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Antagonistic effects of IL‐4 and TGF‐β1 on Langerhans cell‐related antigen expression by human monocytes
Author(s) -
Guironnet G.,
DezutterDambuyant C.,
Bechetoille C. Vincent N.,
Schmitt D.,
PéguetNavarro J.
Publication year - 2002
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 - 10.1189/jlb.71.5.845
Subject(s) - langerin , birbeck granules , biology , transforming growth factor , monocyte , microbiology and biotechnology , cytokine , c c chemokine receptor type 6 , immunology , cd40 , antigen , langerhans cell , dendritic cell , immune system , cytotoxic t cell , in vitro , chemokine , chemokine receptor , biochemistry
In this study, we analyzed the specific effects of transforming growth factor β (TGF‐β1) and/or IL‐4 on monocyte‐derived cells. Monocytes were cultured with GM‐CSF, GM‐CSF/TGF‐β1, GM‐CSF/IL‐4, or GM‐CSF/IL‐4/TGF‐β1 before cell morphology, phenotype, and function were assessed. As expected, interleukin‐4 is mandatory for monocyte differentiation into potent allostimulatory DC. In its absence, monocyte‐derived cells share many phenotypic and functional features with macrophages. However, it is interesting that the cells express E‐cadherin, independent of exogenous TGF‐β1, and addition of the cytokine induced CCR6 expression. Most importantly, a subset of monocytes cultured with GM‐CSF/TGF‐β1 expresses Langerin, as confirmed by electron microscopy analysis. Langerin engagement with specific monoclonal antibodies induces its internalization and the formation of typical Birbeck granules. Monocytes cultured in GM‐CSF/IL‐4 did not express the LC markers E‐cadherin, CCR6, or Langerin. The simultaneous addition of TGF‐β1 allows most of the cells to express E‐cadherin but rarely CCR6 and Langerin. Taken together, the results add further evidence that LC can derive from monocytes and demonstrate an antagonistic effect of IL‐4 and TGF‐β1 on monocyte differentiation toward the LC pathway.