Cutting Edge: Neutrophil Complement Receptor Signaling Is Required for BAFF-Dependent Humoral Responses in Mice. Academic Article uri icon

Overview

abstract

  • T cell-independent (TI) B cell responses to nonprotein Ags involve multiple cues from the innate immune system. Neutrophils express complement receptors and activated neutrophils can release BAFF, but mechanisms effectively linking neutrophil activation to TI B cell responses are incompletely understood. Using germline and conditional knockout mice, we found that TI humoral responses involve alternative pathway complement activation and neutrophil-expressed C3a and C5a receptors (C3aR1/C5aR1) that promote BAFF-dependent B1 cell expansion and TI Ab production. Conditional absence of C3aR1/C5aR1 on neutrophils lowered serum BAFF levels, led to fewer Peyer's patch germinal center B cells, reduced germinal center B cells IgA class-switching, and lowered fecal IgA levels. Together, the results indicate that sequential activation of complement on neutrophils crucially supports humoral TI and mucosal IgA responses through upregulating neutrophil production of BAFF.

publication date

  • January 1, 2023

Research

keywords

  • B-Lymphocytes
  • Neutrophils

Identity

PubMed Central ID

  • PMC9780177

Scopus Document Identifier

  • 85144539912

Digital Object Identifier (DOI)

  • 10.4049/jimmunol.2200410

PubMed ID

  • 36454023

Additional Document Info

volume

  • 210

issue

  • 1