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Norway

PMID:9653089  

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

K Scharffetter-Kochanek | H Lu | K Norman | N van Nood | F Munoz | S Grabbe | M McArthur | I Lorenzo | S Kaplan | K Ley | C W Smith | C A Montgomery | S Rich | A L Beaudet
The Journal of experimental medicine | 1998

A null mutation was prepared in the mouse for CD18, the beta2 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.

Pubmed ID: 9653089

Research resources used in this publication

None found

Antibodies used in this publication

None found

Associated grants

  • Agency: NIAID NIH HHS, United States
    Id: AI30036
  • Agency: NIGMS NIH HHS, United States
    Id: GM15483
  • Agency: NIAID NIH HHS, United States
    Id: AI32177

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