The Journal of Experimental Medicine
VeriKine-HS Human IFN-Beta
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© The Rockefeller University Press, 0022-1007/1998/7/119/ $5.00
The Journal of Experimental Medicine, Volume 188, Number 1, July 1, 1998 119-131

Articles

Spontaneous Skin Ulceration and Defective T Cell Function in CD18 Null Mice

Karin Scharffetter-Kochanek*, Huifang Lu{ddagger}, Keith Norman**, Nicole van Nood§, Flor Munoz{ddagger}, Stephan Grabbe{dagger}{dagger}, Mark McArthur||, Isabel Lorenzo*,¶, Sheldon Kaplan{ddagger}, Klaus Ley**, C. Wayne Smith{ddagger}, Charles A. Montgomery||, Susan Rich§, and Arthur L. Beaudet*,¶

From the * Department of Molecular and Human Genetics, {ddagger} 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 {dagger}{dagger} Department of Dermatology, University of Münster, 48149 Münster, Germany

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.

Key Words: infection • integrin β2 • leukocyte-adhesion deficiency syndrome • receptors, antigen, T cell • leukocytes

Address correspondence to Arthur L. Beaudet, Department of Molecular and Human Genetics, Baylor College of Medicine, One Baylor Plaza, T619, Houston, TX 77030. Phone: 713-798-4795; Fax: 713-798-7773; E-mail: abeaudet{at}bcm.tmc.edu

Dr. Scharffetter-Kochanek's present address is Department of Dermatology, University of Cologne (Köln), Germany.

Abbreviations used: DNFB, dinitrofluorobenzene; ES cell, embryonic stem cell; ICAM-1, intercellular adhesion molecule-1; LAD, leukocyte adhesion deficiency; Mac-1, macrophage antigen-1; OpZ, opsonized zymosan; SE, staphylococcal enterotoxin; ZAS, zymosan activated serum.


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