IL-17

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IL-17

Postby dignan » Mon Dec 31, 2007 10:01 am

IL-17 has been researched quite a bit over the last couple of years at least. Here is some interesting evidence of its involvment in MS.



Interleukin-17 Production in Central Nervous System-Infiltrating T Cells and Glial Cells Is Associated with Active Disease in Multiple Sclerosis.

Am J Pathol. 2007 Dec 21
Tzartos JS, Friese MA, Craner MJ, Palace J, Newcombe J, Esiri MM, Fugger L.
From the Departments of Neuropathology* and Clinical Neurology, John Radcliffe Hospital, and the Medical Research Council Human Immunology Unit, the Neurosciences Group, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, University of Oxford, Oxford, United Kingdom; NeuroResource, University College London, Institute of Neurology, London, United Kingdom; and the Department of Clinical Immunology, Aarhus University Hospital, Skejby Sygehus, Denmark.

Recent findings in the animal model for multiple sclerosis (MS), experimental autoimmune encephalomyelitis, implicate a novel CD4(+) T-cell subset (TH17), characterized by the secretion of interleukin-17 (IL-17), in disease pathogenesis. To elucidate its role in MS, brain tissues from patients with MS were compared to controls.

We detected expression of IL-17 mRNA (by in situ hybridization) and protein (by immunohistochemistry) in perivascular lymphocytes as well as in astrocytes and oligodendrocytes located in the active areas of MS lesions. Further, we found a significant increase in the number of IL-17(+) T cells in active rather than inactive areas of MS lesions. Specifically, double immunofluorescence showed that IL-17 immunoreactivity was detected in 79% of T cells in acute lesions, 73% in active areas of chronic active lesions, but in only 17% of those in inactive lesions and 7% in lymph node control tissue. CD8(+), as well as CD4(+), T cells were equally immunostained for IL-17 in MS tissues. Interestingly, and in contrast to lymph node T cells, no perivascular T cells showed FoxP3 expression, a marker of regulatory T cells, at any stage of MS lesions.

These observations suggest an enrichment of both IL-17(+)CD4(+) and CD8(+) T cells in active MS lesions as well as an important role for IL-17 in MS pathogenesis, with some remarkable differences from the experimental autoimmune encephalomyelitis model.

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Postby Lyon » Mon Dec 31, 2007 10:23 am

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Last edited by Lyon on Wed Nov 30, 2011 6:10 pm, edited 1 time in total.
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Postby TwistedHelix » Thu Jan 03, 2008 5:18 am

Just to confuse things, I found this piece of research today about the role of IL -17 which suggests a beneficial effect on B cells – in mice, anyway – by slowing down their activity for long enough to allow other regulatory cells to work:

Public release date: 2-Jan-2008
Contact: Troy Goodman
tdgoodman@uab.edu
205-934-8938
University of Alabama at Birmingham

BIRMINGHAM, Ala. - Investigators at the University of Alabama at Birmingham (UAB) have identified the previously unknown role of a chemical 'messenger' leading to autoimmune disorders like rheumatoid arthritis and lupus.

The messenger is the naturally occurring chemical interleukin 17 (IL-17), an immunity protein.

UAB researchers pinpointed an unknown role IL-17 plays in autoimmune and inflammatory responses, aside from its commonly known effects within immunity. Future research will home in on IL-17's unwanted actions and preserve its benefits within the immune system.

The new findings are published in the journal Nature Immunology.

In the study, UAB scientists blocked messenger signals from the IL-17 protein to the immune system of mice. This disruption significantly reduced the number of white blood cells, namely disease-causing B cells, clustered in the mice's spleen.

The number of B-cell clusters dropped from 17 percent to 2 percent when the IL-17 protein signals were blocked, the study authors said.

The drop was a clear sign that IL-17 plays a major role on shaping B cells' ability to create more and more disease-causing antibodies.

"The effect of IL-17 to slow down B cells, thereby enhancing their interaction with other immune regulatory cells a new and exciting discovery," said John D. Mountz, M.D., Ph.D., UAB professor of medicine and senior author on the study.

"This is surprising since previously IL-17 was thought to increase, but not decrease, cell motion. Now the effects of IL-17 on B cells can be explored more fully," Mountz said.

Many types of B cells make up the human immune system, which is regulated to sense and fight infection without attacking normal, healthy tissue. In autoimmune diseases that regulatory process becomes imbalanced.

"Knowing more about IL-17's ability to regulate unwanted B-cell migration will generate new ideas in the ongoing search for better drug targets in preventing and treating autoimmune disease," said Hui-Chen Hsu, Ph.D. an assistant professor in the UAB Division of Clinical Immunology and Rheumatology and lead author on the study.

###

The research team included UAB investigators from the departments of Medicine, Cell Biology, Pathology, Microbiology and Dermatology and from Children's Hospital of Pittsburgh and the University of Tennessee Health Science Center in Memphis.

Funding for the study came from the Arthritis Foundation, the American College of Rheumatology, the U.S. Department of Veterans Affairs, the National Institutes of Health and Tokyo-based Daiichi Sankyo Co., Ltd.


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