bcl-2抑制中性粒细胞的凋亡，但不抑制巨噬细胞对它们的吞噬作用。
bcl-2 inhibits apoptosis of neutrophils but not their engulfment by macrophages.
作者信息
Lagasse E, Weissman I L
机构信息
Department of Pathology and Developmental Biology, Stanford University School of Medicine, California 94305.
出版信息
J Exp Med. 1994 Mar 1;179(3):1047-52. doi: 10.1084/jem.179.3.1047.
Neutrophils, the most common inflammatory leukocytes, have the most limited life span of all blood cells. After they undergo apoptosis, they are recognized and engulfed by macrophages. bcl-2, a proto-oncogene rearranged and deregulated in B cell lymphomas bearing the t(14;18) translocation, is known to inhibit programmed death. bcl-2 expression is localized in early myeloid cells of the bone marrow but is absent in mature neutrophils. Transgenic mice that expressed bcl-2 in mature neutrophils showed that bcl-2 blocked neutrophil apoptosis. Despite this, homeostasis of neutrophil population is essentially unaffected. In fact, macrophage uptake of neutrophils expressing bcl-2 still occurred. This transgenic model indicates that the mechanism that triggers phagocytosis of aging neutrophils operates independently of the process of apoptosis regulated by bcl-2.
中性粒细胞是最常见的炎性白细胞，在所有血细胞中寿命最短。它们发生凋亡后，会被巨噬细胞识别并吞噬。bcl-2是一种原癌基因，在携带t(14;18)易位的B细胞淋巴瘤中发生重排并失调，已知其可抑制程序性死亡。bcl-2表达定位于骨髓早期髓样细胞，但在成熟中性粒细胞中不存在。在成熟中性粒细胞中表达bcl-2的转基因小鼠表明，bcl-2可阻断中性粒细胞凋亡。尽管如此，中性粒细胞群体的稳态基本未受影响。事实上，表达bcl-2的中性粒细胞仍会被巨噬细胞摄取。该转基因模型表明，触发衰老中性粒细胞吞噬作用的机制独立于由bcl-2调节的凋亡过程。
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