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Blood, 1 March 2002, Vol. 99, No. 5, pp. 1572-1577
CLINICAL OBSERVATIONS, INTERVENTIONS, AND THERAPEUTIC TRIALS
Effect of tolerance to noninherited maternal antigens on
the occurrence of graft-versus-host disease after bone marrow
transplantation from a parent or an HLA-haploidentical
sibling
Jon J. van Rood,
Fausto R. Loberiza Jr,
Mei-Jie Zhang,
Machteld Oudshoorn,
Frans Claas,
Mitchell S. Cairo,
Richard E. Champlin,
Robert Peter Gale,
Olle Ringdén,
Jill M. Hows, and
Mary H. Horowitz
From Leiden University Medical Center, The Netherlands
(J.J.V., M.O., F.C.); Histocompatibility Committee of the International
Bone Marrow Transplant Registry, Health Policy Institute, Medical
College of Wisconsin, Milwaukee (F.R.L., M.J.Z., M.M.H.); Children's
Hospital of New York (M.S.C.); University of Texas MD Anderson Cancer
Center, Houston (R.E.C.); Center for Advanced Studies in Leukemia, Los
Angeles, CA (R.P.G.); Huddinge University Hospital, Sweden (O.R.); and
University of Bristol, United Kingdom (J.M.H.).
In haploidentical transplantation, the mismatched haplotype of the
donor can originate from either of the parents. We refer to such
mismatched haplotypes as noninherited maternal antigens (NIMA
haplotype) or noninherited paternal antigens (NIPA haplotype). To
determine whether exposure to maternal HLA antigens benefits patients
undergoing bone marrow transplantation, we analyzed graft failure and
graft-versus-host disease (GVHD) after transplantations from parental
or haploidentical sibling donors. We studied 269 patients receiving 1 or 2 HLA-A, -B, -DR antigen-mismatched sibling or parental
non-T-cell-depleted bone marrow transplants for acute myelogenous
leukemia, acute lymphoblastic leukemia, or chronic myelogenous leukemia
between 1985 and 1997 that were reported to the International Bone
Marrow Transplant Registry. Included were 121 (45%) NIMA-mismatched
and 148 (55%) NIPA-mismatched transplantations. Sixty-three
(52%) of the NIMA-mismatched transplants and 69 (47%) of the
NIPA-mismatched transplants were from haploidentical sibling donors.
Sibling transplantations mismatched for NIMA had similar rates of graft
failure but lower rates of acute GVHD (P < .02) than
NIPA-mismatched sibling transplantations. In the first 4 months after
transplantation, mother-to-child transplantations involved
significantly less chronic GVHD than father-to-child transplantations
(P < .02). Treatment-related mortality (TRM) was
significantly higher after parental transplantations
(P = .009 for mother; P = .03 for father)
than after haploidentical sibling transplantations mismatched for the
NIMA. Non-T-cell-depleted bone marrow transplants donated by
haploidentical siblings to recipients mismatched for NIPA and
transplants donated by parents caused more acute and chronic GVHD and
TRM than transplants donated by haploidentical siblings mismatched for NIMA.
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