作者: Richard Sullivan
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摘要: Through use of semisolid tissue culture techniques that sup port the clonal growth hemopoietic progenitor cells, it has become clear during recent years blood cell production within bone marrow is regulated by a family glycopro teins referred to as colony-stimulating factors (CSFs) (1). A large body evidence indicates these cytokines constitute endocrine hormones responsible for regulating most if not all cells enter bloodstream. As illustrated data Nakamura and colleagues, which are reported in present edition this journal (2), CSFs capable operating both individually synergistically at various ontogenetic stages hemopoiesis stimulate vari ous classes arising from marrow. Many genes encode regulatory glycoproteins have been cloned, and, result, number synthetic recombinant made widely available in vestigation well treatment disorders as sociated with failure (3). To date, least 14 affect proliferation phagocytes ' identified. Most prominent among GM-CSF, stimulates neutrophils, eosinophils, macrophages vitro; IL-3, supports phagocytes; G-CSF, primarily prolifer ation neutrophils; M-CSF, effects limited committed macrophage development. While G-CSF M-CSF appear be re stricted single lineages, GM-CSF IL-3 promiscuous early hemopoiesis, stimulating prolifera tion virtually every class 1 Granulocyte/macrophage factor (GM-CSF), granu locyte (G-CSF), (M-CSF), interleukins I through 9 (IL-I IL-9) , tumor necro sis factor-alpha, interferon-gamma.