z-logo
Premium
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.

This content is not available in your region!

Continue researching here.

Having issues? You can contact us here