Mohan C, Morel L, Yang P, Wakeland E K
College of Medicine, University of Florida, Gainesville 32610-0275, USA.
Arthritis Rheum. 1998 Sep;41(9):1652-62. doi: 10.1002/1529-0131(199809)41:9<1652::AID-ART17>3.0.CO;2-W.
In order to shed light on the role of splenic B1 cells in disease pathogenesis in lupus-prone mice, this study was undertaken to determine how efficiently these cells can serve as antigen-presenting cells (APC) and to ascertain which murine lupus susceptibility loci dictate the expansion of these cells.
Spleens and peritoneal cavities (PerC) of NZM2410 lupus-prone mice, as well as of control B6 and New Zealand white mice, were examined for the prevalence, surface phenotype, and possible anatomic location of B1 cells. The antigen-presenting ability of fluorescence-sorted splenic B1a cells was assessed. Levels of B1 cells were examined in B6 mice congenic for 4 different lupus susceptibility intervals.
NZM2410 lupus mice showed an expansion of splenic and PerC B1a cells at all ages. These cells expressed high levels of B71, B72, CD24, lymphocyte function-associated antigen 1, and intercellular adhesion molecule 1, and had the functional capability to serve as APC. Among the lupus susceptibility intervals studied, Sle2, but not Sle1, Sle3, or the H2 locus, affected the expansion of B1 cells.
These findings raise the possibility that the genetically determined expansion of splenic B1a cells in lupus-prone mice might contribute to disease pathogenesis by augmenting the presentation of autoantigens to pathogenic T cells.
为了阐明脾脏B1细胞在狼疮易感小鼠疾病发病机制中的作用，本研究旨在确定这些细胞作为抗原呈递细胞（APC）的效率，并确定哪些小鼠狼疮易感基因座决定了这些细胞的扩增。
检查了NZM2410狼疮易感小鼠以及对照B6和新西兰白兔小鼠的脾脏和腹腔（PerC）中B1细胞的患病率、表面表型和可能的解剖位置。评估了荧光分选的脾脏B1a细胞的抗原呈递能力。在4个不同狼疮易感区间的同源B6小鼠中检测了B1细胞水平。
NZM2410狼疮小鼠在所有年龄段脾脏和PerC B1a细胞均出现扩增。这些细胞高水平表达B71、B72、CD24、淋巴细胞功能相关抗原1和细胞间黏附分子1，并具有作为APC的功能能力。在所研究的狼疮易感区间中，Sle2而非Sle1、Sle3或H2基因座影响B1细胞的扩增。
这些发现提示，狼疮易感小鼠中脾脏B1a细胞的基因决定的扩增可能通过增加自身抗原向致病性T细胞的呈递而促进疾病发病机制。
