T-cell hybridomas from HLA-transgenic mice as tools for analysis of human antigen processing

被引：36

作者：

Canaday, DH

Gehring, A

Leonard, EG

Eilertson, B

Schreiber, JR

Harding, CV

Boom, WH

机构：

[1] Case Western Reserve Univ, Div Infect Dis, Cleveland, OH 44106 USA

[2] Univ Hosp, Cleveland, OH 44106 USA

[3] Case Western Reserve Univ, Dept Pediat, Cleveland, OH 44106 USA

[4] Univ Hosp, Rainbow Babies & Childrens Hosp, Cleveland, OH 44106 USA

[5] Case Western Reserve Univ, Dept Pathol, Cleveland, OH 44106 USA

[6] Univ Hosp, Cleveland, OH 44106 USA

来源：

JOURNAL OF IMMUNOLOGICAL METHODS | 2003年 / 281卷 / 1-2期

关键词：

antigen presentation; human; hybridoma; mouse; macrophage;

D O I：

10.1016/j.jim.2003.07.004

中图分类号：

Q5 [生物化学];

学科分类号：

071010 ; 081704 ;

摘要：

The study of antigen processing and presentation by human antigen presenting cells (APC) has been limited by difficulties of producing and maintaining human T-cell clones. Murine T-cell hybridomas have advantages for detecting specific peptide-MHC complexes on APC. Human antigen-specific immortalized T-cell lines have not been successfully produced. We report and validate the use of transgenic mice with human MHC genes for HLA-A2, DR1 and DR4 to produce murine T-cell hybridomas that are restricted to human HLA alleles and respond to human macrophages, dendritic cells (DC), and B-cell lines. Hybridomas restricted by human MHC-I and -II specific for influenza matrix protein, tetanus toxoid, diphtheria antigen CRM197, and various M. tuberculosis antigens were produced. Epitope specificity was determined for several hybridomas. T hybridomas recognized peptide-MHC complexes on fixed APC for analysis of kinetics or susceptibility to inhibitors of antigen processing. T hybridomas restricted by human MHC represent convenient and powerful tools for the study of antigen processing by human APC. (C) 2003 Elsevier B.V. All rights reserved.

引用

页码：129 / 142

页数：14

共 32 条

[21] Toll-like receptor 2-dependent inhibition of macrophage class II MHC expression and antigen processing by 19-kDa lipoprotein of Mycobacterium tuberculosis [J].