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CCL5 modulates mucosal immunity against chlamydial infection
Author(s) -
Lillard James W,
Singh Udai P,
Sakthivel Senthilkumar K,
Dove Terri M,
Singh Shailesh,
Igietseme Joseph U
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.853.13
Subject(s) - ccl5 , immunology , immunity , chemokine , immune system , biology , humoral immunity , spleen , cellular immunity , antibody , chlamydia , t cell , il 2 receptor
Following genital chlamydial infection, an early T helper type 1 (Th1)‐associated immune response precedes the activation of recruitment of specific Th1 cells bearing distinct chemokine receptors, subsequently leading to the clearance of Chlamydia. We have shown that CCR5, a receptor for CCL5, is crucial for protective chlamydial immunity. Our laboratory and others have also demonstrated that CCL5 deficiencies found in man and animals can increase the susceptibility and progression of infectious diseases by modulating mucosal immunity. These findings suggest the CCR5‐CCL5 axis is critical for chlamydial immunity. We hypothesized CCL5 is required for protective humoral and cellular Chlamydia immunity. The present study revealed that CCR5 and CCL5 mRNAs are elevated in the spleen, iliac lymph nodes (ILNs), and genital mucosa following Chlamydia challenge. Antibody (Ab)‐mediated inhibition of CCL5 during genital chlamydial infection suppressed humoral and Th1 > Th2 cellular responses by splenic‐, ILN‐, and genital mucosa‐derived lymphocytes. Antigen (Ag)‐specific proliferative responses of CD4 + T cells from spleen, ILNs, and genital organs also declined after CCL5 inhibition. The suppression of these responses correlated with delayed clearance of the chlamydial infection. These results indicate that chlamydial immunity is mediated by Th1 immune responses driven in part by CCL5.