|Posted by Simone on June 5, 2013 at 3:10 PM||comments (0)|
The same factor in our immune system that is instrumental in enabling us to fight off severe and dangerous inflammatory ailments is also a player in doing the opposite at a later stage, causing the suppression of our immune response.
Why and how this happens and what can be done to mediate this process for the benefit of mankind is the subject of an article published online in the journal Immunity by Ph.D. student Moshe Sade-Feldman and Prof. Michal Baniyash of the Lautenberg Center for General and Tumor Immunology at the Institute for Medical Research Israel-Canada at the Hebrew University Faculty of Medicine.
Chronic inflammation poses a major global health problem and is common to different pathologies -- such as autoimmune diseases (diabetes, rheumatoid arthritis, lupus and Crohn's), chronic inflammatory disorders, chronic infections (HIV, leprosy, leishmaniasis) and cancer. Cumulative data indicate that at a certain stage of each of these diseases, the immune system becomes suppressed and results in disease progression.
In their previous work, the Hebrew University researchers had shown that in the course of chronic inflammation, unique immune system cells with suppressive features termed myeloid derived suppressor cells (MDSCs) are generated in the bone marrow and migrate into the body's organs and blood, imposing a general immune suppression.
A complex network of inflammatory compounds persistently secreted by the body's normal or cancerous cells support MDSC accumulation, activation and suppressive functions. One of these compounds is tumor necrosis factor-a (TNF-a), which under acute immune responses (short episodes), displays beneficial effects in the initiation of immune responses directed against invading pathogens and tumor cells.
However, TNF-a also displays harmful features under chronic responses, as described in pathologies such as rheumatoid arthritis, psoriasis, type II diabetes, Crohn's disease and cancer, leading to complications and disease progression. Therefore, today several FDA- approved TNF-a blocking reagents are used in the clinic for the treatment of such pathologies.
What has remained unclear until now, however, is just how TNF-a plays its deleterious role in manipulating the host's immune system towards the generaation of a suppressive environment.
In their work, the Hebrew University researchers discovered the mechanisms underlying the TNF-a function, a key to controlling this factor and manipulating it, perhaps, for the benefit of humans. Using experimental mouse models, they showed unequivocally how TNF-a is critical in the induction of immune suppression generated during chronic inflammation. The TNF-a was seen to directly affect the accumulation and suppressive function of MDSCs, leading to an impaired host's immune responses as reflected by the inability to respond against invading pathogens or against developing tumors.
Further, the direct role of how TNF-a works in humans was mimicked by injecting the FDA-approved anti-TNF-a drug, etanercept, into mice at the exacerbated stage of an inflammatory response, when MDSC accumulation was observed in the blood. The etanercept treatment changed the features of MDSCs and abolished their suppressive activity, leading to the restoration of the host's immune function.
Taken together, the results show clearly how the TNF-a-mediated inflammatory response, whether acute or chronic, will dictate its beneficial or harmful consequence on the immune system. While during acute inflammation TNF-a is vital for immediate immune defense against pathogens and clearance of tumor cells, during chronic inflammation -- under conditions where the host is unable to clear the pathogen or the tumor cells -- TNF-a is harmful due to the induction of immune suppression.
|Posted by Simone on June 14, 2011 at 1:52 AM||comments (0)|
☀ Men's Health Month
☀ Home Safety Month
☀ National Aphasia Awareness Month
☀ Cataract Awareness Month
☀ National Scleroderma Awareness Month
☀ National Cancer Survivor's Day (5)
☀ World Sickle Cell Day (19)
☀ National HIV Testing Day (27)
☀ Men's Health Week (13-19)
|Posted by Simone on May 19, 2011 at 8:26 PM||comments (0)|
|Posted by Simone on May 11, 2011 at 9:45 PM||comments (0)|
ScienceDaily (May 9, 2011) — Five million people worldwide suffer from the chronic rheumatic disease SLE, systemic lupus erythematosus. Together with rheumatologists, researchers at Lund University in Sweden are on the way to developing a new test that could resolve a number of question marks surrounding the disease and in the long run improve the lives of SLE patients.
Their research is published in the next issue of the journal Molecular and Cellular Proteomics.
