IL-21 Receptor Signaling Is Essential for Optimal CD4+ T Cell Function and Control of Mycobacterium tuberculosis Infection in Mice
In: The Journal of Immunology, Jg. 199 (2017-10-15), S. 2815-2822
Online
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Zugriff:
In this study, we determined the role of IL-21R signaling in Mycobacterium tuberculosis infection, using IL-21R knockout (KO) mice. A total of 50% of M. tuberculosis H37Rv–infected IL-21R KO mice died in 6 mo compared with no deaths in infected wild type (WT) mice. M. tuberculosis–infected IL-21R KO mice had enhanced bacterial burden and reduced infiltration of Ag-specific T cells in lungs compared with M. tuberculosis–infected WT mice. Ag-specific T cells from the lungs of M. tuberculosis–infected IL-21R KO mice had increased expression of T cell inhibitory receptors, reduced expression of chemokine receptors, proliferated less, and produced less IFN- γ, compared with Ag-specific T cells from the lungs of M. tuberculosis–infected WT mice. T cells from M. tuberculosis–infected IL-21R KO mice were unable to induce optimal macrophage responses to M. tuberculosis. This may be due to a decrease in the Ag-specific T cell population. We also found that IL-21R signaling is associated with reduced expression of a transcriptional factor Eomesodermin and enhanced functional capacity of Ag-specific T cells of M. tuberculosis–infected mice. The sum of our findings suggests that IL-21R signaling is essential for the optimal control of M. tuberculosis infection.
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IL-21 Receptor Signaling Is Essential for Optimal CD4+ T Cell Function and Control of Mycobacterium tuberculosis Infection in Mice
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Autor/in / Beteiligte Person: | Paidipally, Padmaja ; Nurieva, Roza ; Tripathi, Deepak ; Venkatasubramanian, Sambasivan ; Tvinnereim, Amy R. ; Vankayalapati, Ramakrishna ; Welch, Elwyn ; Satyanarayana Swamy Cheekatla |
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Zeitschrift: | The Journal of Immunology, Jg. 199 (2017-10-15), S. 2815-2822 |
Veröffentlichung: | The American Association of Immunologists, 2017 |
Medientyp: | unknown |
ISSN: | 1550-6606 (print) ; 0022-1767 (print) |
DOI: | 10.4049/jimmunol.1601231 |
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