Jagadeesh Bayry
CD4+ T cells are highly heterogeneous with respect to their phenotype, secretion of effector molecules, transcription factors and functions. In the periphery, CD4+ T cells can be polarized into distinct subsets under the influence of antigen presenting cells and cytokine milieu. Recently, Th17 cells that express lineage-specific transcription factor RORC (ROR?t in mice) and produce cytokines IL-17A and IL-17F were identified as distinct lineage of CD4+ T cells [1]. Th17 cells are important to clear extracellular bacteria and fungi. However, when tolerance mechanisms breach, these Th17 cells can also mediate inflammation and can play critical role in the pathogenesis of several autoimmune diseases. In fact, a large number of autoimmune and inflammatory diseases such as multiple sclerosis, rheumatoid arthritis, asthma, lupus, psoriasis and others are characterized by an aberrant activation of Th17 cells and hyper-expression of Th17 inflammatory mediators such as IL-17, IL-21, IL-22, CCL20 and GM-CSF [2,3]. Therefore, Th17 cells are one of the potential targets to treat these diseases.
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Journal of Blood & Lymph received 443 citations as per Google Scholar report
