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艾滋病相关淋巴瘤的免疫学

The immunology of AIDS-associated lymphomas.

作者信息

Ng V L, McGrath M S

机构信息

Department of Laboratory Medicine, University of California San Francisco, USA.

出版信息

Immunol Rev. 1998 Apr;162:293-8. doi: 10.1111/j.1600-065x.1998.tb01449.x.

DOI:10.1111/j.1600-065x.1998.tb01449.x
PMID:9602372
Abstract

Lymphomas that occur in patients with human immunodeficiency virus (HIV) infection are predominantly of B-cell origin and subsets show evidence for Epstein-Barr virus (EBV) infection or chromosomal translocations in the c-myc locus. The only subset of lymphoma clearly related to the immunodeficiency caused by HIV infection (similar to transplantation-associated lymphomas) is the EBV+ primary central nervous system lymphoma. The systemic AIDS-related lymphomas (ARLs) represent a complex set of disease processes histologically categorized as large cell or small non-cleaved (Burkitt's-like) lymphomas. Molecular analyses of the ARLs have demonstrated polyclonal lymphomas as likely early representatives of monoclonal immunoglobulin (Ig)-expressing B-cell lymphomas. Variable region analysis of lymphoma-associated Ig has shown evidence for extensive somatic mutation with little evidence for appropriate affinity maturation. These observations suggest that abnormal control of B-cell maturation in response to polyclonal antigenic stimulation may play a central role in the pathogenesis of ARL. The recent finding of clonal HIV integrated within macrophages in a subset of early lymphomas also provides evidence for abnormalities outside the B-cell compartment playing roles in this disease. Overall, ARLs generally appear to be outgrowths of antigen-driven B-cells with significant growth control influence provided by abnormal T-cell and antigen-presenting cell processes.

摘要

发生在人类免疫缺陷病毒(HIV)感染患者中的淋巴瘤主要起源于B细胞,部分亚型显示有爱泼斯坦-巴尔病毒(EBV)感染或c-myc基因座染色体易位的证据。唯一明确与HIV感染所致免疫缺陷相关的淋巴瘤亚型(类似于移植相关淋巴瘤)是EBV阳性原发性中枢神经系统淋巴瘤。系统性艾滋病相关淋巴瘤(ARL)代表了一组复杂的疾病过程,在组织学上归类为大细胞或小无裂(伯基特样)淋巴瘤。对ARL的分子分析表明,多克隆淋巴瘤可能是表达单克隆免疫球蛋白(Ig)的B细胞淋巴瘤的早期代表。对淋巴瘤相关Ig的可变区分析显示有广泛体细胞突变的证据,而几乎没有适当亲和力成熟的证据。这些观察结果表明,多克隆抗原刺激下B细胞成熟的异常调控可能在ARL的发病机制中起核心作用。最近在一部分早期淋巴瘤的巨噬细胞中发现克隆性HIV整合,这也为B细胞外的异常在该疾病中发挥作用提供了证据。总体而言,ARL通常似乎是抗原驱动的B细胞的产物,异常的T细胞和抗原呈递细胞过程对其生长控制有显著影响。

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