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TNF‐α and IL‐4 regulate expression of fractalkine (CX 3 CL1) as a membrane‐anchored proadhesive protein and soluble chemotactic peptide on human fibroblasts
Author(s) -
Yoshikawa Mamoru,
Nakajima Toshiharu,
Matsumoto Kenji,
Okada Naoko,
Tsukidate Toshiharu,
Iida Makoto,
Otori Nobuyoshi,
Haruna Shin-ichi,
Moriyama Hiroshi,
Imai Toshio,
Saito Hirohisa
Publication year - 2004
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/s0014-5793(04)00132-2
Subject(s) - chemokine , chemotaxis , monocyte , tumor necrosis factor alpha , microbiology and biotechnology , interleukin 8 , ccl2 , chemistry , peptide , cytokine , inflammation , biology , immunology , biochemistry , receptor
The CX 3 C chemokine, fractalkine (FKN, CX 3 CL1), has multiple functions and exists as two distinct forms, a membrane‐anchored protein and a soluble chemotactic peptide that cleaves from the cell surface FKN. In this study, we first demonstrated the expression of FKN in tumor necrosis factor (TNF)‐α‐ and interleukin (IL)‐4‐stimulated human fibroblasts. The induction of FKN was observed for both forms. We also demonstrated monocyte chemotactic activity in the culture supernatant from the fibroblasts stimulated with these cytokines. These results suggest that TNF‐α‐ and IL‐4‐stimulated fibroblasts may play an important role in accumulation of monocytes at inflammatory sites.