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Short-circuiting long-lived humoral immunity by the heightened engagement of CD40
Loren D. Erickson, … , Hitoshi Kikutani, Randolph J. Noelle
Loren D. Erickson, … , Hitoshi Kikutani, Randolph J. Noelle
Published March 1, 2002
Citation Information: J Clin Invest. 2002;109(5):613-620. https://doi.org/10.1172/JCI14110.
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Article Immunology

Short-circuiting long-lived humoral immunity by the heightened engagement of CD40

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Abstract

Agonistic αCD40 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.

Authors

Loren D. Erickson, Brigit G. Durell, Laura A. Vogel, Brian P. O’Connor, Marilia Cascalho, Teruhito Yasui, Hitoshi Kikutani, Randolph J. Noelle

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Figure 3

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αCD40 administration prevents the generation of bone marrow ASCs. Cells ...
αCD40 administration prevents the generation of bone marrow ASCs. Cells from spleen and bone marrow were isolated from the indicated recipients on day 7 (a) and day 21 (b) after immunization and assayed for total NP-specific IgG1a or high-affinity NP-specific IgG1a (c) by ELISPOT using normalized numbers of Tg B cells. Results shown are representative of three independent experiments.

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