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Blood, Vol. 92 No. 6 (September 15), 1998:
pp. 2169-2176
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, and
Takeo Juji
From the Department of Research, Kyoto Red Cross Blood Center, Kyoto,
Japan; the Department of Internal Medicine, Saku Central Hospital,
Nagano, Japan; the Department of Transfusion Medicine, Yamaguchi
University Hospital, Yamaguchi, Japan; the Division of
Hematology/Oncology, Japanese Red Cross Nagoya First Hospital, Nagoya,
Japan; the Department of Transfusion Medicine, Hyogo Medical College,
Nishinomiya, Japan; the Department of Internal Medicine, Osaka Medical
Center for Cancer and Cardiovascular Disease, Osaka, Japan; the
Department of Pediatrics, Osaka Medical Center and Research Institute
for Maternal and Child Health, Osaka, Japan; the Department of
Transfusion Medicine, Tokyo Jikei University School of Medicine, Tokyo,
Japan; the Department of Transfusion Medicine, Kyoto University
Hospital, Kyoto, Japan; and the Japanese Red Cross Central Blood
Center, Tokyo, Japan.
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) (Pcorrected = .018), and CD31 (codons 563/670) + CD62L (Pcorrected = .018) in patients with
the HLA-B44-like superfamily. In patients with the HLA-A3-like
superfamily, the compatibility of CD62L (Pcorrected = .03) and CD62L + CD49b (P = .004, Pcorrected = .078) was associated with acute
GVHD. Therefore, CD31, CD49b, and CD62L might be candidates for
immunodominant mHa.
© 1998 by The American Society of Hematology.
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