Th1 lymphocytes are critical in the cellular immune response and they play an important role in host defense systems for intracellular microbial agents and viruses. Th1 cell promoting factors include IFNγ, IL-12 (p70), and the activation of the transcription factors STAT1 and STAT4. The expression of the Interleukin-12 receptor β2-chain (IL-12Rβ2) is required for Th1 cellular differentiation since it allows for the responsiveness to IL-12 on the Th1 cells. IL-12R activation increases IFNγ expression through STAT1 signals to induce the Th1 master regulator T-bet. This further increases IFNγ expression while suppressing IL-4. Th1 cells are the primary source for the inflammatory cytokines lFNγ, IL-2, and TNFβ (LTα). Th1 cytokines stimulate macrophages, lymphocytes, and PMNs in the destruction of bacterial pathogens. These cytokines also help foster the development of cytotoxic lymphocytes (CTL & NK cells) that are responsible for the cell-mediated immune response against viruses and tumor cells. Due to the central role of Th1 cells in immune system, over activation or misdirected activation also makes them key players in Th1-dominant autoimmune diseases such as multiple sclerosis, type-1 diabetes, rheumatoid arthritis, and delayed-type hypersensitivity responses.
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