Abstract |
We have reported that Burkitt lymphomas (BL) that arise in HLA-A11 positive individuals are resistant to lysis by HLA-A11-specific and HLA-A11-restricted CTLs(10,11). Here we show that this phenomenon can be explained by a selective loss of the HLA-A11 polypeptide. The HLA-A11 negative phenotype is due to a regulatory phenomenon, rather than a structural defect, as proven by the ability to rescue expression of HLA-A11 in in vitro Epstein-Barr virus (EBV)-converted sublines of EBV negative BLs.
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Authors | M G Masucci, N J Stam, S Torsteinsdottir, J J Neefjes, G Klein, H L Ploegh |
Journal | Cellular immunology
(Cell Immunol)
Vol. 120
Issue 2
Pg. 396-400
(May 1989)
ISSN: 0008-8749 [Print] Netherlands |
PMID | 2541930
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S.)
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Chemical References |
- Histocompatibility Antigens Class I
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Topics |
- Alleles
- Burkitt Lymphoma
(immunology)
- Genes, MHC Class I
- Herpesvirus 4, Human
- Histocompatibility Antigens Class I
(analysis)
- Humans
- Tumor Cells, Cultured
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