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ARS Home » Plains Area » Houston, Texas » Children's Nutrition Research Center » Research » Publications at this Location » Publication #162658
Title: DEFICIENCY OF CD11B OR CD11D RESULTS IN REDUCED STAPHYLOCOCCAL ENTEROTOXIN-INDUCED T CELL RESPONSE AND T CELL PHENOTYPIC CHANGES

Author
item WU, HUAIZHU - BAYLOR COLLEGE MED
item RODGERS, JOHN - BAYLOR COLLEGE MED
item PERRARD, XIAO-YUAN - BAYLOR COLLEGE MED
item PRINCE, JOSEPH - BAYLOR COLLEGE MED
item ABE, YASUNORI - BAYLOR COLLEGE MED
item DAVIS, BECKLEY - BAYLOR COLLEGE MED
item DIETSCH, GREG - ICOS CORPORATION
item Smith, Wayne
item BALLANTYNE, CHRISTIE - BAYLOR COLLEGE MED
item PERRARD, JERRY - BAYLOR COLLEGE MED

Submitted to: Journal of Immunology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 4/26/2004
Publication Date: 7/1/2004
Citation: Wu, H., Rodgers, J.R., Perrard, X.D., Prince, J.E., Abe, Y., Davis, B.K., Dietsch, G., Smith, W.C., Ballantyne, C.M. 2004. Deficiency of cd11b or cd11d results in reduced staphylococcal enterotoxin-induced t cell response and t cell phenotypic changes. Journal of Immunology. 173:297-306.

Interpretive Summary: This paper analyzes a potential mechanism by which some bacteria cause tissue injury. That is the production of toxins that cause direct activation of white blood cells. We study a toxin from Staphylococcus organisms and its ability to activate lymphocytes from mice with engineered genetic deficiencies in adhesion molecules. The results demonstrate that two leukocyte adhesion molecules Mac-1 and CR4 are necessary for an efficient response.

Technical Abstract: The 2 integrin CD11a is involved in T cell-APC interactions, but the roles of CD11b, CD11c, and CD11d in such interactions have not been examined. To evaluate the roles of each CD11/CD18 integrin in T cell-APC interactions, we tested the ability of splenocytes of CD11-knockout (KO) mice to respond to staphylococcal enterotoxins (SEs), a commonly used superantigen. The defect in T cell proliferation with SEA was more severe in splenocytes from mice deficient in CD18, CD11b, or CD11d than in CD11a-deficient splenocytes, with a normal response in CD11c-deficient splenocytes. Mixing experiments showed that the defect of both CD11b-KO and CD11d-KO splenocytes was, unexpectedly, in T cells rather than in APC. Cytometric analysis failed to detect CD11b or CD11d on resting or activated T cells or on thymocytes of wild-type adult mice, nor did Abs directed to these integrins block responses in culture, suggesting that T cells educated in CD11b-KO or CD11d-KO mice were phenotypically altered. Consistent with this hypothesis, T cells from CD11b-KO and CD11d-KO splenocytes exhibited reduced intensity of CD3 and CD28 expression and decreased ratios of CD4/ CD8 cells, and CD4 T cells were reduced among CD11b-KO and CD11d-KO thymocytes. CD11b and CD11d were coexpressed on a subset of early wild-type fetal thymocytes. We postulate that transient thymocyte expression of both CD11b and CD11d is nonredundantly required for normal thymocyte and T cell development, leading to phenotypic changes in T cells that result in the reduced response to SE stimulation.