IL-21/IL-21R Signaling Aggravated Respiratory Inflammation Induced by Intracellular Bacteria through Regulation of CD4 T Cell Subset Responses.

J Immunol

Tianjin Key Laboratory of Cellular and Molecular Immunology and Key Laboratory of the Educational Ministry of China, Department of Immunology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin 300070, People's Republic of China

Published: April 2021

The IL-21/IL-21R interaction plays an important role in a variety of immune diseases; however, the roles and mechanisms in intracellular bacterial infection are not fully understood. In this study, we explored the effect of IL-21/IL-21R on chlamydial respiratory tract infection using a chlamydial respiratory infection model. The results showed that the mRNA expression of IL-21 and IL-21R was increased in -infected mice, which suggested that IL-21 and IL-21R were involved in host defense against lung infection. IL-21R mice exhibited less body weight loss, a lower bacterial burden, and milder pathological changes in the lungs than wild-type (WT) mice during lung infection. The absolute number and activity of CD4 T cells and the strength of Th1/Th17 responses in IL-21R mice were significantly higher than those in WT mice after lung infection, but the Th2 response was weaker. Consistently, IL-21R mice showed higher mRNA expression of Th1 transcription factors (T-bet/STAT4), IL-12p40, a Th17 transcription factor (STAT3), and IL-23. The mRNA expression of Th2 transcription factors (GATA3/STAT6), IL-4, IL-10, and TGF-β in IL-21R mice was significantly lower than that in WT mice. Furthermore, the administration of recombinant mouse IL-21 aggravated chlamydial lung infection in C57BL/6 mice and reduced Th1 and Th17 responses following lung infection. These findings demonstrate that IL-21/IL-21R may aggravate chlamydial lung infection by inhibiting Th1 and Th17 responses.

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Source
http://dx.doi.org/10.4049/jimmunol.2001107DOI Listing

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