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Blood, Vol. 93 No. 1 (January 1), 1999:
pp. 43-50
Murine T Lymphocytes Incapable of Producing Macrophage Inhibitory
Protein-1 Are Impaired in Causing Graft-Versus-Host Disease Across a
Class I But Not Class II Major Histocompatibility Complex
Barrier
Jonathan S. Serody,
Donald N. Cook,
Suzanne L. Kirby,
Elizabeth Reap,
Thomas C. Shea, and
Jeffrey A. Frelinger
From the Lineberger Comprehensive Cancer Center, and the Departments
of Medicine, Microbiology, and Immunology, University of North Carolina
at Chapel Hill, Chapel Hill, NC; and the Schering Plough Research
Institute, Kenilworth, NJ.
The routine use of bone marrow transplantation is limited by the
occurrence of acute and chronic graft-versus-host disease (GVHD).
Current approaches to decreasing the occurrence of GVHD after
allogeneic transplantation use T-cell depletion, use immunosuppressive agents, or block costimulatory molecule function. The role of proteins
in the recruitment of alloreactive lymphocytes has not been well
characterized. Chemokines are a large family of proteins that mediate
recruitment of mononuclear cells in vitro and in vivo. To investigate
the role of T-cell production of the chemokine macrophage inhibitory
protein-1 (MIP-1) in the occurrence of GVHD, splenocytes either
from wild-type or from MIP-1 / mice were administered to class
I (B6.C-H2bm1) and class II disparate mice
(B6-C-H2bm12). The incidence and severity of GVHD was
markedly reduced in bm1 mice receiving splenocytes from MIP-1/
mice as compared with mice receiving wild-type splenocytes. Bm1 mice
receiving MIP-1/ splenocytes had significantly less weight
loss and markedly reduced inflammatory responses in the lung and liver
than mice receiving C57BL/6 splenocytes. Bm1 mice receiving
MIP-1/ splenocytes had a markedly decreased production of
antichromatin autoantibodies and impaired generation of bm1-specific T
lymphocytes versus wild-type mice. However, MIP-1/ splenocytes
easily induced GVHD when administered to bm12 mice. This data show that
blockade of chemokine production or function may provide a new approach
to the prevention or treatment of GVHD but that chemokines that recruit
both CD4+ and CD8+ lymphocytes may need to
be targeted.
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