A Common Variant in the Adaptor Mal Regulates Interferon Gamma Signaling
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- 作者：Clí ; ona Ní ; Cheallaigh1 ; 2 ; nicheacm@tcd.ie" class="auth_mail" title="E-mail the corresponding author ; Frederick J. Sheedy1 ; James Harris3 ; Natalia Muñ ; oz-Wolf2 ; Jinhee Lee4 ; Kim West4 ; Eva Palsson McDermott5 ; Alicia Smyth6 ; Laura E. Gleeson1 ; Michelle Coleman1 ; Nuria Martinez4 ; Claire H.A. Hearnden2 ; Graham A. Tynan2 ; Elizabeth C. Carroll2 ; Sarah A. Jones3 ; Siné ; ad C. Corr5 ; Nicholas J. Bernard5 ; Mark M. Hughes5 ; Sarah E. Corcoran5 ; Mary O&rsquo ; Sullivan1 ; Ciara M. Fallon1 ; Hardy Kornfeld4 ; Douglas Golenbock4 ; Stephen V. Gordon6 ; Luke A.J. O&rsquo ; Neill5 ; Ed C. Lavelle2 ; 7 ; 8 ; lavellee@tcd.ie" class="auth_mail" title="E-mail the corresponding author ; Joseph Keane1 ; 8
- 关键词：Mal ; TIRAP ; interferon gamma ; tuberculosis ; phagolysosome maturation ; autophagy
- 刊名：Immunity
- 出版年：2016
- 出版时间：16 February 2016
- 年：2016
- 卷：44
- 期：2
- 页码：368-379
- 全文大小：3004 K
文摘
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Mal has a TLR-independent role in IFNGR signaling
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IFNGR signaling via Mal leads to p38 phosphorylation, autophagy, and killing of TB
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The S180L mutation attenuates responses to IFN-γ stimulation
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S180L mutations impair in vitro and in vivo responses to TB