A role for CD28 in lymphopenia-induced proliferation of CD4 T cells

Karin A. Hagen, Christina T. Moses, Erin F. Drasler, Kelly M. Podetz-Pedersen, Stephen C. Jameson, Alexander Khoruts

Research output: Contribution to journalArticlepeer-review

50 Scopus citations


The peripheral mechanisms that regulate the size and the repertoire of the T cell compartment during recovery from a lymphopenic state are incompletely understood. In particular, the role of costimulatory signals, such as those provided by CD28, which have a critical importance for the immune response toward foreign Ags in nonlymphopenic animals, has been unclear in lymphopenia-induced proliferation (LIP). In this study, we show that accumulation of highly divided CD4 T cells characterized by great potential to make IFN-γ is significantly delayed in the absence of B7:CD28 costimulation during LIP. Furthermore, CD28-sufficient CD4 T cells show great competitive advantage over CD28-deficient CD4 T cells when transferred together into the same lymphopenic hosts. Administration of CTLA-4-Ig removed this competitive advantage. Interestingly, CTLA-4-Ig treatment resulted in modest inhibition of LIP by CD28-deficient responders, suggesting that some of its effects may be independent of mere B7 blockade.

Original languageEnglish (US)
Pages (from-to)3909-3915
Number of pages7
JournalJournal of Immunology
Issue number6
StatePublished - Sep 15 2004


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