Evidence that CD31, CD49b, and CD62L are immunodominant minor histocompatibility antigens in HLA identical sibling bone marrow transplants

Etsuko Maruya, Hiroh Saji, Shigeki Seki, Yasuhiko Fujii, Koji Kato, Syunro Kai, Akira Hiraoka, Keisei Kawa, Yasutaka Hoshi, Kazuhiko Ito, Shigeki Yokoyama, Takeo Juii

Research output: Contribution to journalArticle

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Abstract

Despite complete matching of siblings for the HLA loci, after bone marrow transplantation (BMT), approximately 20% develop graft-versus-host disease (GVHD). This is presumably due to incompatibility of minor histocompatibility antigens (mHa). We investigated the polymorphisms of 14 adhesion molecules (CD2, CD28, CD31, CD34, CD36, CD42, CD44, CD48, CD49b, CD54, CD62L, CD86, CD102, and CD106) in Japanese subjects and their association with the occurrence of GVHD after allogeneic HLA identical BMT. Six molecules (CD2, CD31, CD42, CD49b, CD54, and CD62L), which were found to be polymorphic, were then examined in 118 HLA identical sibling donors and recipients who had undergone BMT. Association of the incompatibility of the polymorphic molecules with the presence or absence of GVHD was examined. In these six, we observed a significant correlation between acute GVHD and the compatibility of CD31 (codons 563/670) (P(corrected) = .018), and CD31 (codons 563/670) + CD62L (P(corrected) = .018) in patients with the HLA-B44- like superfamily. In patients with the HLA-A3-like superfamily, the compatibility of CD62L (P(corrected) =03) and CD62L + CD49b (P = .004, P(corrected) = .078) was associated with acute GVHD. Therefore, CD31, CD49b, and CD62L might be candidates for immunodominant mHa.

Original languageEnglish
Pages (from-to)2169-2176
Number of pages8
JournalBlood
Volume92
Issue number6
Publication statusPublished - Sep 15 1998
Externally publishedYes

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Minor Histocompatibility Antigens
Transplants
Graft vs Host Disease
Grafts
Siblings
Bone
Bone Marrow
Bone Marrow Transplantation
Transplantation (surgical)
Codon
Molecules
HLA-B44 Antigen
HLA-A3 Antigen
Polymorphism
Adhesion
Tissue Donors

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Immunology
  • Hematology
  • Cell Biology

Cite this

Evidence that CD31, CD49b, and CD62L are immunodominant minor histocompatibility antigens in HLA identical sibling bone marrow transplants. / Maruya, Etsuko; Saji, Hiroh; Seki, Shigeki; Fujii, Yasuhiko; Kato, Koji; Kai, Syunro; Hiraoka, Akira; Kawa, Keisei; Hoshi, Yasutaka; Ito, Kazuhiko; Yokoyama, Shigeki; Juii, Takeo.

In: Blood, Vol. 92, No. 6, 15.09.1998, p. 2169-2176.

Research output: Contribution to journalArticle

Maruya, E, Saji, H, Seki, S, Fujii, Y, Kato, K, Kai, S, Hiraoka, A, Kawa, K, Hoshi, Y, Ito, K, Yokoyama, S & Juii, T 1998, 'Evidence that CD31, CD49b, and CD62L are immunodominant minor histocompatibility antigens in HLA identical sibling bone marrow transplants', Blood, vol. 92, no. 6, pp. 2169-2176.
Maruya, Etsuko ; Saji, Hiroh ; Seki, Shigeki ; Fujii, Yasuhiko ; Kato, Koji ; Kai, Syunro ; Hiraoka, Akira ; Kawa, Keisei ; Hoshi, Yasutaka ; Ito, Kazuhiko ; Yokoyama, Shigeki ; Juii, Takeo. / Evidence that CD31, CD49b, and CD62L are immunodominant minor histocompatibility antigens in HLA identical sibling bone marrow transplants. In: Blood. 1998 ; Vol. 92, No. 6. pp. 2169-2176.
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T1 - Evidence that CD31, CD49b, and CD62L are immunodominant minor histocompatibility antigens in HLA identical sibling bone marrow transplants

AU - Maruya, Etsuko

AU - Saji, Hiroh

AU - Seki, Shigeki

AU - Fujii, Yasuhiko

AU - Kato, Koji

AU - Kai, Syunro

AU - Hiraoka, Akira

AU - Kawa, Keisei

AU - Hoshi, Yasutaka

AU - Ito, Kazuhiko

AU - Yokoyama, Shigeki

AU - Juii, Takeo

PY - 1998/9/15

Y1 - 1998/9/15

N2 - Despite complete matching of siblings for the HLA loci, after bone marrow transplantation (BMT), approximately 20% develop graft-versus-host disease (GVHD). This is presumably due to incompatibility of minor histocompatibility antigens (mHa). We investigated the polymorphisms of 14 adhesion molecules (CD2, CD28, CD31, CD34, CD36, CD42, CD44, CD48, CD49b, CD54, CD62L, CD86, CD102, and CD106) in Japanese subjects and their association with the occurrence of GVHD after allogeneic HLA identical BMT. Six molecules (CD2, CD31, CD42, CD49b, CD54, and CD62L), which were found to be polymorphic, were then examined in 118 HLA identical sibling donors and recipients who had undergone BMT. Association of the incompatibility of the polymorphic molecules with the presence or absence of GVHD was examined. In these six, we observed a significant correlation between acute GVHD and the compatibility of CD31 (codons 563/670) (P(corrected) = .018), and CD31 (codons 563/670) + CD62L (P(corrected) = .018) in patients with the HLA-B44- like superfamily. In patients with the HLA-A3-like superfamily, the compatibility of CD62L (P(corrected) =03) and CD62L + CD49b (P = .004, P(corrected) = .078) was associated with acute GVHD. Therefore, CD31, CD49b, and CD62L might be candidates for immunodominant mHa.

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