在体内以及EML造血祖细胞中，小鼠白血病病毒感染后B淋巴细胞分化潜能降低。
Diminished potential for B-lymphoid differentiation after murine leukemia virus infection in vivo and in EML hematopoietic progenitor cells.
作者信息
Finstad Samantha L, Rosenberg Naomi, Levy Laura S
机构信息
Department of Microbiology and Immunology, Tulane University School of Medicine, 1430 Tulane Avenue SL-38, New Orleans, LA 70112, USA.
出版信息
J Virol. 2007 Jul;81(13):7274-9. doi: 10.1128/JVI.00250-07. Epub 2007 Apr 11.
Abstract
Infection with a recombinant murine-feline gammaretrovirus, MoFe2, or with the parent virus, Moloney murine leukemia virus, caused significant reduction in B-lymphoid differentiation of bone marrow at 2 to 8 weeks postinfection. The suppression was selective, in that myeloid potential was significantly increased by infection. Analysis of cell surface markers and immunoglobulin H gene rearrangements in an in vitro model demonstrated normal B-lymphoid differentiation after infection but significantly reduced viability of differentiating cells. This reduction in viability may confer a selective advantage on undifferentiated lymphoid progenitors in the bone marrow of gammaretrovirus-infected animals and thereby contribute to the establishment of a premalignant state.
摘要
感染重组鼠-猫γ逆转录病毒MoFe2或其亲本病毒莫洛尼鼠白血病病毒，在感染后2至8周会导致骨髓B淋巴细胞分化显著减少。这种抑制具有选择性，因为感染会使髓系潜能显著增加。在体外模型中对细胞表面标志物和免疫球蛋白H基因重排的分析表明，感染后B淋巴细胞分化正常，但分化细胞的活力显著降低。这种活力降低可能赋予γ逆转录病毒感染动物骨髓中未分化淋巴祖细胞选择性优势，从而有助于建立癌前状态。
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