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Characterization of Thymus-dependent and Thymus-independent Immunoglobulin Isotype Responses in Mice Using Enzyme-linked Immunosorbent Assay
Published on: September 7, 2018
Mechanisms of antibody-mediated enhancement of immune responses
Melissa Cipolla1, Andrew J MacLean1, Brianna Hernandez1
1Laboratory of Molecular Immunology, The Rockefeller University, New York, NY, USA.
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.
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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