Journal
JOURNAL OF IMMUNOLOGY
Volume 180, Issue 2, Pages 1148-1157Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.180.2.1148
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Funding
- NCI NIH HHS [CA103642, R01 CA103642, P30 CA023108, R01 CA103642-05] Funding Source: Medline
- NIAID NIH HHS [R01 AI069943-02, R01 AI069943] Funding Source: Medline
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Memory CD8(+) T cell responses have been considered to be independent of CD80/CD86-CD28 costimulation. However, recall responses are often severely blunted in CD28(-/-) mice. Whether this impairment represents a requirement for CD28 costimulation for proper memory CD8(+) T cell development or a requirement during the recall response is unknown. Furthermore, how CD28 costimulation affects the phenotype and function of memory CD8(+) T cells has not been characterized in detail. In this study, we investigate these questions by studying the role of the CD28 costimulatory pathway in memory CD8(+) T cell responses to acute and persistent DNA virus infections. Memory CD8(+) T cells against vaccinia virus (VV) infection which develop without CD28 costimulation exhibit lower expression of differentiation markers CD27 and CD122 (IL-15R beta). These memory CD8(+) T cells also fail to produce IL-2. Our data indicate that for an optimal recall response, CD28 costimulation is required both for T cell priming and also during the recall response. Similar requirements were observed for memory CD8(+) T cell responses during persistent infection with murine gammaherpesvirus 68 (MHV-68) infection, indicating CD28 may play the same role in both acute and persistent infections. Finally, we show deficits in the recall response are restored by IL-2 signaling during recall, but not during priming. The data presented show that CD28 costimulation not only controls the magnitude of the primary response but also affects development of memory CD8(+) T cells and is required during the recall response in addition to initial T cell priming.
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