Kanost D, McCluskey J
Centre for Transfusion Medicine and Immunology, Flinders Medical Centre, Bedford Park, Australia.
Eur J Immunol. 1994 May;24(5):1186-93. doi: 10.1002/eji.1830240527.
Presentation of hen egg lysozyme (HEL) by HEL-specific B cells was studied in transgenic mice expressing anti-HEL immunoglobulin (Ig-transgenic). In T hybridoma assays, presentation of the HEL46-61 determinant by B cells from Ig-transgenic mice required 10(3)-10(4)-fold lower concentrations of HEL than were required for presentation by B cells from non-transgenic mice. In contrast, presentation of the HEL determinants 112-129 and 25-43 by HEL-specific B cells was either not significantly enhanced, or enhanced only 10-fold compared with B cells from non-transgenic mice. Enhanced presentation of HEL determinants by B cells from Ig-transgenic donors was specific for HEL, since keyhole limpet hemocyanin or synthetic HEL46-61 peptide were presented comparably by B cells from Ig-transgenic mice and non-transgenic littermates. A minimum of 1-4% Ig-transgenic B cells was required to detect enhanced presentation of HEL46-61 in vitro. Constitutive presentation of the HEL46-61 determinant, but not the HEL25-43 or HEL112-129 determinants, was detectable on anergic HEL-specific B cells from double (HEL/Ig)-transgenic mice. In the presence of exogenously added HEL, anergic B cells presented all three HEL determinants. Constitutively presented HEL46-61 was not due to endogenous synthesis of HEL antigen by anergic B cells from double-transgenic mice, as comparable levels of the HEL46-61 determinant were constitutively presented by B cells from Ig-Tg-->HEL-Tg irradiation bone marrow chimeric mice. Firstly, these results indicate that the enhanced antigen presentation mediated by Ig receptors on B cells is not equivalent for all antigenic determinants. Secondly, the data demonstrate that anergic, autoreactive B cells efficiently process and present nominal antigens in addition to constitutively presenting specific self antigen in vivo.
在表达抗鸡卵清溶菌酶（HEL）免疫球蛋白的转基因小鼠（Ig转基因）中，研究了HEL特异性B细胞对HEL的呈递情况。在T杂交瘤试验中，与非转基因小鼠的B细胞相比，Ig转基因小鼠的B细胞呈递HEL46 - 61决定簇所需的HEL浓度要低10³ - 10⁴倍。相比之下，HEL特异性B细胞呈递HEL决定簇112 - 129和25 - 43时，与非转基因小鼠的B细胞相比，要么没有显著增强，要么仅增强了10倍。Ig转基因供体的B细胞对HEL决定簇呈递的增强是HEL特异性的，因为来自Ig转基因小鼠和非转基因同窝小鼠的B细胞对钥孔戚血蓝蛋白或合成的HEL46 - 61肽的呈递情况相当。在体外检测到HEL46 - 61呈递增强需要至少1 - 4%的Ig转基因B细胞。在双（HEL/Ig）转基因小鼠的无反应性HEL特异性B细胞上可检测到HEL46 - 61决定簇的组成性呈递，但未检测到HEL25 - 43或HEL112 - 129决定簇的组成性呈递。在添加外源性HEL的情况下，无反应性B细胞呈递所有三种HEL决定簇。双转基因小鼠无反应性B细胞组成性呈递的HEL46 - 61并非由于内源性合成HEL抗原，因为来自Ig-Tg→HEL-Tg照射骨髓嵌合小鼠的B细胞也组成性呈递了相当水平的HEL46 - 61决定簇。首先，这些结果表明，B细胞上的Ig受体介导的增强抗原呈递并非对所有抗原决定簇都等效。其次，数据表明，无反应性、自身反应性B细胞除了在体内组成性呈递特异性自身抗原外，还能有效地加工和呈递名义抗原。
