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Interactions of DC‐SIGN with Mac‐1 and CEACAM1 regulate contact between dendritic cells and neutrophils
Author(s) -
van Gisbergen Klaas P.J.M.,
Ludwig Irene S.,
Geijtenbeek Teunis B.H.,
van Kooyk Yvette
Publication year - 2005
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2005.09.089
Subject(s) - dc sign , microbiology and biotechnology , innate immune system , dendritic cell , immune system , t cell , biology , receptor , acquired immune system , chemistry , immunology , biochemistry
Early during infection neutrophils are the most important immune cells that are involved in killing of pathogenic bacteria and regulation of innate immune responses at the site of infection. It has become clear that neutrophils also modulate adaptive immunity through interactions with dendritic cells (DCs) that are pivotal in the induction of T cell responses. Upon activation, neutrophils release TNF‐α and induce maturation of DCs that enables these antigen‐presenting cells to stimulate T cell proliferation and to induce T helper 1 polarization. DC maturation by neutrophils also requires cellular interactions that are mediated by binding of the DC‐specific receptor DC‐SIGN to Mac‐1 on the neutrophil. Here, we demonstrate that also CEACAM1 is an important ligand for DC‐SIGN on neutrophils. Binding of DC‐SIGN to both CEACAM1 and Mac‐1 is required to establish cellular interactions with neutrophils. DC‐SIGN is a C‐type lectin that has specificity for Lewis x , and we show that DC‐SIGN mediates binding to CEACAM1 through Lewis x moieties that are specifically expressed on CEACAM1 derived from neutrophils. This indicates that glycosylation‐driven binding of both Mac‐1 and CEACAM1 to DC‐SIGN is essential for interactions of neutrophils with DCs and enables neutrophils to modulate T cell responses through interactions with DCs.