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Blood, Vol. 92 No. 11 (December 1), 1998:
pp. 4453-4463
A Critical Role for CD48 Antigen in Regulating Alloengraftment and
Lymphohematopoietic Recovery After Bone Marrow Transplantation
Bruce R. Blazar,
Patricia A. Taylor,
Angela Panoskaltsis-Mortari,
Hideo Yagita,
Jonathan S. Bromberg, and
Daniel A. Vallera
From the University of Minnesota Cancer Center and the Department of
Pediatrics, Division of Bone Marrow Transplantation and the Department
of Therapeutic Radiology-Radiation Oncology, University of Minnesota
Hospital and Cancer Center, Minneapolis, MN; Jutendo University School
of Medicine, Tokyo, Japan; and the University of Michigan, Ann Arbor,
MI.
The binding of CD2, present on T cells, to its counterreceptor CD48
facilitates adhesion, signaling, alloantigen-induced cytokine production, and cytotoxic T-lymphocyte responses. Because
these T-cell functions have been implicated in graft-versus-host
disease (GVHD) pathogenesis, we have analyzed the effects of the
CD2:CD48 pathway on GVHD mediated by CD4+ and
CD8+ T cells infused into sublethally irradiated
recipients. CD4+ T-cell-mediated, and to a lesser
extent, CD8+ T-cell-mediated GVHD was inhibited by
 CD2 + 48 monoclonal antibody (MoAb) infusion. To assess
the effects of combined MoAb infusion on alloengraftment, two different
alloengraftment bone marrow transplantation (BMT) models were used. In
both, MoAb infusion markedly inhibited alloengraftment and
hematopoietic recovery post-BMT. To determine if the adverse effects on
lymphohematopoiesis in the allogeneic BMT recipients were caused by an
immune or nonimmune mechanism, studies were performed in congenic BMT
recipients to preclude an immune mechanism as the cause for delayed
recovery post-BMT. MoAb infusion resulted in impaired
lymphohematopoietic recovery in congenic BMT recipients and markedly
reduced day 12 colony-forming unit-spleen formation in syngeneic BMT
recipients, consistent with a nonimmune mediated mechanism. Because the
spleen is a site of early hematopoietic recovery post-BMT, studies were performed using adult splenectomized syngeneic BMT recipients. MoAb
infusion delayed recovery in both nonsplenectomized and splenectomized recipients post-BMT, indicating that the delayed hematopoietic recovery
was not the consequence of an abnormal homing pattern of hematopoietic
progenitors to the spleen early post-BMT. CD48 MoAb was necessary
and sufficient for the inhibition of GVHD lethality and delayed
lymphohematopoietic effects of the combined MoAb regimen. CD48 MoAb
was found to induce a profound modulation of CD48 antigen expression on
BM cells, suggesting that the CD48 antigen may have an important
function in hematopoiesis in the BM compartment. Taken together, these
data provide evidence that the CD48 antigen plays a critical role in
regulating hematopoiesis in post-BMT.
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