Rock K L, Rothstein L, Gamble S, Fleischacker C
Division of Lymphocyte Biology, Dana Farber Cancer Institute, Boston, MA 02115.
J Immunol. 1993 Jan 15;150(2):438-46.
Exogenous Ag in the extracellular fluids do not gain access to the class I Ag-presenting pathway in most cells. However, there is an APC resident in spleen that can process and present exogenous Ag in association with class I molecules. We characterize the phenotype of this cell. This APC is of low buoyant density, is adherent to Sepharose and glass, and expresses both class II molecules and FcR. This phenotype identifies this APC as a macrophage. Resident, peptone- and thioglycolate-induced peritoneal macrophages also display this Ag-presenting activity. Analysis with CTL clones suggest that this Ag-presenting pathway may be active in only a subset of macrophages. A similar Ag-presenting activity is also present in dendritic cell-enriched populations from spleen although we cannot rule out the possible involvement of contaminating macrophages. In contrast, B and T cells that are resident in spleen and LPS blasts are unable to present exogenous Ag in association with class I molecules. The presentation of exogenous OVA with class I molecules is not inhibited by the inhibitors of thiol proteases, leupeptin, and antipain. The presence of gelonin, a ribosomal inactivating protein, in the extracellular fluids inhibits the ability of these APC to present exogenous OVA. Under identical conditions, gelonin does not inhibit Con A-stimulated T cell proliferation, or LPS-stimulated B cell proliferation and Ag presentation. These results are discussed in relation to the potential pathways through which an Ag in the extracellular fluids is presented with MHC class I molecules.
细胞外液中的外源性抗原在大多数细胞中无法进入I类抗原呈递途径。然而,脾脏中存在一种抗原呈递细胞(APC),它能够处理并呈递与I类分子相关的外源性抗原。我们对这种细胞的表型进行了表征。这种APC浮力密度低,能黏附于琼脂糖和玻璃,同时表达II类分子和Fc受体。这种表型表明该APC是巨噬细胞。驻留的、经蛋白胨和巯基乙酸盐诱导的腹腔巨噬细胞也表现出这种抗原呈递活性。用细胞毒性T淋巴细胞(CTL)克隆进行分析表明,这种抗原呈递途径可能仅在一部分巨噬细胞中具有活性。来自脾脏的富含树突状细胞的群体中也存在类似的抗原呈递活性,尽管我们不能排除污染巨噬细胞的可能参与。相比之下,脾脏中的B细胞、T细胞以及脂多糖刺激的母细胞无法呈递与I类分子相关的外源性抗原。外源性卵清蛋白(OVA)与I类分子的呈递不受巯基蛋白酶抑制剂亮抑酶肽和抗蛋白酶的抑制。细胞外液中存在的核糖体失活蛋白gelonin会抑制这些APC呈递外源性OVA的能力。在相同条件下,gelonin不会抑制刀豆蛋白A(Con A)刺激的T细胞增殖,也不会抑制脂多糖刺激的B细胞增殖和抗原呈递。我们结合细胞外液中的抗原通过主要组织相容性复合体(MHC)I类分子呈递的潜在途径对这些结果进行了讨论。