Genetics of HLA class II regulation.
Genetics of HLA class II regulation.
复制标题
HLA II 类调控的遗传学。
DOI：
10.1007/bf02918200
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发表时间：
1990
影响因子：
4.4
通讯作者：
Lee,JS
中科院分区：
文献类型：
--
作者：
Hume,CR;Lee,JS
Major histocompatibility complex class II genes are expressed constitutively on relatively few tissues, primarily B lymphocytes [1]. Class II antigens are also expressed transiently along the developmental pathway of many cell types or following stimulation with various soluble factors, such as 7-interferon and IL-4 [2-5]. Curiously, malignant cells derived from many different tissues express class II antigens constitutively or are inducible for expression by 7-interferon [3]. At least three distinct human class II AB heterodimers, HLA-DP, DQ and DR, are expressed at the cell surface and are involved in antigen presentation [6]. In general, B cells express the DR, DP and DQ A and B genes coordinately, suggesting that a common molecular mechanism regulates their expression. As in many other systems, the availability of mutants has begun to reveal mechanisms that are used in regulating class II gene expression. We have extensively studied four independent class II negative B cell mutants, RJ2. 2.5, 6.1. 6, BLS-1 and BLS-2. The first two lines were generated in vitro by immunoselection [7-10], and the latter two were established from patients with class II deficient bare lymphocyte syndrome (BLS). These cell lines show a concomitant decrease in expression of all class II antigens although there are no detectable rearrangements or deletions of the appropriate structural genes.Although the mutants 6.1. 6 and RJ2. 2.5 were selected only for the loss of DR antigens, neither cell line expresses any detectable cell surface class II antigens, and class II RNA levels are greatly reduced [11-13]. B lymphocytes from patients with BLS or B cell lines immortalized from them with Epstein-Barr virus (EBV) resemble the mutants derived in vitro [14-18]. That is, BLS B cells fail to express either protein or mRNA for any of the class II genes, suggesting that they also have defects in trans-acting regulatory factors.
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影响因子：
2.9
作者：
FLING, SP;GREGERSON, DS
通讯作者：
GREGERSON, DS
急性髓系白血病中缺乏髓过氧化物酶的中性粒细胞。
DOI：
--
发表时间：
2009
期刊：
Scandinavian Journal of Haematology
影响因子：
--
作者：
D. Catovsky;D. Galton;J. Robinson
通讯作者：
J. Robinson
影响因子：
20.3
作者：
W. Nauseef
通讯作者：
W. Nauseef
人髓过氧化物酶基因：白血病细胞中的分子克隆和表达。
影响因子：
20.3
作者：
K. Chang;J. Trujillo;R. Cook;S. Stass
通讯作者：
S. Stass
影响因子：
5.3
作者：
P. Ponte;P. Gunning;H. Blau;L. Kedes
通讯作者：
P. Ponte;P. Gunning;H. Blau;L. Kedes