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The T-helper type 1 cell differentiation pathway describes the process by which naïve CD4+ T cells differentiate into Th1 cells. This differentiation is triggered by antigen presentation via MHC class II on antigen-presenting cells, along with co-stimulatory signals and a cytokine environment rich in interleukin-12 (IL-12) and interferon-gamma (IFN-γ). The transcription factor T-bet is the master regulator of this process, enhancing expression of IFN-γ and further promoting the Th1 phenotype, which is essential for defense against intracellular pathogens and in mediating inflammation. Aberrations in this pathway are implicated in autoimmunity, chronic inflammation, infection susceptibility, and some cancers[1][2][3][4][5][6].
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