Toll-Like Receptor 3 Deficiency Leads to Altered Immune Responses to Chlamydia trachomatis Infection in Human Oviduct Epithelial Cells-Reference-Cited by-同舟云学术

Toll-Like Receptor 3 Deficiency Leads to Altered Immune Responses to Chlamydia trachomatis Infection in Human Oviduct Epithelial Cells

Published:2019-10 Issue:10 Volume:87 Page:
ISSN:0019-9567
Container-title:Infection and Immunity
language:en
Short-container-title:Infect Immun

Author:

Xu Jerry Z.¹,Kumar Ramesh¹,Gong Haoli²,Liu Luyao²,Ramos-Solis Nicole¹,Li Yujing³,Derbigny Wilbert A.¹^ORCID

Affiliation:

1. Department of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, Indiana, USA

2. Xiangya Second Hospital, Central South University, Changsha, Hunan Province, People’s Republic of China

3. Department of Medical and Molecular Genetics, Indiana University School of Medicine, Indianapolis, Indiana, USA

Abstract

Reproductive tract pathology caused by Chlamydia trachomatis infection is an important global cause of human infertility. To better understand the mechanisms associated with Chlamydia -induced genital tract pathogenesis in humans, we used CRISPR genome editing to disrupt Toll-like receptor 3 (TLR3) function in the human oviduct epithelial (hOE) cell line OE-E6/E7 in order to investigate the possible role(s) of TLR3 signaling in the immune response to Chlamydia .

Funder

HHS | National Institutes of Health

Publisher

American Society for Microbiology

Subject

Infectious Diseases,Immunology,Microbiology,Parasitology

Link

https://journals.asm.org/doi/pdf/10.1128/IAI.00483-19

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