Journal
JOURNAL OF IMMUNOLOGY
Volume 190, Issue 11, Pages 5485-5495Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1202951
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Funding
- Division of Intramural Research of the National Institute of Allergy and Infectious Diseases/National Institutes of Health
- German Research Foundation [TRR60, GRK1045-2]
- National Institutes of Health [R01 CA167053]
- United Kingdom Medical Research Council [U117581330]
- Medical Research Council [MC_U117581330] Funding Source: researchfish
- MRC [MC_U117581330] Funding Source: UKRI
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Friend virus infection of mice induces the expansion and activation of regulatory T cells (Tregs) that dampen acute immune responses and promote the establishment and maintenance of chronic infection. Adoptive transfer experiments and the expression of neuropilin-1 indicate that these cells are predominantly natural Tregs rather than virus-specific conventional CD4(+) T cells that converted into induced Tregs. Analysis of Treg TCR V beta chain usage revealed a broadly distributed polyclonal response with a high proportionate expansion of the V beta 5(+) Treg subset, which is known to be responsive to endogenous retrovirus-encoded superantigens. In contrast to the major population of Tregs, the V beta 5(+) subset expressed markers of terminally differentiated effector cells, and their expansion was associated with the level of the antiviral CD8(+) T cell response rather than the level of Friend virus infection. Surprisingly, the expansion and accumulation of the V beta 5(+) Tregs was IL-2 independent but dependent on TNF-alpha. These experiments reveal a subset-specific Treg induction by a new pathway.
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