Premium
CCL5 modulates pneumococcal surface protein A (PspA) peptide‐specific T helper cell responses
Author(s) -
SINGH RAJESH,
SINGH SHAILESH,
SINGH UDAI P,
BRILES DAVID E,
LILLARD JAMES W
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.853.15
Subject(s) - ccl5 , immune system , t cell , biology , streptococcus pneumoniae , spleen , immunology , chemokine , il 2 receptor , microbiology and biotechnology , antibiotics
Pneumococcal surface protein A (PspA) is a cell surface protein present on Streptococcus pneumonia . We have previously shown that CCL5 blockade alters PspA‐specific humoral and cellular pneumococcal immunity, during S.pneumoniae strain EF3030‐induced carriage. Here we show that CCL5 blockade decreases the number of IFNγ + and increases the number of IL10 + CD4 + T cells in the spleen and nasal tract (NT) during the recognition phase of the pneumococcal adaptive immune response. Residues 287 to 378 of PspA caused the greatest cytokine secretion and proliferation recall responses by splenic and NT CD4 + T cells isolated from F 1 (B6 × BALB/c) mice. CCL5 inhibition significant reduction in the capacity for IFNγ, but not TNFα or IL4, secretion by mucosal and systemic PspA peptide specific CD4 + T cells. CCL5 blockade also resulted in a significant increase in PspA peptide specific IL 10 producing CD4 + T cells compared to control Ab treated mice. In support CCL5 deficiency resulted in a higher number of CCL5 + CD11b + CD11c + and IL‐10 + CD11b + cells, but lower number of CCR5 + CD11b + CD11c − cells in the spleen compared to similarly challenged mice that received control Ab. Together, these changes corresponded with the transition from pneumococcal carriage to lethal pneumonia. These data suggest that CCL5 is an essential factor for the induction and maintenance of protective pneumococcal immunity.