期刊
BLOOD
卷 125, 期 11, 页码 1826-1829出版社
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2014-09-603464
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资金
- National Institutes of Health (National Heart, Lung, and Blood Institute) [PO1 HL44612, R01 HL13629]
- National Institutes of Health (National Institute of Allergy and Infectious Diseases) [R01 AI079087]
Antibodies specific for platelet factor 4 (PF4)/heparin complexes are central to the pathogenesis of heparin-induced thrombocytopenia. Marginal zone B cells appear to be the source of such antibodies, but whether T-cell help is required is unclear. Here, we showed that induction of PF4/heparin-specific antibodies by PF4/heparin complexes was markedly impaired in mice depleted of CD4 T cells by anti-CD4 antibodies. Furthermore, Rag1-deficient recipient mice produced PF4/heparin-specific antibodies upon PF4/heparin challenge when reconstituted with a mixture of wild-type splenic B cells and splenocytes from B-cell-deficient (mu MT) mice but not splenocytes from T-and B-cell-deficient (Rag1 knockout) mice. Lastly, mice with B cells lacking CD40, a B-cell costimulatory molecule that helps T-cell-dependent B-cell responses, displayed a marked reduction of PF4/heparin-specific antibody production following PF4/heparin challenge. Together, these findings show that helper T cells play a critical role in production of PF4/heparin-specific antibodies.
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