Type I IFN-dependent FcγRIV signaling in murine monocytes promotes lethal anaphylaxis during viral infections.

ABSTRACT: Anaphylaxis is a life-threatening hypersensitivity reaction. Clinical observations suggest heightened susceptibility during viral infections, yet the mechanisms remain poorly defined. Here, we show that both active and passive IgG-mediated anaphylaxis were exacerbated in the setting of acute viral infection. In mice, this enhancement was driven predominantly by FcγRIV, the homolog of human FcγRIIIa. FcγRIV crosslinking induced anaphylactic symptoms selectively in infected animals, with no effect in naive conditions. Among leukocytes, inflammatory monocytes emerged as the principal drivers of this lethal reaction. Viral infection triggered a strong upregulation of FcγRIV on inflammatory monocytes, an effect absent in type I IFN receptor-deficient (Ifnar1-deficient) mice. Extending these fin

SUBMITTER: Elwy A 

PROVIDER: S-EPMC12904709 | biostudies-literature | 2026 Feb

REPOSITORIES: biostudies-literature