Th1 Differentiation Pathway
Click on one of the links shown in the Explore Pathways box below to see the processes that promote Th1 differentiation and the transcription factors, secreted molecules, and some of the cell surface markers that distinguish a differentiated Th1 cell from the other T helper cell subtypes.
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Overview of Th1 Differentiation
CD4+ T cells play a central role in the adaptive immune response. Following T cell receptor activation and co-stimulation by antigen-presenting cells, naïve CD4+ T cells differentiate into one of several lineages of T helper cell subtypes depending primarily on cytokines present in the extracellular environment. In the presence of IL-27 and IL-12, naïve CD4+ T cells differentiate into T helper type 1 (Th1) cells. Th1 cells are required for host defense against intracellular viral and bacterial pathogens. IL-27 promotes early commitment to the Th1 lineage by activating STAT1 signaling to induce expression of the Th1-specific transcription factor, T-bet, and inhibit expression of the Th2-specific transcription factor, GATA-3. T-bet serves as the master regulator of Th1 differentiation. It promotes expression of both IL-12 R beta 2 and IFN-gamma, the signature cytokine produced by Th1 cells. IL-12 R beta 2 dimerizes with IL-12 R beta 1 to form a functional IL-12 receptor complex. This renders the cells responsive to IL-12, which is critical for Th1 differentiation. IL-12 signaling stimulates STAT4-dependent expression of IFN-gamma and IL-18 R beta. Formation of the IL-18 receptor complex allows IL-18 signaling to further drive IFN-gamma expression through AP-1-dependent transcription. In addition to activation of STAT4, IL-12, along with IFN-gamma, activates STAT1 to maintain T-bet expression and Th1-specific cytokine production.
To learn more, please visit our Th1 Cells Research Area.
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