scholarly journals IRF1 and BATF: key drivers of type 1 regulatory T-cell differentiation

2017 ◽  
Vol 14 (8) ◽  
pp. 652-654 ◽  
Author(s):  
Sophia Giang ◽  
Antonio La Cava
2013 ◽  
Vol 110 (19) ◽  
pp. 7802-7807 ◽  
Author(s):  
C. Wu ◽  
C. Pot ◽  
L. Apetoh ◽  
T. Thalhamer ◽  
B. Zhu ◽  
...  

2015 ◽  
Vol 21 (6) ◽  
pp. 638-646 ◽  
Author(s):  
Ivan D Mascanfroni ◽  
Maisa C Takenaka ◽  
Ada Yeste ◽  
Bonny Patel ◽  
Yan Wu ◽  
...  

2015 ◽  
Vol 195 (9) ◽  
pp. 4154-4161 ◽  
Author(s):  
Ruan Zhang ◽  
Christopher M. Borges ◽  
Martin Y. Fan ◽  
John E. Harris ◽  
Laurence A. Turka

2020 ◽  
Vol 117 (24) ◽  
pp. 13740-13749 ◽  
Author(s):  
Yusuke Higuchi ◽  
Jun-ichirou Yasunaga ◽  
Yu Mitagami ◽  
Hirotake Tsukamoto ◽  
Kazutaka Nakashima ◽  
...  

Human T cell leukemia virus type 1 (HTLV-1) is the etiologic agent of a T cell neoplasm and several inflammatory diseases. A viral gene, HTLV-1 bZIP factor (HBZ), induces pathogenic Foxp3-expressing T cells and triggers systemic inflammation and T cell lymphoma in transgenic mice, indicating its significance in HTLV-1–associated diseases. Here we show that, unexpectedly, a proinflammatory cytokine, IL-6, counteracts HBZ-mediated pathogenesis. Loss of IL-6 accelerates inflammation and lymphomagenesis in HBZ transgenic mice. IL-6 innately inhibits regulatory T cell differentiation, suggesting that IL-6 functions as a suppressor against HBZ-associated complications. HBZ up-regulates expression of the immunosuppressive cytokine IL-10. IL-10 promotes T cell proliferation only in the presence of HBZ. As a mechanism of growth promotion by IL-10, HBZ interacts with STAT1 and STAT3 and modulates the IL-10/JAK/STAT signaling pathway. These findings suggest that HTLV-1 promotes the proliferation of infected T cells by hijacking the machinery of regulatory T cell differentiation. IL-10 induced by HBZ likely suppresses the host immune response and concurrently promotes the proliferation of HTLV-1 infected T cells.


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