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Interleukin‐1β triggers the differentiation of macrophages with enhanced capacity to present mycobacterial antigen to T cells
Author(s) -
Schenk Mirjam,
Fabri Mario,
Krutzik Stephan R.,
Lee Delphine J.,
Vu David M.,
Sieling Peter A.,
Montoya Dennis,
Liu Philip T.,
Modlin Robert L.
Publication year - 2014
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1111/imm.12167
Subject(s) - cd36 , phagocytosis , innate immune system , biology , microbiology and biotechnology , immune system , tlr2 , immunology , cd16 , receptor , antigen , cd14 , cd64 , biochemistry , cd3 , cd8
Summary The rapid differentiation of monocytes into macrophages ( M Φ) and dendritic cells is a pivotal aspect of the innate immune response. Differentiation is triggered following recognition of microbial ligands that activate pattern recognition receptors or directly by pro‐inflammatory cytokines. We demonstrate that interleukin‐1β ( IL ‐1β) induces the rapid differentiation of monocytes into CD 209 + M Φ, similar to activation via Toll‐like receptor 2/1, but with distinct phenotypic and functional characteristics. The IL ‐1β induced M Φ express higher levels of key markers of phagocytosis, including the Fc‐receptors CD 16 and CD 64, as well as CD 36, CD 163 and CD 206. In addition, IL ‐1β‐induced M Φ exert potent phagocytic activity towards inert particles, oxidized low‐density lipoprotein and mycobacteria. Furthermore, IL ‐1β‐induced M Φ express higher levels of HLA ‐ DR and effectively present mycobacterial antigens to T cells. Therefore, the ability of IL ‐1β to induce monocyte differentiation into M Φ with both phagocytosis and antigen‐presenting function is a distinct part of the innate immune response in host defence against microbial infection.