Mechanism of Suppression of Cell-Mediated Immunity by Measles Virus

TLDR

Measles causes profound suppression of cell‑mediated immunity, a process linked to IL‑12 production from monocytes/macrophages and the complement regulator CD46 that connects complement to cellular immune responses. Cross‑linking of CD46, the cellular receptor for MV, with antibody or with the complement activation product C3b similarly inhibited monocyte IL‑12 production, providing a plausible mechanism for MV‑induced immunosuppression. Measles virus infection of primary human monocytes specifically down‑regulated IL‑12 production.

Abstract

The mechanisms underlying the profound suppression of cell-mediated immunity (CMI) accompanying measles are unclear. Interleukin-12 (IL-12), derived principally from monocytes and macrophages, is critical for the generation of CMI. Measles virus (MV) infection of primary human monocytes specifically down-regulated IL-12 production. Cross-linking of CD46, a complement regulatory protein that is the cellular receptor for MV, with antibody or with the complement activation product C3b similarly inhibited monocyte IL-12 production, providing a plausible mechanism for MV-induced immunosuppression. CD46 provides a regulatory link between the complement system and cellular immune responses.