Please use this identifier to cite or link to this item: https://doi.org/10.1084/jem.20171704
Title: Bhlhe40 is an essential repressor of IL-10 during Mycobacterium tuberculosis infection
Authors: Huynh, JP
Lin, CC
Kimmey, JM
Jarjour, NN
Schwarzkopf, EA
Bradstreet, TR
Shchukina, I
Shpynov, O
Weaver, CT
Taneja, R 
Artyomov, MN
Edelson, BT
Stallings, CL
Issue Date: 1-Jul-2018
Publisher: Rockefeller University Press
Citation: Huynh, JP, Lin, CC, Kimmey, JM, Jarjour, NN, Schwarzkopf, EA, Bradstreet, TR, Shchukina, I, Shpynov, O, Weaver, CT, Taneja, R, Artyomov, MN, Edelson, BT, Stallings, CL (2018-07-01). Bhlhe40 is an essential repressor of IL-10 during Mycobacterium tuberculosis infection. Journal of Experimental Medicine 215 (7) : 1823-1838. ScholarBank@NUS Repository. https://doi.org/10.1084/jem.20171704
Abstract: © 2018 Huynh et al. The cytokine IL-10 antagonizes pathways that control Mycobacterium tuberculosis (Mtb) infection. Nevertheless, the impact of IL-10 during Mtb infection has been difficult to decipher because loss-of-function studies in animal models have yielded only mild phenotypes. We have discovered that the transcription factor basic helix-loop-helix family member e40 (Bhlhe40) is required to repress Il10 expression during Mtb infection. Loss of Bhlhe40 in mice results in higher Il10 expression, higher bacterial burden, and early susceptibility similar to that observed in mice lacking IFN-γ. Deletion of Il10 in Bhlhe40−/− mice reverses these phenotypes. Bhlhe40 deletion in T cells or CD11c+ cells is sufficient to cause susceptibility to Mtb. Bhlhe40 represents the first transcription factor found to be essential during Mtb infection to specifically regulate Il10 expression, revealing the importance of strict control of IL-10 production by innate and adaptive immune cells during infection. Our findings uncover a previously elusive but significant role for IL-10 in Mtb pathogenesis.
Source Title: Journal of Experimental Medicine
URI: https://scholarbank.nus.edu.sg/handle/10635/155221
ISSN: 00221007
15409538
DOI: 10.1084/jem.20171704
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