Cargando…
A Human Minor Histocompatibility Antigen Specific for B Cell Acute Lymphoblastic Leukemia
Human minor histocompatibility antigens (mHags) play an important role in the induction of cytotoxic T lymphocyte (CTL) reactivity against leukemia after human histocompatibility leukocyte antigen (HLA)-identical allogeneic bone marrow transplantation (BMT). As most mHags are not leukemia specific b...
Autores principales: | , , , , , , , , , |
---|---|
Formato: | Texto |
Lenguaje: | English |
Publicado: |
The Rockefeller University Press
1999
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2192993/ https://www.ncbi.nlm.nih.gov/pubmed/9892612 |
_version_ | 1782147365969330176 |
---|---|
author | Dolstra, Harry Fredrix, Hanny Maas, Frans Coulie, Pierre G. Brasseur, Francis Mensink, Ewald Adema, Gosse J. de Witte, Theo M. Figdor, Carl G. van de Wiel-van Kemenade, Elly |
author_facet | Dolstra, Harry Fredrix, Hanny Maas, Frans Coulie, Pierre G. Brasseur, Francis Mensink, Ewald Adema, Gosse J. de Witte, Theo M. Figdor, Carl G. van de Wiel-van Kemenade, Elly |
author_sort | Dolstra, Harry |
collection | PubMed |
description | Human minor histocompatibility antigens (mHags) play an important role in the induction of cytotoxic T lymphocyte (CTL) reactivity against leukemia after human histocompatibility leukocyte antigen (HLA)-identical allogeneic bone marrow transplantation (BMT). As most mHags are not leukemia specific but are also expressed by normal tissues, antileukemia reactivity is often associated with life-threatening graft-versus-host disease (GVHD). Here, we describe a novel mHag, HB-1, that elicits donor-derived CTL reactivity in a B cell acute lymphoblastic leukemia (B-ALL) patient treated by HLA-matched BMT. We identified the gene encoding the antigenic peptide recognized by HB-1–specific CTLs. Interestingly, expression of the HB-1 gene was only observed in B-ALL cells and Epstein-Barr virus–transformed B cells. The HB-1 gene–encoded peptide EEKRGSLHVW is recognized by the CTL in association with HLA-B44. Further analysis reveals that a polymorphism in the HB-1 gene generates a single amino acid exchange from His to Tyr at position 8 within this peptide. This amino acid substitution is critical for recognition by HB-1–specific CTLs. The restricted expression of the polymorphic HB-1 Ag by B-ALL cells and the ability to generate HB-1–specific CTLs in vitro using peptide-loaded dendritic cells offer novel opportunities to specifically target the immune system against B-ALL without the risk of evoking GVHD. |
format | Text |
id | pubmed-2192993 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 1999 |
publisher | The Rockefeller University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-21929932008-04-16 A Human Minor Histocompatibility Antigen Specific for B Cell Acute Lymphoblastic Leukemia Dolstra, Harry Fredrix, Hanny Maas, Frans Coulie, Pierre G. Brasseur, Francis Mensink, Ewald Adema, Gosse J. de Witte, Theo M. Figdor, Carl G. van de Wiel-van Kemenade, Elly J Exp Med Articles Human minor histocompatibility antigens (mHags) play an important role in the induction of cytotoxic T lymphocyte (CTL) reactivity against leukemia after human histocompatibility leukocyte antigen (HLA)-identical allogeneic bone marrow transplantation (BMT). As most mHags are not leukemia specific but are also expressed by normal tissues, antileukemia reactivity is often associated with life-threatening graft-versus-host disease (GVHD). Here, we describe a novel mHag, HB-1, that elicits donor-derived CTL reactivity in a B cell acute lymphoblastic leukemia (B-ALL) patient treated by HLA-matched BMT. We identified the gene encoding the antigenic peptide recognized by HB-1–specific CTLs. Interestingly, expression of the HB-1 gene was only