作者: Joseph P. Mizgerd , Claire M. Doerschuk , Arthur L. Beaudet , Daniel C. Bullard , M. John Hicks
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摘要: Mutant mice triply deficient in ICAM-1, E-selectin, and P-selectin did not develop the neutrophilic skin lesions that spontaneously arise mutants doubly E-selectin P-selectin. Thus, ICAM-1 is essential to disease resulting from endothelial selectin deficiency. During experimental dermatitis, acute neutrophil emigration was completely prevented young both selectins (E/P E/P/I mutants). However, older E/P with spontaneous displayed an selectin-independent pathway for emigration. In contrast, remained compromised CD18 regardless of age or lesions. Experimentally induced chronic elicited this mutants. by inflammation at distant sites, may contribute