期刊
NATURE COMMUNICATIONS
卷 9, 期 -, 页码 -出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/s41467-018-06686-0
关键词
-
资金
- NIH [R01AI045050, R01 AI128901]
- Alliance for Lupus Research [TIL-416522]
Follicular helper T (T-FH) cells are expanded in systemic lupus erythematosus, where they are required to produce high affinity autoantibodies. Eliminating T-FH cells would, however compromise the production of protective antibodies against viral and bacterial pathogens. Here we show that inhibiting glucose metabolism results in a drastic reduction of the frequency and number of T-FH cells in lupus-prone mice. However, this inhibition has little effect on the production of T-cell-dependent antibodies following immunization with an exogenous antigen or on the frequency of virus-specific T-FH cells induced by infection with influenza. In contrast, glutaminolysis inhibition reduces both immunization-induced and autoimmune T-FH cells and humoral responses. Solute transporter gene signature suggests different glucose and amino acid fluxes between autoimmune T-FH cells and exogenous antigen-specific T-FH cells. Thus, blocking glucose metabolism may provide an effective therapeutic approach to treat systemic autoimmunity by eliminating autoreactive T-FH cells while preserving protective immunity against pathogens.
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