Pharmacologically Inferred Glycolysis and Glutaminolysis Requirement of B Cells in Lupus-Prone Mice.
Pharmacologically Inferred Glycolysis and Glutaminolysis Requirement of B Cells in Lupus-Prone Mice.
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DOI:
10.4049/jimmunol.2100356
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发表时间:
2022-05-01
影响因子:
4.4
通讯作者:
Morel, Laurence
中科院分区:
文献类型:
--
作者:
Choi, Seung-Chul;Li, Wei;Zhang, Xiaojuan;Kanda, Nathalie;Zeumer-Spataro, Leilani;Teng, Xiangyu;Morel, Laurence
Several studies have shown an enhanced metabolism in the CD4+ T cells of lupus patients and lupus-prone mice. Little is known on the metabolism of B cells in lupus. Here we compared the metabolism of B cells between lupus-prone B6.Sle1.Sle2.Sle3 (TC) mice and B6 controls at steady state relative to autoantibody production, as well as during T cell-dependent (TD) and T cell-independent (TI) immunizations. Starting before the onset of autoimmunity, B cells from TC mice showed an elevated glycolysis and mitochondrial respiration, which were normalized in vivo by inhibiting glycolysis with a 2-deoxy-D-glucose (2DG) treatment. 2DG greatly reduced the production of TI-antigen-specific antibodies, but showed minimal effect with TD-antigens. In contrast, the inhibition of glutaminolysis with 6-Diazo-5-oxo-L-norleucine (DON) had a greater effect on TD than TI Ag-specific antibodies in both strains. Analysis of the TI and TD responses in purified B cells in vitro suggests, however, that the glutaminolysis requirement is not B cell-intrinsic. Thus, B cells have a greater requirement for glycolysis in TI than TD-responses, as inferred from pharmacological interventions. B cells from lupus-prone and control mice have different intrinsic metabolic requirement, or different responses towards 2DG and DON. which mirrors our previous results obtained with follicular helper T cells. Overall, these results predict that targeting glucose metabolism may provide an effective therapeutic approach for systemic autoimmunity by eliminating both autoreactive TFH and B cells, although it may also impair TI-responses.
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影响因子:
16.6
作者:
Choi SC;Titov AA;Abboud G;Seay HR;Brusko TM;Roopenian DC;Salek-Ardakani S;Morel L
通讯作者:
Morel L
影响因子:
7.3
作者:
Bacalao MA;Satterthwaite AB
通讯作者:
Satterthwaite AB
影响因子:
4.4
作者:
Dufort, Fay J.;Bleiman, Blair F.;Chiles, Thomas C.
通讯作者:
Chiles, Thomas C.
影响因子:
4.4
作者:
Jayachandran, Nipun;Mejia, Edgard M.;Marshall, Aaron J.
通讯作者:
Marshall, Aaron J.
影响因子:
4.4
作者:
Sang, Allison;Niu, Haitao;Morel, Laurence
通讯作者:
Morel, Laurence