C1q restrains autoimmunity and viral infection by regulating CD8 + T cell metabolism
2018; American Association for the Advancement of Science; Volume: 360; Issue: 6388 Linguagem: Inglês
10.1126/science.aao4555
ISSN1095-9203
AutoresGuang Sheng Ling, Greg Crawford, Norzawani B Buang, I Bartók, Kunyuan Tian, Nicole M. Thielens, Isabelle Bally, James A. Harker, Philip G. Ashton‐Rickardt, Sophie Rutschmann, Jessica Strid, Marina Botto,
Tópico(s)Immune Cell Function and Interaction
ResumoComplement is a CD8 + T cell metabolic rheostat Systemic 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, Ling et 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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