by GE Healthcare
When helper cells aren’t helpful
[Via Eureka! Science News]
Current research suggests that T helper-type 1 (Th1) cells, previously thought to mediate autoimmunity, may actual inhibit the development of experimental immune encephalomyelitis (EAE), a mouse model of multiple sclerosis (MS), by suppressing Th17 cells. The related report by Wildbaum et al, “Antigen-specific CD25-Foxp3-IFN-γ high CD4+ T cells restrain the development of experimental allergic encephalomyelitis by suppressing Th17 cells,” appears in the June 2010 issue of The American Journal of Pathology.
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I really feel for the poor person who has to write up releases dealing with immunology. Immunology has its own nomenclature that is not really penetrable if you do not live in the field. The writer actually does a pretty good job, even if this is jargon-rich:
Current research suggests that T helper-type 1 (Th1) cells, previously thought to mediate autoimmunity, may actual inhibit the development of experimental immune encephalomyelitis (EAE), a mouse model of multiple sclerosis (MS), by suppressing Th17 cells. The related report by Wildbaum et al, “Antigen-specific CD25-Foxp3-IFN-γ high CD4+ T cells restrain the development of experimental allergic encephalomyelitis by suppressing Th17 cells,” appears in the June 2010 issue of The American Journal of Pathology. MS is believed to be an autoimmune disorder, where damage to the nervous system is caused by the patient’s own immune system. Th1 cells, which secrete high levels of the inflammatory mediator interferon-γ(IFN-γ), have been previously implicated as being pathogenic in autoimmune diseases such as MS. More recent data, however, suggests that antigen-specific T cells that produce the molecule IL-17 (Th17 cells) initiate the inflammatory process in EAE.
As IFN-γ suppresses Th17 cell development, a group led by Dr. Nathan Karin at the Rappaport Family Institute for Research in the Medical Sciences hypothesized that IFN-γ-expressing T cells may serve as regulatory cells to block the development of autoimmunity. They discovered that EAE development depended on the death of these antigen-specific IFN-γ-expressing regulatory cells at early stages of disease and that inhibiting the killing of these cells at early stages of EAE suppressed disease development. In addition, overexpression of IFN-γ in EAE-mediating T cells caused them to act instead as antigen-specific regulatory cells. Thus, early suppression of Th17 cells may block the development of autoimmunity.
So, Th17 cells, which are probably responsible for some auto-immune diseases, can be regulated by a specific subset of T helper cells. So, inhibiting the death of these specific cells stopped the development of a model for autoimmune diseases. Sounds about as complicated as immunology is today.
When I first took immunology, we had T-cells, B-cells, lymphocytes, leucocytes macrophages and maybe a few other types. All mainly discernible in the microscope.
Now we separate at out cells based on surface markets. Not just 1 or 2 but sometimes up to 13 or more. And our ability to find specific subsets has gotten so much better as we have gained greater experience modulating the immune system.
But come on. Can’t we start coming up with real names for some of these? Antigen-specific CD25-Foxp3-IFN-γ high CD4+ T cells. It’s like chemistry nomenclature, simply adding on more markers.
Perhaps we need to come up with a standard name for these, like we do for interleukins.