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IL‐1beta triggers monocytes to differentiate into CD209+ macrophages
Author(s) -
Schenk Mirjam,
Liu Philip,
Krutzik Stephan R,
Montoya Dennis,
Modlin Robert L
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.2_supplement.539
Subject(s) - innate immune system , microbiology and biotechnology , tlr2 , immune system , cd14 , biology , cd16 , cellular differentiation , immunology , chemistry , cd8 , biochemistry , cd3 , gene
The dual functions of the innate immune system in response to infection‐ capturing pathogens and presenting antigens‐ are mediated by distinct cell subsets that can be induced by TLR2/1: CD209 + macrophages that are phagoytic and CD1b + dendritic cells that are potent antigen‐presenting cells. Given that IL‐1β and TLRs trigger similar signaling pathways, we hypothesize that IL‐1β, as another innate immune signal, may effect monocyte differentiation. Our data demonstrate that IL‐1β induces CD209 + but not CD1b + cells unlike TLR2/1. IL1β induced CD209 + cells, co‐express CD163, CD206 and express higher levels of CD16, CD64, CD36 and HLA‐DR and exert higher phagocytic activity than TLR2/1 induced CD209 + cells. IL‐1β induces IL‐15 at similar levels as TLR2/1 engagement but does not induce GM‐CSF offering a mechanism for the preferential differentiation into CD209 + but not CD1b + cells. In conclusion, IL‐1β is involved in regulating critical host defense mechanisms such as antimicrobial activity and monocyte differentiation. Therefore, these data suggest that the inflammasome may have an important function in monocyte differentiation. The elucidation of these distinct mechanisms will provide new insights for the development of therapeutic strategies against infectious diseases targeting innate immune cell subsets at the level of differentiation.