Combined Genetic Inactivation of β2-Microglobulin and CD58 Reveals Frequent Escape from Immune Recognition in Diffuse Large B Cell Lymphoma

被引：362

作者：

Challa-Malladi, Madhavi ^{[1
]}

Lieu, Yen K. ^{[1
]}

Califano, Olivia ^{[1
]}

Holmes, Antony B. ^{[1
]}

Bhagat, Govind ^{[2
,3
]}

Murty, Vundavalli V. ^{[1
,2
,3
]}

Dominguez-Sola, David ^{[1
]}

Pasqualucci, Laura ^{[1
,2
,3
]}

Dalla-Favera, Riccardo ^{[1
,2
,3
,4
,5
]}

机构：

[1] Columbia Univ, Inst Canc Genet, New York, NY 10032 USA

[2] Columbia Univ, Dept Pathol & Cell Biol, New York, NY 10032 USA

[3] Columbia Univ, Herbert Irving Comprehens Canc Ctr, New York, NY 10032 USA

[4] Columbia Univ, Dept Genet & Dev, New York, NY 10032 USA

[5] Columbia Univ, Dept Microbiol & Immunol, New York, NY 10032 USA

来源：

CANCER CELL | 2011年 / 20卷 / 06期

关键词：

MHC CLASS-I; ADHESION MOLECULES; HODGKIN-LYMPHOMA; T-LYMPHOCYTES; HEAVY-CHAINS; LFA-3; EXPRESSION; MUTATIONS; ANTIGEN; RECEPTOR;

D O I：

10.1016/j.ccr.2011.11.006

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

We report that diffuse large B cell lymphoma (DLBCL) commonly fails to express cell-surface molecules necessary for the recognition of tumor cells by immune-effector cells. In 29% of cases, mutations and deletions inactivate the beta 2-Microglobulin gene, thus preventing the cell-surface expression of the HLA class-I (HLA-I) complex that is necessary for recognition by CD8(+) cytotoxic T cells. In 21 A) of cases, analogous lesions involve the CD58 gene, which encodes a molecule involved in T and natural killer cell-mediated responses. In addition to gene inactivation, alternative mechanisms lead to aberrant expression of HLA-I and CD58 in >60% of DLBCL. These two events are significantly associated in this disease, suggesting that they are coselected during lymphomagenesis for their combined role in escape from immune-surveillance.

引用

页码：728 / 740

页数：13

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