TH17 blocking drugs for uveitis

Addtional information on drugs and medications.

Moderators: Mike Bartolatz, kwork

Post Reply
Mike Bartolatz
Posts: 6595
Joined: Fri Feb 06, 2004 9:58 pm

TH17 blocking drugs for uveitis

Post by Mike Bartolatz »

AIN457
the interlukin 12 FAMILY composed of IL12,IL23 and IL27 impact the production of TH17 cells which in turn produce IL17 an inflammatory cytokine implicated in many autoimmune disease processes and uveitis. Th17 blocking drugs are currently in study for uveitis. so far so good is the response by Dr Foster at the Ocular Immunology and Uveitis Foundation. Lets hope there are no adverse side effects and that they produce long term remission from Uveitis and related disease processes.

Wishing all the very best,
Mike
Mike Bartolatz
Moderator
Mike Bartolatz
Posts: 6595
Joined: Fri Feb 06, 2004 9:58 pm

Re: TH17 blocking drugs for uveitis

Post by Mike Bartolatz »

1: Immunol Res. 2008;41(2):87-102. Links
Th17 cells: a new fate for differentiating helper T cells.Chen Z, O'Shea JJ.
Molecular Immunology and Inflammation Branch, National Institutes of Arthritis, Musculoskeletal and Skin Diseases, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892, USA. zchen@utu.fi

Classically naïve CD4(+) have been thought to differentiate into two possible lineages, T helper 1 (Th1) or T helper 2 (Th2) cells. Within this paradigm the pathogenesis of autoimmunity was suggested to predominantly relate to Th1 cells and the production of IFN-gamma. However, there were many aspects of this model that did not seem to fit, not the least of which was that IFN-gamma was protective in some models of autoimmunity. During the past 2 years, remarkable progress has been made to characterize a new lineage of helper T cells. Designated Th17 cells, this lineage selectively produces proinflammatory cytokines including IL-17, IL-21, and IL-22. In the mouse, the differentiation of this new lineage is initiated by TGFbeta-1 and IL-6 and IL-21, which activate Stat3 and induce the expression of the transcription factor retinoic acid-related orphan receptor (RORgammat). IL-23, which also activates Stat3, apparently serves to maintain Th17 cells in vivo. In human cells, IL-1, IL-6, and IL-23 promote human Th17 differentiation, but TGFbeta-1 is reportedly not needed. Emerging data have suggested that Th17 plays an essential role in the host defense against extracellular bacteria and fungi and in pathogenesis of autoimmune diseases. Selectively targeting the Th17 lineage may be beneficial for the treatment of inflammatory and autoimmune diseases.

PMID: 18172584 [PubMed - indexed for MEDLINE]
Mike Bartolatz
Moderator
Post Reply