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J. Exp. Med.,
Volume 188, Number 1, July 1, 1998 119-131
By
From the * Department of Molecular and Human Genetics, A null mutation was prepared in the mouse for CD18, the Department of Pediatrics, § Department of
Microbiology and Immunology, Center for Comparative Medicine, Baylor College of Medicine, and ¶ Howard Hughes Medical Institute, Houston, Texas 77030; ** Department of Biomedical
Engineering, University of Virginia, Charlottesville, Virginia 22908; and Department of
Dermatology, University of Münster, 48149 Münster, Germany
2 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.
2;
leukocyte-adhesion deficiency syndrome;
receptors,
antigen, T cell;
leukocytes
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