Maecker H T, Do M S, Levy S
Department of Medicine/Oncology, Stanford University Medical Center, Stanford, CA 94305, USA.
Proc Natl Acad Sci U S A. 1998 Mar 3;95(5):2458-62. doi: 10.1073/pnas.95.5.2458.
Mice lacking CD81 (TAPA-1), a widely expressed tetraspanin molecule, have impaired antibody responses to protein antigens. This defect is specific to antigens that preferentially stimulate a T helper 2 response (ovalbumin or keyhole limpet hemocyanin in alum) and is only seen with T cell-dependent antigens. Absence of CD81 on B cells is sufficient to cause the defect. Also, antigen-specific interleukin (IL) 4 production is greatly reduced in the spleen and lymph nodes of CD81-null mice compared with heterozygous littermates. Thus, expression of CD81 on B cells is critical for inducing optimal IL-4 and antibody production during T helper 2 responses. These findings suggest that CD81 may interact with a ligand on T cells to signal IL-4 production. By using a soluble form of CD81 as a probe, a putative ligand for CD81 was identified on a subset of B and T cells. Two possible models for the interaction of CD81 on B cells with a potential ligand on either B or T cells are proposed.
缺乏CD81（TAPA - 1）的小鼠，CD81是一种广泛表达的四跨膜蛋白分子，其对蛋白质抗原的抗体反应受损。这种缺陷特定于优先刺激辅助性T细胞2型反应的抗原（明矾中的卵清蛋白或钥孔血蓝蛋白），并且仅在T细胞依赖性抗原中出现。B细胞上缺乏CD81足以导致这种缺陷。此外，与杂合子同窝小鼠相比，CD81基因敲除小鼠的脾脏和淋巴结中抗原特异性白细胞介素（IL）-4的产生大幅减少。因此，B细胞上CD81的表达对于在辅助性T细胞2型反应期间诱导最佳的IL - 4和抗体产生至关重要。这些发现表明CD81可能与T细胞上的配体相互作用以信号传导IL - 4的产生。通过使用可溶性形式的CD81作为探针，在一部分B细胞和T细胞上鉴定出了CD81的推定配体。提出了B细胞上的CD81与B细胞或T细胞上潜在配体相互作用的两种可能模型。
