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Regulation of CD4 cell memory by PSGL‐1
Author(s) -
Lin Melissa Michelle,
Bradley Linda M
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.846.1
Subject(s) - selectin , microbiology and biotechnology , effector , cd8 , biology , cytotoxic t cell , glycosylation , t cell , immune system , immunology , cell adhesion molecule , in vitro , biochemistry
Long‐term immunity against infections depends upon the generation and maintenance of memory T cells. CD4 cells play a pivotal role in the induction of immunity to influenza viruses by regulating the responses of both CD8 cells and B cells. A fundamental feature of CD4 cells is their capacity to generate functionally distinct subsets that confer different protective functions. Recently, we found that the capacity to generate glycosylated, biologically active selectin ligands is acquired by a subset of CD4 effectors after influenza virus infection and that P‐selectin is induced in the lungs. In this study, we used CD4 cells from OT‐II TCR transgenic mice that lack the fucosyl transferases necessary for glycosylation (FucT IV/IV) of selectins to investigate the role of those receptors in the CD4 cell response to influenza. We demonstrate that selectin binding is not required to generate a normal primary response to PR8 influenza virus. However, FucT IV/VII −/− OT‐II cells exhibit elevated production of IFN‐gamma, increased homeostatic turnover, and a failure to undergo secondary expansion as memory cells. Our data support the overall hypothesis that mechanisms regulated by adhesion molecules can be essential for the delivery of signals which control CD4 cell responses and their homeostatic maintenance, thereby sanctioning the development and persistence of memory. This research is supported by NIH Grant P01 AI046530.