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Experimental study reveals FcγR-dependent enhancement of germinal center responses, indicating distinct mechanisms regulate B cell recruitment thresholds.
Immune memory responses are rapid and qualitatively distinct from primary responses. They typically develop in the presence of antigen-experienced memory T and B cells and preexisting antibodies. Although the contribution of T and B cells to recall responses is well defined, the contribution of antibody "memory" and the mechanisms by which preexisting antibodies modulate the development of germinal center (GC) and plasma cell responses is not precisely understood. Here, we report on mechanisms that mediate antibody enhancement of GC and plasmablast (PB) compartments, and the parallel process by which antibodies change the affinity threshold for B cell recruitment into immune responses. The data indicate that antibody-mediated enhancement of GC and PB responses is Fc gamma receptor (FcγR) dependent and largely complement receptor 1 and 2 (CR1/2) independent. In contrast, the reduction in the affinity threshold for GC entry is independent of both FcγRs and CR1/2.
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Cipolla et al. (2026) studied this question.
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