Spontaneous skin ulceration and defective T cell function in CD18 null mice

Karin Scharffetter-Kochanek, Huifang Lu, Keith Norman, Nicole Van Nood, Flor Munoz, Stephan Grabbe, Mark McArthur, Isabel Lorenzo, Sheldon Kaplan, Klaus Ley, C. Wayne Smith, Charles A. Montgomery, Susan Rich, Arthur L. Beaudet

Research output: Contribution to journalArticle

286 Scopus citations

Abstract

A null mutation was prepared in the mouse for CD18, the β2 subunit of leukocyte integrins. Homozygous CD18 null mice develop chronic dermatitis with extensive facial and submandibular erosions. The phenotype includes elevated neutrophil counts, increased immunoglobulin levels, lymphadenopathy, splenomegaly, and abundant plasma cells in skin, lymph nodes, gut, and kidney. Very few neutrophils were found in spontaneously occurring skin lesions or with an induced toxic dermatitis. Intravital microscopy in CD18 null mice revealed a lack of firm neutrophil attachment to venules in the cremaster muscle in response to N-formyl-methionyl-leucyl-phenylalanine. A severe defect in T cell proliferation was found in the CD18 null mice when T cell receptors were stimulated either by staphylococcal enterotoxin A or by major histocompatibility complex alloantigens demonstrating a greater role of CD11/CD18 integrins in T cell responses than previously documented. The null mice are useful for delineating the functions of CD18 in vivo.

Original languageEnglish (US)
Pages (from-to)119-131
Number of pages13
JournalJournal of Experimental Medicine
Volume188
Issue number1
DOIs
StatePublished - Jul 6 1998

Keywords

  • Infection
  • Integrin β
  • Leukocyte-adhesion deficiency syndrome
  • Leukocytes
  • Receptors, antigen, T cell

ASJC Scopus subject areas

  • Immunology

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