Journal
IMMUNITY
Volume 13, Issue 3, Pages 291-301Publisher
CELL PRESS
DOI: 10.1016/S1074-7613(00)00029-7
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Funding
- NIAID NIH HHS [AI 37554] Funding Source: Medline
- NIGMS NIH HHS [GM 56689] Funding Source: Medline
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI037554] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R01GM056689] Funding Source: NIH RePORTER
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Proliferation and differentiation of CD4(+) T cells are often correlated, but it is not clear whether they are mechanistically linked. When antigen-specific T cells are present at high frequency in vivo, they all respond to antigenic peptide stimulation by expressing activation markers, but only a subset begins to proliferate. However, noncycling cells may synthesize the effector cytokine IFN gamma even though their cell cycle is blocked in G1. These data show that proliferation and effector function are not rigidly linked in T cells. Instead, CD4(+) T cells have the flexibility to engage in or bypass clonal expansion based on the integration of multiple signals, including the frequency of other responding T cells.
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