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CD62L high IL7R high CD4+ T cells with memory potential are primed early following infection with Leishmania major
Author(s) -
Colpitts Sara Lynn,
Dalton Nicole,
Rodriguez Carlos,
Scott Phillip
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.855.5
Subject(s) - population , biology , immunology , homing (biology) , leishmania major , interleukin 21 , cytotoxic t cell , memory t cell , t cell , immune system , leishmania , medicine , in vitro , genetics , ecology , parasite hosting , environmental health , world wide web , computer science
The development of vaccines against diseases requiring cell‐mediated immunity has been hampered by our lack of understanding of the memory T cells required to maintain immunity. Our lab has shown that a population of CD62L high central memory T (T CM ) cells mediates long‐term immunity to the intracellular protozoan Leishmania major. Our current studies are aimed at how TCM cells develop following infection. Using both polyclonal and transgenic donor T cells, we have identified two populations of Leishmania‐specific CD4 + T cells that emerge early following infection. One population has undergone greater than six rounds of division, expresses low levels of CD62L, and produces IFNγ in accordance with an effector phenotype (T EFF ). We believe the second population to be themselves, or the precursors of, T CM cells based on their expression of high levels of CD62L and CCR7, which mediate lymph node (LN)‐homing, the IL‐7R, which promotes memory T cell survival, and the production of IL‐2. Sorting the two populations and restimulating them in vivo with antigen revealed only the CD62L high cells could survive, consistent with their potential to become memory T cells. We have also found that while both cell types are primed in the first few days following infection, TEFF cells emerge from cells resident in the draining LN at the time of infection, and cells that are recruited into the LN at later times contribute to the T CM population.