Identification of a graft versus host disease-associated human minor histocompatibility antigen

J M den Haan, N E Sherman, E Blokland, E Huczko, F Koning, J W Drijfhout, J Skipper, J Shabanowitz, D F Hunt, V H Engelhard

Research output: Contribution to journalArticleAcademicpeer-review

Abstract

Minor histocompatibility antigen disparities between human leukocyte antigen (HLA)-matched bone marrow donors and recipients are a major risk factor for graft versus host disease (GVHD). An HLA-A2.1-restricted cytotoxic T cell clone that recognized the minor histocompatibility antigen HA-2 was previously isolated from a patient with severe GVHD after HLA-identical bone marrow transplantation. The HLA-A2.1-bound peptide representing HA-2 has now been identified. This peptide appears to originate from a member of the non-filament-forming class I myosin family. Because HA-2 has a phenotype frequency of 95 percent in the HLA-A2.1-positive population, it is a candidate for immunotherapeutic intervention in bone marrow transplantation.

Original languageEnglish
Pages (from-to)1476-80
Number of pages5
JournalScience
Volume268
Issue number5216
Publication statusPublished - 9 Jun 1995

Cite this

den Haan, J. M., Sherman, N. E., Blokland, E., Huczko, E., Koning, F., Drijfhout, J. W., ... Engelhard, V. H. (1995). Identification of a graft versus host disease-associated human minor histocompatibility antigen. Science, 268(5216), 1476-80.
den Haan, J M ; Sherman, N E ; Blokland, E ; Huczko, E ; Koning, F ; Drijfhout, J W ; Skipper, J ; Shabanowitz, J ; Hunt, D F ; Engelhard, V H. / Identification of a graft versus host disease-associated human minor histocompatibility antigen. In: Science. 1995 ; Vol. 268, No. 5216. pp. 1476-80.
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abstract = "Minor histocompatibility antigen disparities between human leukocyte antigen (HLA)-matched bone marrow donors and recipients are a major risk factor for graft versus host disease (GVHD). An HLA-A2.1-restricted cytotoxic T cell clone that recognized the minor histocompatibility antigen HA-2 was previously isolated from a patient with severe GVHD after HLA-identical bone marrow transplantation. The HLA-A2.1-bound peptide representing HA-2 has now been identified. This peptide appears to originate from a member of the non-filament-forming class I myosin family. Because HA-2 has a phenotype frequency of 95 percent in the HLA-A2.1-positive population, it is a candidate for immunotherapeutic intervention in bone marrow transplantation.",
keywords = "Amino Acid Sequence, Bone Marrow Transplantation, Epitopes, Female, Graft vs Host Disease/immunology, HLA-A2 Antigen/immunology, Humans, Mass Spectrometry, Minor Histocompatibility Antigens/chemistry, Molecular Sequence Data, Neoplasm Proteins/chemistry, Oligopeptides/chemistry, T-Lymphocytes, Cytotoxic/immunology",
author = "{den Haan}, {J M} and Sherman, {N E} and E Blokland and E Huczko and F Koning and Drijfhout, {J W} and J Skipper and J Shabanowitz and Hunt, {D F} and Engelhard, {V H}",
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den Haan, JM, Sherman, NE, Blokland, E, Huczko, E, Koning, F, Drijfhout, JW, Skipper, J, Shabanowitz, J, Hunt, DF & Engelhard, VH 1995, 'Identification of a graft versus host disease-associated human minor histocompatibility antigen' Science, vol. 268, no. 5216, pp. 1476-80.

Identification of a graft versus host disease-associated human minor histocompatibility antigen. / den Haan, J M; Sherman, N E; Blokland, E; Huczko, E; Koning, F; Drijfhout, J W; Skipper, J; Shabanowitz, J; Hunt, D F; Engelhard, V H.

In: Science, Vol. 268, No. 5216, 09.06.1995, p. 1476-80.

Research output: Contribution to journalArticleAcademicpeer-review

TY - JOUR

T1 - Identification of a graft versus host disease-associated human minor histocompatibility antigen

AU - den Haan, J M

AU - Sherman, N E

AU - Blokland, E

AU - Huczko, E

AU - Koning, F

AU - Drijfhout, J W

AU - Skipper, J

AU - Shabanowitz, J

AU - Hunt, D F

AU - Engelhard, V H

PY - 1995/6/9

Y1 - 1995/6/9

N2 - Minor histocompatibility antigen disparities between human leukocyte antigen (HLA)-matched bone marrow donors and recipients are a major risk factor for graft versus host disease (GVHD). An HLA-A2.1-restricted cytotoxic T cell clone that recognized the minor histocompatibility antigen HA-2 was previously isolated from a patient with severe GVHD after HLA-identical bone marrow transplantation. The HLA-A2.1-bound peptide representing HA-2 has now been identified. This peptide appears to originate from a member of the non-filament-forming class I myosin family. Because HA-2 has a phenotype frequency of 95 percent in the HLA-A2.1-positive population, it is a candidate for immunotherapeutic intervention in bone marrow transplantation.

AB - Minor histocompatibility antigen disparities between human leukocyte antigen (HLA)-matched bone marrow donors and recipients are a major risk factor for graft versus host disease (GVHD). An HLA-A2.1-restricted cytotoxic T cell clone that recognized the minor histocompatibility antigen HA-2 was previously isolated from a patient with severe GVHD after HLA-identical bone marrow transplantation. The HLA-A2.1-bound peptide representing HA-2 has now been identified. This peptide appears to originate from a member of the non-filament-forming class I myosin family. Because HA-2 has a phenotype frequency of 95 percent in the HLA-A2.1-positive population, it is a candidate for immunotherapeutic intervention in bone marrow transplantation.

KW - Amino Acid Sequence

KW - Bone Marrow Transplantation

KW - Epitopes

KW - Female

KW - Graft vs Host Disease/immunology

KW - HLA-A2 Antigen/immunology

KW - Humans

KW - Mass Spectrometry

KW - Minor Histocompatibility Antigens/chemistry

KW - Molecular Sequence Data

KW - Neoplasm Proteins/chemistry

KW - Oligopeptides/chemistry

KW - T-Lymphocytes, Cytotoxic/immunology

M3 - Article

VL - 268

SP - 1476

EP - 1480

JO - Science

JF - Science

SN - 0036-8075

IS - 5216

ER -

den Haan JM, Sherman NE, Blokland E, Huczko E, Koning F, Drijfhout JW et al. Identification of a graft versus host disease-associated human minor histocompatibility antigen. Science. 1995 Jun 9;268(5216):1476-80.