Expression of complement receptor CR2 (CD21) on human subcorneal keratinocytes in normal and diseased skin

J. Hunyadi, M. Simon, A. S. Kenderessy, A. Dobozy

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

Human keratinocytes are able to synthesize and express cell surface moieties characteristic of effector and/or accessory cells of the immune system (CD16, CD36, HLA-DR, intercellular adhesion molecule-1). In the present study, skin biopsies from healthy volunteers, from patients with psoriasis vulgaris (PV), mycosis fungoides (MF), purpura pigmentosa chronica (PPC), acute urticaria (AU) and from positive tuberculin skin tests were investigated with regard to the reactivity with the monoclonal antibodies to complement receptors CR1 CR2 and CR3 by means of a multistep immunoperoxidase method. In the clinically involved skin of all patients with PV, MF or PPC, and in biopsies obtained from positive tuberculin tests, specific epidermal intercellular staining with OKB7 and Leu anti-CR2 was seen on subcorneal keratinocytes. This finding suggests a differentiation-linked expression of CR2 on human keratinocytes in cytokine-mediated skin diseases whereas CR1 and CR3 are apparently not expressed.

Original languageEnglish
Pages (from-to)184-186
Number of pages3
JournalDermatologica
Volume183
Issue number3
Publication statusPublished - 1991

Fingerprint

Complement Receptors
Keratinocytes
Skin Diseases
Mycosis Fungoides
Tuberculin Test
Purpura
Psoriasis
Biopsy
Skin
Urticaria
HLA-DR Antigens
Intercellular Adhesion Molecule-1
Skin Tests
Immune System
Healthy Volunteers
Monoclonal Antibodies
Staining and Labeling
Cytokines

Keywords

  • C3d receptor
  • CD21 antigen
  • CR2
  • keratinocytes
  • psoriasis
  • skin diseases

ASJC Scopus subject areas

  • Dermatology

Cite this

Expression of complement receptor CR2 (CD21) on human subcorneal keratinocytes in normal and diseased skin. / Hunyadi, J.; Simon, M.; Kenderessy, A. S.; Dobozy, A.

In: Dermatologica, Vol. 183, No. 3, 1991, p. 184-186.

Research output: Contribution to journalArticle

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