observed in B-ALL cells and Epstein-Barr virus–transformed B cells. The HB-1 gene–encoded peptide EEKRGSLHVW is recognized by the CTL in association with HLA-B44. Further analysis reveals that a polymorphism in the HB-1 gene generates a single amino acid exchange from His to Tyr at position 8 within this peptide. This amino acid substitution is critical for recognition by HB-1–specific CTLs. The restricted expression of the polymorphic HB-1 Ag by B-ALL cells and the ability to generate HB-1–specific CTLs in vitro using peptide-loaded dendritic cells offer novel opportunities to specifically target the immune system against B-ALL without the risk of evoking GVHD. The Rockefeller University Press 1999-01-18 /pmc/articles/PMC2192993/ /pubmed/9892612 Text en This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/). |
spellingShingle | Articles Dolstra, Harry Fredrix, Hanny Maas, Frans Coulie, Pierre G. Brasseur, Francis Mensink, Ewald Adema, Gosse J. de Witte, Theo M. Figdor, Carl G. van de Wiel-van Kemenade, Elly A Human Minor Histocompatibility Antigen Specific for B Cell Acute Lymphoblastic Leukemia |
title | A Human Minor Histocompatibility Antigen Specific for B Cell Acute Lymphoblastic Leukemia |
title_full | A Human Minor Histocompatibility Antigen Specific for B Cell Acute Lymphoblastic Leukemia |
title_fullStr | A Human Minor Histocompatibility Antigen Specific for B Cell Acute Lymphoblastic Leukemia |
title_full_unstemmed | A Human Minor Histocompatibility Antigen Specific for B Cell Acute Lymphoblastic Leukemia |
title_short | A Human Minor Histocompatibility Antigen Specific for B Cell Acute Lymphoblastic Leukemia |
title_sort | human minor histocompatibility antigen specific for b cell acute lymphoblastic leukemia |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2192993/ https://www.ncbi.nlm.nih.gov/pubmed/9892612 |
work_keys_str_mv | AT dolstraharry ahumanminorhistocompatibilityantigenspecificforbcellacutelymphoblasticleukemia AT fredrixhanny ahumanminorhistocompatibilityantigenspecificforbcellacutelymphoblasticleukemia AT maasfrans ahumanminorhistocompatibilityantigenspecificforbcellacutelymphoblasticleukemia AT couliepierreg ahumanminorhistocompatibilityantigenspecificforbcellacutelymphoblasticleukemia AT brasseurfrancis ahumanminorhistocompatibilityantigenspecificforbcellacutelymphoblasticleukemia AT mensinkewald ahumanminorhistocompatibilityantigenspecificforbcellacutelymphoblasticleukemia AT ademagossej ahumanminorhistocompatibilityantigenspecificforbcellacutelymphoblasticleukemia AT dewittetheom ahumanminorhistocompatibilityantigenspecificforbcellacutelymphoblasticleukemia AT figdorcarlg ahumanminorhistocompatibilityantigenspecificforbcellacutelymphoblasticleukemia AT vandewielvankemenadeelly ahumanminorhistocompatibilityantigenspecificforbcellacutelymphoblasticleukemia AT dolstraharry humanminorhistocompatibilityantigenspecificforbcellacutelymphoblasticleukemia AT fredrixhanny humanminorhistocompatibilityantigenspecificforbcellacutelymphoblasticleukemia AT maasfrans humanminorhistocompatibilityantigenspecificforbcellacutelymphoblasticleukemia AT couliepierreg humanminorhistocompatibilityantigenspecificforbcellacutelymphoblasticleukemia AT brasseurfrancis humanminorhistocompatibilityantigenspecificforbcellacutelymphoblasticleukemia AT mensinkewald humanminorhistocompatibilityantigenspecificforbcellacutelymphoblasticleukemia AT ademagossej humanminorhistocompatibilityantigenspecificforbcellacutelymphoblasticleukemia AT dewittetheom humanminorhistocompatibilityantigenspecificforbcellacutelymphoblasticleukemia AT figdorcarlg humanminorhistocompatibilityantigenspecificforbcellacutelymphoblasticleukemia AT vandewielvankemenadeelly humanminorhistocompatibilityantigenspecificforbcellacutelymphoblasticleukemia |