Journal
JOURNAL OF IMMUNOLOGY
Volume 167, Issue 10, Pages 5636-5644Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.167.10.5636
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Funding
- NIAID NIH HHS [T32 AI07313, P01 AI35296] Funding Source: Medline
- NIGMS NIH HHS [R01 GM54706] Funding Source: Medline
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CD4(+) T cells that undergo multiple rounds of cell division during primary Ag challenge in vivo produce IL-2 on secondary Ag rechallenge, whereas cells that fail to progress through the cell cycle are anergic to restimulation. Anti-CTLA-4 mAb treatment during primary Ag exposure increases cell cycle progression and enhances recall Ag responsiveness; however, simultaneous treatment with rapamycin, an inhibitor of the mammalian target of rapamycin and potent antiproliferative agent, prevents both effects. The data suggest that cell cycle progression plays a primary role in the regulation of recall Ag responsiveness in CD4(+) T cells in vivo. CTLA-4 molecules promote clonal anergy development only indirectly by limiting cell cycle progression during the primary response.
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