title: RANTES production in a conjunctival epithelial cell line.
abstract: OBJECTIVE
  Although corneal tissue damage in allergic ocular diseases is thought to be induced by inflammatory cells that infiltrate from conjunctival tissue, the mechanisms of recruiting these cells remain unclear. The objective of this study was to demonstrate whether conjunctival epithelial cells have the ability to produce "regulated on activation, normal T-cell expressed and secreted" (RANTES). To test this hypothesis, we investigated RANTES expression in the conjunctival tissue and also RANTES production by cytokine stimulation in a human conjunctival epithelial cell line.
  
  
  METHODS
  We investigated the expression of the chemokine RANTES in conjunctival epithelium from two patients with atopic keratoconjunctivitis (AKC) and one patient with vernal keratoconjunctivitis (VKC) by using immunohistochemistry. We also investigated the production and suppression of RANTES from a human conjunctival epithelial cell line, Wong-Kilbourne-derived human conjunctiva (WK-hC) by using enzyme-linked immunosorbent assay (ELISA).
  
  
  RESULTS
  Conjunctival epithelium from a patient with AKC stained positively for RANTES. We found that tumor necrosis factor-alpha (TNF-alpha) induced de novo production of RANTES, and interferon-gamma (IFN-gamma) synergistically increased the TNF-alpha-dependent production of RANTES from WK-hC cells. Dexamethasone suppressed the RANTES production from the cell line.
  
  
  CONCLUSIONS
  Taken together, human conjunctival epithelial cells were capable of producing RANTES in response to inflammatory stimuli such as TNF-alpha and may play a role in recruiting inflammatory cells such as eosinophils and T lymphocytes toward the ocular surface.
authors.affiliation: Department of Allergy and Immunology, National Children's Medical Research Center, Tokyo, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Fukagawa
authors.forename: H
authors.initials: H
authors.lastname: Saito
authors.forename: K
authors.initials: K
authors.lastname: Tsubota
authors.forename: S
authors.initials: S
authors.lastname: Shimmura
authors.forename: H
authors.initials: H
authors.lastname: Tachimoto
authors.forename: A
authors.initials: A
authors.lastname: Akasawa
authors.forename: Y
authors.initials: Y
authors.lastname: Oguchi
mesh_terms: D000293:Adolescent; D000328:Adult; D000970:Antineoplastic Agents / Q000494:pharmacology; D002460:Cell Line / Q000187:drug effects; D018946:Chemokine CCL5 / Q000096:biosynthesis*; D002648:Child; D003228:Conjunctiva / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D016572:Cyclosporine / Q000494:pharmacology; D003907:Dexamethasone / Q000494:pharmacology; D004797:Enzyme-Linked Immunosorbent Assay; D004847:Epithelial Cells; D004848:Epithelium / Q000187:drug effects / Q000378:metabolism; D005260:Female; D005938:Glucocorticoids / Q000494:pharmacology; D006801:Humans; D007166:Immunosuppressive Agents / Q000494:pharmacology; D007371:Interferon-gamma / Q000494:pharmacology; D008297:Male; D008875:Middle Aged; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology
chemical_list: D000970:Antineoplastic Agents; D018946:Chemokine CCL5; D005938:Glucocorticoids; D007166:Immunosuppressive Agents; D014409:Tumor Necrosis Factor-alpha; D003907:Dexamethasone; D007371:Interferon-gamma; D016572:Cyclosporine