Enhanced upper genital tract pathologies by blocking Tim-3 and PD-L1 signaling pathways in mice intravaginally infected with <it>Chlamydia muridarum</it>
<p>Abstract</p> <p>Background</p> <p>Although Tim-3 & PD-L1 signaling pathways play important roles in negatively regulating immune responses, their roles in chlamydial infection have not been evaluated.</p> <p>Methods</p> <p>Neutralization a...
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BMC
2011-12-01
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Online Access: | http://www.biomedcentral.com/1471-2334/11/347 |
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author | Peng Bo Lu Chunxue Tang Lingli Yeh I-Tien He Zhimin Wu Yimou Zhong Guangming |
author_facet | Peng Bo Lu Chunxue Tang Lingli Yeh I-Tien He Zhimin Wu Yimou Zhong Guangming |
author_sort | Peng Bo |
collection | DOAJ |
description | <p>Abstract</p> <p>Background</p> <p>Although Tim-3 & PD-L1 signaling pathways play important roles in negatively regulating immune responses, their roles in chlamydial infection have not been evaluated.</p> <p>Methods</p> <p>Neutralization antibodies targeting Tim-3 and PD-L1 were used to treat mice. Following an intravaginal infection with <it>C. muridarum </it>organisms, mice with or without the dual antibody treatment were compared for live chlamydial organism shedding from the lower genital tract and inflammatory pathology in the upper genital tract.</p> <p>Results</p> <p>Mice treated with anti-Tim-3 and anti-PD-L1 antibodies displayed a time course of live organism shedding similar to that of mice treated with equivalent amounts of isotype-matched IgG molecules. The combined antibody blocking failed to alter either the lower genital tract cytokine or systemic humoral and cellular adaptive responses to <it>C. muridarum </it>infection. However, the antibody blocking significantly enhanced <it>C. muridarum</it>-induced pathologies in the upper genital tract, including more significant hydrosalpinx and inflammatory infiltration in uterine horn and oviduct tissues.</p> <p>Conclusions</p> <p>The Tim-3 and PD-L1-mediated signaling can significantly reduce pathologies in the upper genital tract without suppressing immunity against chlamydial infection, suggesting that Tim-3 and PD-L1-mediated negative regulation may be manipulated to attenuate tubal pathologies in women persistently infected with <it>C. trachomatis </it>organisms.</p> |
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issn | 1471-2334 |
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spelling | doaj.art-337d1e55dc8a4d34ac191c4ed7c748142022-12-22T01:19:06ZengBMCBMC Infectious Diseases1471-23342011-12-0111134710.1186/1471-2334-11-347Enhanced upper genital tract pathologies by blocking Tim-3 and PD-L1 signaling pathways in mice intravaginally infected with <it>Chlamydia muridarum</it>Peng BoLu ChunxueTang LingliYeh I-TienHe ZhiminWu YimouZhong Guangming<p>Abstract</p> <p>Background</p> <p>Although Tim-3 & PD-L1 signaling pathways play important roles in negatively regulating immune responses, their roles in chlamydial infection have not been evaluated.</p> <p>Methods</p> <p>Neutralization antibodies targeting Tim-3 and PD-L1 were used to treat mice. Following an intravaginal infection with <it>C. muridarum </it>organisms, mice with or without the dual antibody treatment were compared for live chlamydial organism shedding from the lower genital tract and inflammatory pathology in the upper genital tract.</p> <p>Results</p> <p>Mice treated with anti-Tim-3 and anti-PD-L1 antibodies displayed a time course of live organism shedding similar to that of mice treated with equivalent amounts of isotype-matched IgG molecules. The combined antibody blocking failed to alter either the lower genital tract cytokine or systemic humoral and cellular adaptive responses to <it>C. muridarum </it>infection. However, the antibody blocking significantly enhanced <it>C. muridarum</it>-induced pathologies in the upper genital tract, including more significant hydrosalpinx and inflammatory infiltration in uterine horn and oviduct tissues.</p> <p>Conclusions</p> <p>The Tim-3 and PD-L1-mediated signaling can significantly reduce pathologies in the upper genital tract without suppressing immunity against chlamydial infection, suggesting that Tim-3 and PD-L1-mediated negative regulation may be manipulated to attenuate tubal pathologies in women persistently infected with <it>C. trachomatis </it>organisms.</p>http://www.biomedcentral.com/1471-2334/11/347<it>Chlamydia muridarum</it>Oviduct pathologyTim-3 &PD-L1 signaling pathways |
spellingShingle | Peng Bo Lu Chunxue Tang Lingli Yeh I-Tien He Zhimin Wu Yimou Zhong Guangming Enhanced upper genital tract pathologies by blocking Tim-3 and PD-L1 signaling pathways in mice intravaginally infected with <it>Chlamydia muridarum</it> BMC Infectious Diseases <it>Chlamydia muridarum</it> Oviduct pathology Tim-3 & PD-L1 signaling pathways |
title | Enhanced upper genital tract pathologies by blocking Tim-3 and PD-L1 signaling pathways in mice intravaginally infected with <it>Chlamydia muridarum</it> |
title_full | Enhanced upper genital tract pathologies by blocking Tim-3 and PD-L1 signaling pathways in mice intravaginally infected with <it>Chlamydia muridarum</it> |
title_fullStr | Enhanced upper genital tract pathologies by blocking Tim-3 and PD-L1 signaling pathways in mice intravaginally infected with <it>Chlamydia muridarum</it> |
title_full_unstemmed | Enhanced upper genital tract pathologies by blocking Tim-3 and PD-L1 signaling pathways in mice intravaginally infected with <it>Chlamydia muridarum</it> |
title_short | Enhanced upper genital tract pathologies by blocking Tim-3 and PD-L1 signaling pathways in mice intravaginally infected with <it>Chlamydia muridarum</it> |
title_sort | enhanced upper genital tract pathologies by blocking tim 3 and pd l1 signaling pathways in mice intravaginally infected with it chlamydia muridarum it |
topic | <it>Chlamydia muridarum</it> Oviduct pathology Tim-3 & PD-L1 signaling pathways |
url | http://www.biomedcentral.com/1471-2334/11/347 |
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