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Down‐regulation of the β‐chemokine receptor CCR6 in dendritic cells mediated by TNF‐α and IL‐4
Author(s) -
Carramolino Laura,
Kremer Leonor,
Goya íñigo,
Varona Rosa,
Buesa Jose María,
Gutiérrez Julio,
Zaballos Angel,
MartínezA. Carlos,
Márquez Gabriel
Publication year - 1999
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.66.5.837
Subject(s) - biology , c c chemokine receptor type 6 , dendritic cell , chemokine , microbiology and biotechnology , cd14 , tumor necrosis factor alpha , c c chemokine receptor type 7 , chemokine receptor , immunology , ccl20 , immune system
Chemokines are involved in the control of dendritic cell (DC) trafficking, which is critical for the immune response. We have generated DC from human umbilical cord blood CD34 + progenitors cultured with granulocyte‐macrophage colony‐stimulating factor, tumor necrosis factor α (TNF‐α), and stem cell factor. Using an anti‐CCR6 monoclonal antibody, we observed that these cells showed maximum expression of this β‐chemokine receptor when they were immature, as determined by their relatively low expression of several DC maturation markers such as CD1a, CD11c, CD14, CD40, CD80, and CD83. Immature DC responded strongly to macrophage inflammatory protein‐3α (MIP‐3α), the CCR6 ligand, in migration and calcium mobilization assays. CCR6 expression decreased in parallel with the DC maturation induced by prolonged TNF‐α treatments. Interleukin‐4 was also able to decrease CCR6 protein levels. Our findings suggest that the MIP‐3α/CCR6 interaction plays an important role in the trafficking of immature DC to chemokine production sites such as injured or inflamed peripheral tissues, where DC undergo maturation on contact with antigens. J. Leukoc. Biol. 66: 837–844; 1999.