Nemazee D, Russell D, Arnold B, Haemmerling G, Allison J, Miller J F, Morahan G, Buerki K
Dept. of Pediatrics, National Jewish Center for Immunology and Respiratory Medicine, Denver, CO 80206.
Immunol Rev. 1991 Aug;122:117-32. doi: 10.1111/j.1600-065x.1991.tb00600.x.
Using mice transgenic for functional, rearranged immunoglobulin heavy and light chain genes, it can be demonstrated that B lymphocytes reactive with cell surface-bound class I MHC antigen can be controlled by clonal elimination. Even low-affinity cell-bound ligands can induce deletion. Deletion can occur in the pre-B to B cell transitional stage or after the B cells exist the bone marrow, depending on where the cells first encounter autoantigen. IgD appears to play no role in protecting cells from deletion. It is argued that defects in B-cell tolerance alone may be sufficient to lead to systemic autoimmunity.
利用转有功能性重排免疫球蛋白重链和轻链基因的小鼠，可以证明与细胞表面结合的I类MHC抗原发生反应的B淋巴细胞可通过克隆清除得到控制。即使是低亲和力的细胞结合配体也能诱导清除。清除可发生在前B细胞到B细胞的过渡阶段，或在B细胞离开骨髓之后，这取决于细胞首次遇到自身抗原的位置。IgD似乎在保护细胞免于清除方面不起作用。有人认为，仅B细胞耐受性缺陷可能足以导致全身性自身免疫。
