Anderson D C, Springer T A
Annu Rev Med. 1987;38:175-94. doi: 10.1146/annurev.me.38.020187.001135.
Leukocyte adhesion deficiency (LAD) is a recently recognized autosomal-recessive trait characterized by recurrent bacterial infections, impaired pus formation and wound healing, and abnormalities in a wide spectrum of adherence-dependent functions of granulocytes, monocytes, and lymphoid cells. Features of this disease are attributable to deficiency (or absence) of cell surface expression of a family of functionally and structurally related glycoproteins. These include Mac-1 (complement receptor type 3), lymphocyte function-associated antigen-1 (LFA-1), and p150,95. Defective biosynthesis of the beta chain shared by each molecule (comprised of alpha 1 beta 1 complexes) represents the fundamental molecular basis of this disease. Recognition of the molecular pathogenesis of this disorder has allowed rich insights into the role of cellular adherence reactions in inflammation and host defense.
白细胞黏附缺陷症（LAD）是一种最近才被认识的常染色体隐性性状，其特征为反复发生细菌感染、脓液形成和伤口愈合受损，以及粒细胞、单核细胞和淋巴细胞的多种黏附依赖性功能异常。该疾病的特征归因于一组功能和结构相关糖蛋白的细胞表面表达缺陷（或缺失）。这些糖蛋白包括Mac-1（3型补体受体）、淋巴细胞功能相关抗原-1（LFA-1）和p150,95。每个分子共享的β链（由α1β1复合物组成）生物合成缺陷是该疾病的基本分子基础。对这种疾病分子发病机制的认识使人们对细胞黏附反应在炎症和宿主防御中的作用有了深入了解。
