title: Role of the tumor necrosis factor family member LIGHT in the pathogenesis of atopic dermatitis.
abstract: BACKGROUND
  LIGHT (the name of which is derived from "homologous to lymphotoxins, exhibits inducible expression, competes with herpes simplex virus glycoprotein D for herpes simplex virus entry mediator, and expressed by T lymphocytes"), is a member of the tumor necrosis factor superfamily that is involved in various inflammatory diseases.
  
  
  OBJECTIVE
  To assess serum LIGHT levels in patients with atopic dermatitis (AD) before and after treatment and compare it with controls. To correlate serum LIGHT with the severity scoring of AD (SCORAD) index. Another objective is to compare LIGHT levels between lesional skin in patients with AD and controls.
  
  
  METHODS
  Twenty patients with AD and 20 healthy controls were enrolled in the study. Serum LIGHT levels were examined using an enzyme immunoassay technique. Serum total IgE levels, absolute eosinophil count, and eosinophil percentage were also done for both patients and controls. The SCORAD index was done for every patient before and after treatment. Skin LIGHT levels were analyzed using enzyme-linked immunosorbent assay kit and compared with control skin.
  
  
  RESULTS
  Serum LIGHT levels in patients with AD were significantly higher than that of healthy controls and correlated positively with SCORAD index. LIGHT concentrations decreased as the symptoms were improved by treatment. A significant correlation was found on comparing the LIGHT serum levels and other established markers of disease severity. LIGHT levels in lesional skin in these patients were markedly higher than LIGHT levels in normal skin.
  
  
  CONCLUSIONS
  LIGHT may play an important role in the pathogenesis of AD. This may presumably have possible future implications on the treatment of this chronic disease.
authors.affiliation: Department of Dermatology, Venereology and Andrology, Faculty of Medicine, Ain Shams University, Cairo, Egypt.
authors.forename: Neveen Salah
authors.identifier: http://orcid.org/0000-0002-9705-2186
authors.initials: NS
authors.lastname: Seifeldin
authors.affiliation: Department of Medical Microbiology and Immunology, Faculty of Medicine, Ain Shams University, Cairo, Egypt.
authors.forename: Shereen Bendary
authors.initials: SB
authors.lastname: El Sayed
authors.affiliation: Department of Dermatology, Venereology and Andrology, Faculty of Medicine, Ain Shams University, Cairo, Egypt.
authors.forename: Marwa Kamal
authors.initials: MK
authors.lastname: Asaad
authors.affiliation: Department of Dermatology, Venereology and Andrology, Faculty of Medicine, Ain Shams University, Cairo, Egypt.
authors.forename: Alaa Ahmed
authors.initials: AA
authors.lastname: Aly
mesh_terms: D000293:Adolescent; D000328:Adult; D016022:Case-Control Studies; D003876:Dermatitis, Atopic / Q000097:blood* / Q000188:drug therapy / Q000378:metabolism; D004804:Eosinophils; D005260:Female; D006633:Histamine Antagonists / Q000627:therapeutic use; D006801:Humans; D007073:Immunoglobulin E / Q000097:blood; D007958:Leukocyte Count; D008297:Male; D012720:Severity of Illness Index; D012867:Skin / Q000378:metabolism*; D013256:Steroids / Q000627:therapeutic use; D053326:Tumor Necrosis Factor Ligand Superfamily Member 14 / Q000097:blood* / Q000378:metabolism; D055815:Young Adult
chemical_list: D006633:Histamine Antagonists; D013256:Steroids; D053326:Tumor Necrosis Factor Ligand Superfamily Member 14; D007073:Immunoglobulin E