title: Very late antigen-1 in psoriasis: an immunohistochemical study.
abstract: BACKGROUND
  Currently, psoriasis is thought to be an inflammatory response to an antigenic stimulation, in which angiogenesis plays a fundamental role. Very late antigen-1 (VLA-1) is a beta(1) integrin collagen receptor that is up-regulated in many angiogenic processes. Data on its role in psoriasis are sparse.
  
  
  OBJECTIVE
  In a prospective study, we evaluated the staining of VLA-1 in lesional skin from patients with psoriasis and atopic dermatitis.
  
  
  METHODS
  Frozen sections from skin biopsies of patients with chronic plaque-type psoriasis (n = 18) and chronic atopic dermatitis (n = 7) were stained with a monoclonal antibody to VLA-1. The number of blood vessels stained with VLA-1 and the staining intensity were evaluated. These were correlated with the histologic features.
  
  
  RESULTS
  The absolute number of blood vessels was found to be similar in the atopic and psoriatic samples. However, the number of vessels stained with anti-VLA-1, as well as the staining intensity, was shown to be significantly higher in the psoriasis group (P < 0.05). Differences between psoriatic lesions showing typical histological features of psoriasis and those showing features that overlap with dermatitis were found as well.
  
  
  CONCLUSIONS
  Expression of VLA-1 was found significantly higher in lesional dermal blood vessels of psoriatic patients compared with atopic patients. These findings suggest a possible role for VLA-1 in the pathological angiogenesis of psoriasis. It may be an additional tool for establishing the diagnosis of psoriasis and provide a basis for new strategies in the treatment of psoriasis.
authors.affiliation: Department of Dermatology, Chaim Sheba Medical Center, Tel.Hashomer, Israel.
authors.forename: S
authors.initials: S
authors.lastname: Baum
authors.forename: A
authors.initials: A
authors.lastname: Barzilai
authors.forename: M
authors.initials: M
authors.lastname: Huszar
authors.forename: S
authors.initials: S
authors.lastname: Greenberger
authors.forename: H
authors.initials: H
authors.lastname: Trau
authors.forename: I
authors.initials: I
authors.lastname: Bank
mesh_terms: D000328:Adult; D000368:Aged; D001706:Biopsy; D001808:Blood Vessels / Q000378:metabolism / Q000473:pathology; D003876:Dermatitis, Atopic / Q000378:metabolism* / Q000473:pathology; D005260:Female; D006801:Humans; D039222:Integrin alpha1beta1 / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D009389:Neovascularization, Pathologic / Q000378:metabolism / Q000473:pathology; D011446:Prospective Studies; D011565:Psoriasis / Q000378:metabolism* / Q000473:pathology; D012867:Skin / Q000098:blood supply / Q000473:pathology; D018418:Th2 Cells / Q000473:pathology
chemical_list: D039222:Integrin alpha1beta1