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Marked Expansion of Foxp3+, Vbeta5+ Regulatory T cells during Chronic Lymphocytic Choriomeningitis Virus (LCMV) Infection
Author(s) -
Punkosdy George,
Ahmed Rafi,
Shevach Ethan
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.858.4
Subject(s) - foxp3 , lymphocytic choriomeningitis , clone (java method) , biology , immunology , immune system , population , granzyme b , chronic infection , virology , cd8 , medicine , gene , genetics , environmental health
In order to analyze the potential role that Treg play in viral infection, we have compared the phenotypic changes in Treg during the course of acute (Armstrong) and chronic (Clone 13) LCMV infection in mice. Foxp3+ Treg increased in frequency among CD4+ cells and expressed increased levels of CTLA‐4, GITR, ICOS, and PD‐1 specifically during Clone 13 infection suggesting an increase in Treg activation during chronic infection. Analysis of TCR Vbeta usage revealed a marked increase in a subpopulation of Treg expressing the TCR Vbeta5 during Clone 13 infection (from 7% to ∼25% of total Foxp3+ cells in uninfected or Armstrong infected and Clone 13 infected mice, respectively). Surprisingly, no change in the frequency of CD4+ Vbeta5+Foxp3− was noted during either Armstrong or Clone 13 infections. The Vbeta5+Foxp3+ Treg expressed additional markers that have been associated with Treg activation including high levels of CD101, CD103 and granzyme B. The increase in frequency of Vbeta5+ Treg was due to the preferential expansion of this population early in infection, as determined by BrdU uptake and Ki‐67 staining, and not differentiation of Vbeta5+Foxp3− T cells. We are now in the process of determining the antigen specificity of the Vbeta5+Foxp3+ T cells and determining the specific role these cells may play in the regulating the immune response during chronic viral infection.