What is it about?
Autoimmunity results from the dysregulation of the immune system leading to tissue damage. The specific T cell derived cytokine milieu within the site of inflammation is important during the disease process. Dendritic cell (DCs) subsets that activate pathogenic or protective regulatory T cells are important in mediating autoimmunity. We have found that Th17 cells, once thought to only act as pathogenic cells through production of IL-17, have been shown to have regulatory properties as well with co-production of the anti-inflammatory cytokine IL-10 by regulatory Th17 cells termed as Treg17 cells. Study of the inflammatory process following encounter with agents that stimulate the innate immune responses such as mycobacterial adjuvants such as Bacille Calmette-Guérin (BCG) vaccine opens a new horizon for the discovery of therapeutic agents to protect from autoimmune diseases. These agents function through TLR ligands that interacting with Toll-like receptors (TLR) on antigen-presenting cells such as DCs. Microbial agents such as BCG or Freund's adjuvant (CFA) that induce a Th17 response are protective in models of autoimmune diseases particularly EAE and type 1 diabetes (T1D). The induction of innate immunity by these microbial products alters the balance in the cytokine microenvironment and may be responsible for modulation of the inflammation and protection from autoimmunity.
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Why is it important?
The induction of innate immunity by microbial products that alter the balance in the cytokine microenvironment and may be responsible for modulation of the inflammation and protection from autoimmunity.
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This page is a summary of: Therapeutic Benefits of Regulating Inflammation in Autoimmunity, Inflammation & Allergy - Drug Targets, September 2008, Bentham Science Publishers,
DOI: 10.2174/187152808785748155.
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