Open AccessC1q restrains autoimmunity and viral infection by regulating CD8 + T cell metabolism
Author(s) -
Guang Sheng Ling,
Greg Crawford,
Norzawani B Buang,
I Bartók,
Kunyuan Tian,
Nicole M. Thielens,
Isabelle Bally,
James A. Harker,
Philip G. AshtonRickardt,
Sophie Rutschmann,
Jessica Strid,
Marina Botto
Publication year - 2018
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.aao4555
Subject(s) - complement c1q , autoimmunity , cytotoxic t cell , cd8 , biology , effector , cell metabolism , t cell , immunology , microbiology and biotechnology , immune system , cell , complement system , biochemistry , in vitro
Complement is a CD8+ T cell metabolic rheostatSystemic lupus erythematosus (SLE) is associated with deficiencies in the complement protein C1q. Although C1q plays a role in the clearance of apoptotic cells, there are several redundant clearance pathways. Disruption of one pathway does not lead to an autoimmune defect. In a chronic graft-versus-host disease model of SLE, Linget al. show that C1q dampens CD8+ T cell responses to self-antigens. C1q modulates metabolism through the mitochondrial cell-surface protein p32/gC1qR. The lack of C1q during a viral infection also enhances CD8+ T cell responses. Thus, C1q plays a role as a “metabolic rheostat” for effector CD8+ T cells.Science , this issue p.558
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