A Common Variant in the Adaptor Mal Regulates Interferon Gamma Signaling

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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

•: Mal has a TLR-independent role in IFNGR signaling
•: IFNGR signaling via Mal leads to p38 phosphorylation, autophagy, and killing of TB
•: The S180L mutation attenuates responses to IFN-γ stimulation
•: S180L mutations impair in vitro and in vivo responses to TB

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