Defective lymphopoiesis in bone marrow of motheaten (me/me) and viable motheaten (mev/mev) mutant mice. I. Analysis of development of prothymocytes, early B lineage cells, and terminal deoxynucleotidyl transferase-positive cells.
Defective lymphopoiesis in bone marrow of motheaten (me/me) and viable motheaten (mev/mev) mutant mice. I. Analysis of development of prothymocytes, early B lineage cells, and terminal deoxynucleotidyl transferase-positive cells.
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Motheaten（ME/ME）和可行的Motheaten（MEV/MEV）突变小鼠的骨髓中的淋巴管缺陷。 I.分析促炎细胞，早期B谱系细胞和末端脱氧核苷酸转移酶阳性细胞的发育。
DOI：
10.1084/jem.164.4.1129
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发表时间：
1986-10-01
影响因子：
15.3
通讯作者：
Schultz, L
中科院分区：
文献类型：
--
作者：
Greiner, D L;Goldschneider, I;Komschlies, K L;Medlock, E S;Bollum, F J;Schultz, L
本研究确定了淋巴细胞生成的早期阶段的缺陷，这些缺陷可能导致Motheaten（me/me）和活Motheaten（mev/mev）突变纯合子小鼠外周T和B淋巴细胞的发育和/或功能异常。结果表明，在me/me和mev/mev小鼠中，骨髓中的原胸腺细胞以基本正常的数量存在，如胸腺内注射所确定的，但显然缺乏有效归巢到胸腺的能力，如静脉内转移所确定的;通过B220抗原鉴定的骨髓中的早期B谱系细胞显著减少，包括未成熟B细胞（sIg+）、前B细胞（cIg+，sIg-）和前B细胞（B220+，cIg-，sIg-）; TdT+骨髓细胞，尤其是表达B220 B谱系抗原的亚群，在2周龄时明显减少;正常数量的TdT+胸腺细胞在出生后的前3周出现，但此后迅速减少。结果进一步表明，无论是胸腺细胞的胸腺归巢能力的缺陷，也没有TdT+骨髓细胞的缺陷是由于自身抗体。本文还讨论了me/me和mev/mev小鼠淋巴前体细胞发育缺陷与胸腺退化的过早发生和外周血T、B淋巴细胞异常的可能关系;体外研究的结果也是如此（在一份配套文件中提出），这表明骨髓基质微环境的原发性缺陷是导致淋巴细胞异常发育的原因。前体细胞
This study identifies defects in the early stages of lymphopoiesis that may contribute to the abnormalities in the development and/or function of peripheral T and B lymphocytes in mice homozygous for the motheaten (me/me) and viable motheaten (mev/mev) mutations. The results indicate that in me/me and mev/mev mice prothymocytes in bone marrow are present in essentially normal numbers, as determined by intrathymic injection, but apparently lack the ability to home effectively to the thymus, as determined by intravenous transfer; early B lineage cells in bone marrow, identified by the B220 antigen, are markedly depleted, including immature B cells (sIg+), pre-B cells (cIg+, sIg-), and pro-B cells (B220+, cIg-, sIg-); TdT+ bone marrow cells, especially a subset that expresses the B220 B lineage antigen, are markedly depleted by two weeks of age; normal numbers of TdT+ thymocytes are present during the first 3 wk of postnatal life, but rapidly decrease thereafter. The results further indicate that neither the defective thymus homing capacity of prothymocytes nor the deficiency of TdT+ bone marrow cells is due to autoantibodies. The possible relationship of the defective development of lymphoid precursor cells to the premature onset of thymic involution and to the abnormalities of peripheral T and B lymphocytes in me/me and mev/mev mice is discussed; as are the results of in vitro studies (presented in a companion paper), which suggest that a primary defect in the stromal microenvironment of the bone marrow is responsible for the abnormal development of the lymphoid precursor cells.