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Blood, 1 October 2006, Vol. 108, No. 7, pp. 2485-2492.
Prepublished online as a Blood First Edition Paper on June 20, 2006; DOI 10.1182/blood-2006-04-016063.
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Submitted April 10, 2006
Accepted May 29, 2006
Host B cells produce IL-10 following TBI and attenuate
acute GVHD after allogeneic bone marrow transplantation
Vanessa Rowe, Tatjana Banovic, Kelli P MacDonald, Rachel Kuns, Alistair L Don, Edward S Morris, Angela C Burman, Helen M Bofinger, Andrew D Clouston, and Geoffrey R Hill*
The Queensland Institute of Medical Research, QLD, Australia
Department of Pathology, University of Queensland, Brisbane, Australia
* Corresponding author; email: geoffh{at}qimr.edu.au.
Host antigen presenting cells (APC) are known to be
critical for the induction of graft versus host disease
(GVHD) after allogeneic bone marrow transplantation
(BMT) but the relative contribution of specific APC
subsets remains unclear. We have studied the role of
host B cells in GVHD by using B cell deficient µMT
mice as BMT recipients in a model of CD4-dependent GVHD to MHC antigens. We demonstrate that acute GVHD is
augmented in µMT recipients relative to wild-type
(wt) recipients (mortality: 85% v 44%, P<0.01) and this is the result of an increase in donor T cell proliferation, expansion and inflammatory cytokine production early after BMT. Recipient B cells were depleted 28-fold at the day of BMT by total body irradiation (TBI) administered 24 hours earlier and we demonstrate that TBI rapidly induces IL-10 generation from B cells but not DC or other cellular populations within spleen. Finally, recipient mice in which B cells are unable to produce IL-10 due to
homologous gene deletion develop more severe acute GVHD
than recipient mice in which B cells are wild type.
Thus the induction of IL-10 in host B cells during
conditioning attenuates experimental acute GVHD.
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