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- W349641292 abstract "IL-36 cytokines are members of the IL-1 family of cytokines that stimulate dendritic cells and T cells leading to enhanced T helper 1 responses in vitro and in vivo; however, their role in host defense has not been fully addressed thus far. The objective of this study was to examine the role of IL-36R signaling in the control of mycobacterial infection, using models of systemic attenuated M. bovis BCG infection and virulent aerogenic M. tuberculosis infection. IL-36γ expression was increased in the lung of M. bovis BCG infected mice. However, IL-36R deficient mice infected with M. bovis BCG showed similar survival and control of the infection as compared to wild-type mice, although their lung pathology and CXCL1 response were transiently different. While highly susceptible TNF-α deficient mice succumbed with overwhelming M. tuberculosis infection, and IL-1RI deficient mice showed intermediate susceptibility, IL-36R-deficient mice controlled the infection, with bacterial burden, lung inflammation and pathology, similar to wild-type controls. Therefore, IL-36R signaling has only limited influence in the control of mycobacterial infection." @default.
- W349641292 created "2016-06-24" @default.
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- W349641292 date "2015-05-07" @default.
- W349641292 modified "2023-10-18" @default.
- W349641292 title "Limited Contribution of IL-36 versus IL-1 and TNF Pathways in Host Response to Mycobacterial Infection" @default.
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- W349641292 doi "https://doi.org/10.1371/journal.pone.0126058" @default.
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