"At present, it can take up to a year before a patient is diagnosed with SLE. This is because the symptoms are diffuse and are often mistaken for other diseases. However, with this blood-based test, it is possible to determine quickly whether someone has the disease or not," says Christer Wingren, associate professor in Immunotechnology at CREATE Health, Lund University.
The test can also determine how far the disease has progressed. There are three different variants of SLE, and all require different treatment. With current methods, it is often difficult to find out which variant a patient has, which makes it difficult for doctors to prescribe the right medication. A third advantage of the new technique is that it also makes it possible to predict when the disease will become active.
"Characteristic of SLE is that the disease goes in waves, or flares. Without warning, the disease can flare up and put the patient out of action for a long time. With our test, we hope to be able to predict when an episode is about to happen and in this way prevent it using the right medication," explains Christer Wingren.
If all goes well, hospitals could start using the technique in two to three years.
The test itself comprises a small chip, smaller than a little fingernail, on which the researchers create a grid pattern, known as an array, using specially selected antibodies. The antibodies serve as 'capture molecules'; by placing a drop of blood on the chip, the antibodies bind the proteins, or biomarkers, in the body. In this way, a unique 'fingerprint' is produced for each patient, which reflects the disease.
"In our article, we show which pattern of biomarkers (the 'fingerprint') to look for. From a technical point of view, we get a large number of data signals that say whether the marker is present and in what quantity. These measurements are then entered into a computer, which can present them to the doctors in a way that is easy to understand. It is this fingerprint which doctors could use in the future in clinical practice," explains Christer Wingren, who has spent most of the past decade developing the technique, and the past two years adapting it for SLE in particular.
According to Christer Wingren, a number of researchers around the world have attempted to develop something similar, but without success. The Lund researchers' success in the task is partly due to them having found a way to make the antibodies stable and thus more functional. The method has also become highly sensitive.
In order for the research to benefit patients, a number of key biomarker signatures, which form the basis for the test, have been patented. The findings have also been transferred to a newly started company, Immunovia, which was founded by Christer Wingren and three of his colleagues at the Department of Immunotechnology.
The research has its origins in the cancer research that Christer Wingren and a number of other researchers at the translational cancer centre CREATE Health work on. Together with Carl Borrebaeck, Dr Wingren uses an equivalent technological platform that can detect and diagnose different types of cancer. They have very promising data for predicting breast cancer recurrence and diagnosing pancreatic cancer.
The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by Lund University, via AlphaGalileo.
|Posted by Simone on April 20, 2011 at 1:22 AM||comments (0)|
How does methotrexate induce hair loss?
To understand methotrexate induced hair loss, let us first understand the life cycle of a hair. Hair is made by a hair follicle. Each hair has a growth phase known as anagen & a resting phase known as telogen. A hair follicle grows hair for upto 3- 4 years. This is the end of the life cycle of the hair. It falls, the follicle then rests for about 3- 4 months & starts making a new hair. Normally most scalp hair (about 85%) are in the growth phase & only about 100 scalp hair fall every day. Methotrexate triggers a process called telogen effluvium wherein a greater proportion of hairs suddenly enter the resting phase. The hair thus stops growing & fall out.
How can one take care of methotrexate induced hair loss?
|Posted by Simone on April 10, 2011 at 12:34 AM||comments (0)|
☂ National Donate Life Month
☂ National Autism Awareness Month
☂ National Minority Health Month
☂ Alcohol Awareness Month
☂ World Health Day (7)
☂ World Meningitis Day (24)
☂ National Infant Immunization Week (23-30)
|Posted by Simone on April 10, 2011 at 12:23 AM||comments (0)|
March - National Nutrition Month
February - American Heart Month
January - Cervical Health Awareness Month
December - Safe Toys and Gifts Month
See full postings on http://www.icantfitmyjeans.blogspot.com
|Posted by Simone on April 7, 2011 at 6:17 PM||comments (0)|
What is World Health Day?
"World Health Day is celebrated on 7 April to mark the founding of WHO. Each year, the Organization selects a key health issue, and encourages people from all ages and all backgrounds to hold events that highlight the signiﬁ cance of this issue for good health and well-being. World Health Day provides a unique opportunity for communities from across the world to come together for one day to promote actions that can improve our health."
WHD Brochure > http://www.who.int/world-health-day/2011/world-health-day2011-brochure.pdf
World Health Day Website > http://www.who.int/world-health-day/2011/en/index.html
News Releases from WHO Website