Rovere P, Vallinoto C, Bondanza A, Crosti M C, Rescigno M, Ricciardi-Castagnoli P, Rugarli C, Manfredi A A
Divisione di Medicina II, Istituto Scientifico H S. Raffaele and University of Milan, Italy.
J Immunol. 1998 Nov 1;161(9):4467-71.
Physiologic cell death via apoptosis occurs without inflammation or autoimmunity. Here, we investigated the outcome of the interaction of apoptotic cells with dendritic cells (DCs), which are potent professional APCs. DCs internalized apoptotic cells and processed them for presentation to both MHC class I- and class II-restricted T cells with an efficiency that was dependent upon the number of apoptotic cells. The latter event was accompanied by the autocrine/paracrine secretion of IL-1beta and TNF-alpha, with eventual DC maturation. High numbers of apoptotic cells, mimicking a failure of their in vivo clearance, are therefore sufficient to trigger DC maturation and the presentation of intracellular Ags from apoptotic cells, even in the absence of exogenous "danger" signals.
通过凋亡发生的生理性细胞死亡不会引发炎症或自身免疫反应。在此,我们研究了凋亡细胞与树突状细胞(DCs)相互作用的结果,树突状细胞是强大的专职抗原呈递细胞(APCs)。DCs内化凋亡细胞并对其进行处理,以便将其呈递给MHC I类和II类限制性T细胞,其效率取决于凋亡细胞的数量。后一事件伴随着IL-1β和TNF-α的自分泌/旁分泌分泌,最终导致DC成熟。因此,即使在没有外源性“危险”信号的情况下,大量模仿其体内清除失败的凋亡细胞也足以触发DC成熟并呈递凋亡细胞内的抗原。