Journal
ANNUAL REVIEW OF IMMUNOLOGY, VOL 38
Volume 38, Issue -, Pages 705-725Publisher
ANNUAL REVIEWS
DOI: 10.1146/annurev-immunol-103019-085803
Keywords
CD4(+) T cell differentiation; T follicular helper cell; T effector cell; memory T cell; transcription factor; CD4(+) subset
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Funding
- NIAID NIH HHS [R01 AI108626] Funding Source: Medline
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The discovery of CD4(+) T cell subset-defining master transcription factors and framing of the Th1/Th2 paradigm ignited the CD4(+) T cell field. Advances in in vivo experimental systems, however, have revealed that more complex lineage-defining transcriptional networks direct CD4(+) T cell differentiation in the lymphoid organs and tissues. This review focuses on the layers of fate decisions that inform CD4(+) T cell differentiation in vivo. Cytokine production by antigen-presenting cells and other innate cells influences the CD4(+) T cell effector program [e.g., T helper type 1 (Th1), Th2, Th17]. Signals downstream of the T cell receptor influence whether individual clones bearing hallmarks of this effector program become T follicular helper cells, supporting development of B cells expressing specific antibody isotypes, or T effector cells, which activate microbicidal innate cells in tissues. These bifurcated, parallel axes allow CD4(+) T cells to augment their particular effector program and prevent disease.
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