title: Expression of fractalkine and its receptor, CX3CR1, in atopic dermatitis: possible contribution to skin inflammation.
abstract: BACKGROUND
  Fractalkine (FKN) induces activation and adhesion of leukocytes expressing its receptor, CX(3)CR1. FKN is released from the cell surface through proteolytic cleavage as soluble FKN (sFKN).
  
  
  OBJECTIVE
  We sought to assess FKN and CX(3)CR1 expression in the skin, serum sFKN levels, and CX(3)CR1 expression on blood leukocytes in patients with atopic dermatitis (AD).
  
  
  METHODS
  FKN and CX(3)CR1 expression in the skin was examined immunohistochemically. mRNA expression of FKN, thymus and activation-regulated chemokine, and macrophage-derived chemokine in the skin was assessed by means of real-time RT-PCR. Serum sFKN levels were assessed by using ELISA. Blood leukocytes were stained for CX(3)CR1 by means of flow cytometric analysis.
  
  
  RESULTS
  FKN was strongly expressed on endothelial cells in skin lesions of patients with AD and psoriasis but not in normal skin. FKN mRNA levels in AD lesional skin increased to a similar extent to thymus and activation-regulated chemokine and macrophage-derived chemokine mRNA levels. CX(3)CR1-expressing cells in the affected skin of patients with AD or psoriasis increased compared with those in normal skin. Serum sFKN levels were increased in patients with AD but not in patients with psoriasis relative to levels in healthy control subjects. Serum sFKN levels were associated with the disease severity and decreased with the improvement of skin lesions in patients with AD. CX(3)CR1(+) cell frequencies and CX(3)CR1 expression levels were decreased in CD8(+) T cells, monocytes, and natural killer cells from patients with AD, but this was not observed in patients with psoriasis.
  
  
  CONCLUSIONS
  These results suggest that through functions in both membrane-bound and soluble forms, FKN plays an important role in the trafficking of CX(3)CR1(+) leukocytes during the inflammation caused by AD.
authors.affiliation: Department of Dermatology, Kanazawa University Graduate School of Medical Science, 13-1 Takaramachi, Kanazawa, Ishikawa 920-8641, Japan.
authors.forename: Takeshi
authors.initials: T
authors.lastname: Echigo
authors.forename: Minoru
authors.initials: M
authors.lastname: Hasegawa
authors.forename: Yuka
authors.initials: Y
authors.lastname: Shimada
authors.forename: Kazuhiko
authors.initials: K
authors.lastname: Takehara
authors.forename: Shinichi
authors.initials: S
authors.lastname: Sato
mesh_terms: D000293:Adolescent; D000328:Adult; D000073883:CX3C Chemokine Receptor 1; D016022:Case-Control Studies; D054414:Chemokine CCL17; D054422:Chemokine CCL22; D054428:Chemokine CX3CL1; D019742:Chemokines, CC / Q000235:genetics; D020523:Chemokines, CX3C / Q000097:blood / Q000235:genetics / Q000378:metabolism*; D003876:Dermatitis, Atopic / Q000209:etiology / Q000235:genetics / Q000276:immunology*; D003877:Dermatitis, Contact / Q000235:genetics / Q000276:immunology; D005260:Female; D006801:Humans; D007962:Leukocytes / Q000276:immunology; D008297:Male; D008565:Membrane Proteins / Q000097:blood / Q000235:genetics / Q000378:metabolism*; D011565:Psoriasis / Q000235:genetics / Q000276:immunology; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D018121:Receptors, Cytokine / Q000378:metabolism*; D015728:Receptors, HIV / Q000378:metabolism*; D012867:Skin / Q000276:immunology; D012995:Solubility
chemical_list: C106230:CCL17 protein, human; C515482:CCL22 protein, human; D000073883:CX3C Chemokine Receptor 1; C515538:CX3CL1 protein, human; D054414:Chemokine CCL17; D054422:Chemokine CCL22; D054428:Chemokine CX3CL1; D019742:Chemokines, CC; D020523:Chemokines, CX3C; D008565:Membrane Proteins; D012333:RNA, Messenger; D018121:Receptors, Cytokine; D015728:Receptors, HIV