期刊
JOURNAL OF CLINICAL INVESTIGATION
卷 109, 期 5, 页码 613-620出版社
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI200214110
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资金
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI042234, R37AI026296, F32AI010302, R01AI026296] Funding Source: NIH RePORTER
- NIAID NIH HHS [R01 AI026296, F32 AI010302, AI-26296, AI-42234, AI-10302-01A1, R37 AI026296] Funding Source: Medline
Agonistic alphaCD40 Ab's have been shown to be potent immune adjuvants for both cell- and humoral-mediated immunity. While enhancing short-lived humoral immunity, the administration of a CD40 agonist during, thymus-dependent immune responses ablates germinal center formation prematurely terminates the humoral immune response, blocks the generation of B cell memory, and prevents the generation of long-lived bone marrow plasma cells. Interestingly, some of these effects of heightened CD40 engagement could be mimicked by enhancing the magnitude of antigen-specific T cell help. Taken together, these studies demonstrate that as the magnitude of CD40 signaling intensifies, the fate of antigen-reactive B cells can be dramatically altered. These are the first studies to describe the multifaceted function of CD40 in determining the fate of antigen-reactive B cells and provide novel insights into how CD40 agonists; can short-circuit humoral immunity.
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