T helper 1 immunity requires complement-driven NLRP3 inflammasome activity in CD4 + T cells
Author(s) -
Giuseppina Arbore,
Erin E. West,
Rosanne Spolski,
Avril A. B. Robertson,
Andreas Klos,
Claudia Rheinheimer,
Pavel Dutow,
Trent M. Woodruff,
Zu Xi Yu,
Luke O'neill,
Rebecca C. Coll,
Alan Sher,
Warren J. Leonard,
Jörg Köhl,
Peter N. Monk,
Matthew A. Cooper,
Matthew Arno,
Behdad Afzali,
Helen J. Lachmann,
Andrew P. Cope,
Katrin D. Mayer-Barber,
Claudia Kemper
Publication year - 2016
Publication title -
science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 12.556
H-Index - 1186
eISSN - 1095-9203
pISSN - 0036-8075
DOI - 10.1126/science.aad1210
Subject(s) - complement (music) , immunity , inflammasome , chemistry , immune system , immunology , biology , virology , inflammation , biochemistry , gene , complementation , phenotype
Innate immune crosstalk in T cells The classical view of immune activation is that innate immune cells, such as macrophages and dendritic cells, recognize invading microbes and then alert adaptive immune cells, such as T cells, to respond. Arboreet al. now show that innate and adaptive immunity converge in human and mouse T cells. Activated T cells express components of the complement cascade, which in turn leads to the assembly of NLRP3 inflammasomes—both critical components of innate immunity that help hosts detect and eliminate microbes. In T cells, complement and inflammasomes work together to push T cells to differentiate into a specialized subset of T cells important for eliminating intracellular bacteria.Science , this issue p.10.1126/science.aad1210
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