasive test that could identify and predict the course of the disease, helping clinicians tailor therapies to disease progression.”
Source: newswise
Brain tumours: artificial stimulation of the immune system could mean less aggressive treatments
Brain metastases are common secondary complications of other types of cancer, particularly lung, breast and skin cancer. The body’s own immune response in the brain is rendered powerless in the fight against these metastases by inflammatory reactions. Researchers at the MedUni Vienna have now, for the first time, precisely characterised the brain’s immune response to infiltrating metastases. This could pave the way to the development of new, less aggressive treatment options.
“The active phagocytes are quite literally overwhelmed by the tumour and even the white blood cells are too weak to fight off these metastases on their own; they have to be stimulated before they can have any effect,” explains oncologist Matthias Preusser from the University Department of Internal Medicine I and the Comprehensive Cancer Center (CCC), a joint institution operated by the MedUni Vienna and the Vienna General Hospital.
Brain tissue was obtained for investigation from autopsies carried out on people who had metastatic disease secondary to breast, lung or skin cancer. These are also the most common types of primary tumour. Brain metastases develop because they spread from the tumours into other parts of the body right up to the brain.
The scientists at the Clinical Institute of Neurology, the Centre for Brain Research, the CCC and the University Department of Internal Medicine I have discovered that metastases in the brain do encounter a wall of phagocytes, but it is too weak to successfully arrest the tumour’s development. To do this, white blood cells (lymphocytes) need to be mobilised in greater numbers as the second instance of the immune defence system.
These findings could lead to new therapeutic strategies being developed that will aim to increase the activation of white blood cells or other parts of the immune system – perhaps through medication such as antibody treatments or vaccines.
300 to 400 patients with brain metastases are treated each year at the MedUni Vienna. The standard treatment in most cases is radiotherapy to the head or generalised irradiation of the brain – which is associated with certain risks and possible side effects. Only in very few cases are drug-based treatment methods available for certain types of cancer. Says Preusser: “Our findings could represent an important step towards the development of less aggressive forms of treatment.”
(Source: meduniwien.ac.at)
Discovery of Immune Cells That Protect Against Multiple Sclerosis Offers Hope for New Treatment
ScienceDaily (Aug. 16, 2012) — In multiple sclerosis, the immune system attacks nerves in the brain and spinal cord, causing movement problems, muscle weakness and loss of vision. Immune cells called dendritic cells, which were previously thought to contribute to the onset and development of multiple sclerosis, actually protect against the disease in a mouse model, according to a study published by Cell Press in the August issue of the journal Immunity. These new insights change our fundamental understanding of the origins of multiple sclerosis and could lead to the development of more effective treatments for the disease.
"By transfusing dendritic cells into the blood, it may be possible to reduce autoimmunity," says senior study author Ari Waisman of University Medical Center of Johannes Gutenberg University Mainz. "Beyond multiple sclerosis, I can easily imagine that this approach could be applied to other autoimmune diseases, such as inflammatory bowel disease and psoriasis."
In an animal model of multiple sclerosis known as experimental autoimmune encephalomyelitis (EAE), immune cells called T cells trigger the disease after being activated by other immune cells called antigen-presenting cells (APCs). Dendritic cells are APCs capable of activating T cells, but it was not known whether dendritic cells are the APCs that induce EAE.
In the new study, Waisman and his team used genetic methods to deplete dendritic cells in mice. Unexpectedly, these mice were still susceptible to EAE and developed worse autoimmune responses and disease clinical scores, suggesting that dendritic cells are not required to induce EAE and other APCs stimulate T cells to trigger the disease. The researchers also found that dendritic cells reduce the responsiveness of T cells and lower susceptibility to EAE by increasing the expression of PD-1 receptors on T cells.
"Removing dendritic cells tips the balance toward T cell-mediated autoimmunity," says study author Nir Yogev of University Medical Center of Johannes Gutenberg University Mainz. "Our findings suggest that dendritic cells keep immunity under check, so transferring dendritic cells to patients with multiple sclerosis could cure defects in T cells and serve as an effective intervention for the disease."
Source: Science Daily
Unique Cell Type Implicated in Multiple Sclerosis
The new study, published in Science Translational Medicine, shows that one effect of daclizumab is to thin the ranks of lymphoid tissue inducer (LTi) cells. These cells are known to promote the development of lymph nodes and related tissues during fetal life, but their role during adulthood has been unclear. The new study marks the first time that LTi cells have been implicated in any human autoimmune disorder.
"While further study is required to confirm the role of LTi cells in autoimmunity, our results point to the cells as a promising target for the development of new drugs to treat autoimmune disorders," said Bibiana Bielekova, M.D., an investigator at NIH’s National Institute of Neurological Disorders and Stroke (NINDS).
Autoantibodies damage blood vessels in the brain — important factor in development of dementia
July 31, 2012
The presence of specific autoantibodies of the immune system is associated with blood vessel damage in the brain. These findings were made by Marion Bimmler, a graduate engineer of medical laboratory diagnostics at the Max Delbrück Center for Molecular Medicine Berlin-Buch and Dr. Peter Karczewski of the biotech company E.R.D.E.-AAK-Diagnostik GmbH in studies on a rat model. The researchers’ results suggest that autoimmune mechanisms play a significant role in the pathogenesis and progression of Alzheimer’s and vascular dementia.
(MR Angiography/Copyright: MDC)
Antibodies are the defense molecules of the body’s immune system against foreign invaders. If the antibodies cease to distinguish between “foreign” and “self”, they attack the cells of the own body, and are thus referred to as autoantibodies. These can trigger autoimmune diseases. Using MR angiography and other methods, Marion Bimmler and her colleagues have now shown that the autoantibodies bind to specific surface proteins (alpha1 andrenergic receptors) of vascular cells and thereby damage the blood vessels of the brain. The reason: The autoantibodies generate a continual stimulation of the receptor and at the same time trigger an increase in intracellular calcium ion levels. As a result, the blood vessel walls thicken, and blood flow to the brain is disturbed.
First Encouraging Results after Removal of Autoantibodies by Immunoadsorption
In earlier studies, Marion Bimmler and her research team examined blood samples of patients with Alzheimer’s or vascular dementia and showed that half of them had comparable autoantibodies. A first clinical trial together with Charité – Universitätsmedizin Berlin is currently ongoing with a collective of patients with Alzheimer’s or vascular dementia. The patients were divided into two groups – a small group whose autoantibodies were removed from the blood via immunoadsorption and a control group that did not receive this treatment. Until now, over an observation period of 6 and subsequently 12 months, the patient group who had undergone immunoadsorption improved in their memory performance and in their ability to cope with their everyday lives. In contrast, the condition of the patients who did not receive immunoadsorption treatment and continued to have autoantibodies in their blood deteriorated dramatically. Now the researchers are planning further clinical trials with larger numbers of patients.
Provided by Helmholtz Association of German Research Centres
Source: medicalxpress.com