Journal
JOURNAL OF INFECTIOUS DISEASES
Volume 211, Issue 12, Pages 2014-2022Publisher
OXFORD UNIV PRESS INC
DOI: 10.1093/infdis/jiu839
Keywords
Chlamydia; genital infection; oviduct pathology; TNF receptor 1; TNF receptor 2; CD8(+) T cells
Categories
Funding
- Midwestern University
- College of Health Sciences
- National Institutes of Health [1R03AI088342, 1R15AI101920]
- American Heart Association Midwest Affiliate [13SDG17310011]
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Background. We demonstrated previously that tumor necrosis factor a (TNF-alpha)- producing Chlamydia-specific CD8(+) T cells cause oviduct pathological sequelae. Methods.aEuro integral In the current study, we used wild-type C57BL/6J (WT) mice with a deficiency in genes encoding TNF receptor superfamily member 1a (TNFR1; TNFR1 knockout [KO] mice), TNF receptor superfamily member 1b (TNFR2; TNFR2 KO mice), and both TNFR1 and TNFR2 (TNFR1/2 double KO [DKO] mice) and mix-match adoptive transfers of CD8(+) T cells to study chlamydial pathogenesis. Results.aEuro integral TNFR1 KO, TNFR2 KO, and TNFR1/2 DKO mice displayed comparable clearance of primary or secondary genital Chlamydia muridarum infection but significantly reduced oviduct pathology, compared with WT animals. The Chlamydia-specific total cellular cytokine response in splenic and draining lymph nodes and the antibody response in serum were comparable between the WT and KO animals. However, CD8(+) T cells from TNFR2 KO mice displayed significantly reduced activation (CD11a expression and cytokine production), compared with TNFR1 KO or WT animals. Repletion of TNFR2 KO mice with WT CD8(+) T cells but not with TNFR2 KO CD8(+) T cells and repletion of TNFR1 KO mice with either WT or TNFR1 KO CD8(+) T cells restored oviduct pathology to WT levels in both KO groups. Conclusions.aEuro integral Collectively, these results demonstrate that TNFR2-bearing CD8(+) T cells and TNFR1-bearing non-CD8(+) T cells contribute significantly to oviduct pathology following genital chlamydial infection.
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