作者: R. R. Hardy , J. D. Kemp , K. Hayakawa
DOI: 10.1007/978-3-642-74974-2_3
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摘要: C.B-17scid (SCID) mice are characterized by a lack of serum immunoglobulin and the inability to reject skin allografts. The defect has been attributed an lymphoid cells make functional T cell receptor rearrangements, presumably due in recombinase system (Schuler et al. 1986). We have employed sensitive multiparameter FACS (fluorescence activated sorter) analysis enumerate populations present young adult (2–4 month) SCID compared them with those detectable normal (C.B-17) animals order clearly define baseline levels lineage SCID. Such might also help pinpoint stage(s) at which become defective. analyzed tissues expected include both early (bone marrow thymus) later (spleen peritoneal cell) stages B lineages. In course these studies we found that recently described S7 antibody (Gulley 1988), together B220 (Coffman Weissman 1981a,b, 1983) defines previously-unrecognized population bone may constitute set very B-lineage (or lymphoid) progenitors.