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gp49B1-α(v)β3相互作用抑制抗原诱导的肥大细胞活化。

gp49B1-alpha(v)beta3 interaction inhibits antigen-induced mast cell activation.

作者信息

Castells M C, Klickstein L B, Hassani K, Cumplido J A, Lacouture M E, Austen K F, Katz H R

机构信息

Department of Medicine, Harvard Medical School and Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital, Boston, MA 02115, USA.

出版信息

Nat Immunol. 2001 May;2(5):436-42. doi: 10.1038/87749.

Abstract

We have identified the integrin alpha(v)beta3 as a ligand for mouse gp49B1, thus identifying a new class of ligand for a member of the family of inhibitory immunoreceptors that bear C2-type immunoglobulin-like domains. The specific interaction was shown by both cell-protein and cell-cell binding assays. In addition, we found that the interaction of alpha(v)beta3 with gp49B1 on bone marrow-derived mouse mast cells inhibited antigen-induced immunoglobulin E-mediated cell activation. Because neither gp49B1 nor alpha(v)beta3 exhibit substantive allelic variation, their newly appreciated interaction may reflect an innate pathway for down-regulating the activity of mast cells.

摘要

我们已确定整合素α(v)β3是小鼠gp49B1的一种配体,从而为带有C2型免疫球蛋白样结构域的抑制性免疫受体家族成员确定了一类新的配体。细胞-蛋白质和细胞-细胞结合试验均显示了这种特异性相互作用。此外,我们发现α(v)β3与骨髓来源的小鼠肥大细胞上的gp49B1相互作用可抑制抗原诱导的免疫球蛋白E介导的细胞活化。由于gp49B1和α(v)β3均未表现出实质性的等位基因变异,它们新发现的相互作用可能反映了一种下调肥大细胞活性的固有途径。

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