Abstract
Abstract Mast cells play critical roles in allergic and inflammatory diseases as effector and immunoregulatory cells. A well understood mast cell activation pathway is antigen-mediated crosslinkage of IgE bound to its high affinity receptor (FcεRI). Cytokines produced during the immune response may alter mast cell function. We have shown that, contrary to its better-known anti-inflammatory role, IL-10 induces pro-inflammatory cytokines in peritoneal and bone marrow derived mast cells stimulated with IgE+antigen. The increase in pro-inflammatory cytokines and chemokines (IL-6, MCP-1, MIP-1a, and IL-13) is seen both at the mRNA and protein level. Consistent with previously published data, IL-10 suppresses TNF production. Using an in vivo IgE-induced passive systemic anaphylaxis model, we show that IL-10 pre-treatment causes a more severe anaphylactic response and increased serum IL-6 and MIP-1a, suggesting that IL-10-mediated enhancement can occur in vivo. These data support a more nuanced view of IL-10 as a key immunoregulatory cytokine capable of curbing and promoting different inflammatory mediators in hypersensitivity reactions.
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