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*
University of Minnesota Cancer Center and Department of Pediatrics, Division of Bone Marrow Transplantation, Minneapolis, MN 55455;
Department of Opthalmology, Louisiana State University Medical Center, New Orleans, LA 70112;
Immunomodulation Research Center, University of Ulsan, Ulsan, Korea; and
Immunex, Seattle, WA 98101
4-1BB is expressed on activated CD4+ and
CD8+ T cells; its ligand, 4-1BB ligand is expressed on
APCs. Despite expression on both T cell subpopulations, 4-1BB has been
reported to predominantly affect CD8+ T cell responses. By
quantifying graft-vs-host disease alloresponses in vivo, we demonstrate
that both CD4+ and CD8+ T cell-mediated
alloresponses are regulated by 4-1BB/4-1BB ligand interactions to
approximately the same extent. 4-1BB receptor-facilitated
CD4+ T cell-mediated alloresponses were partly CD28
independent. In two distinct marrow graft rejection systems, host
CD8+ and CD4+ T cells each separately
contributed to host anti-donor T cell-mediated allograft rejection.
4-1BB mAb increased the graft-vs-leukemia effect of a suboptimal
number of donor splenocytes given later post bone marrow
transplantation by bolstering allogeneic responses resulting in
leukemia elimination. In summary, 4-1BB ligation is a potent regulator
of CD4+ and CD8+ T cell-mediated allogeneic
responses in vivo. Modifying the ligation of 4-1BB represents a new
approach to altering the graft-vs-host disease and graft-vs-leukemia
effects of allogeneic T cells post bone marrow
transplantation.
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K. Nozawa, J. Ohata, J. Sakurai, H. Hashimoto, H. Miyajima, H. Yagita, K. Okumura, and M. Azuma Preferential Blockade of CD8+ T Cell Responses by Administration of Anti-CD137 Ligand Monoclonal Antibody Results in Differential Effect on Development of Murine Acute and Chronic Graft-Versus-Host Diseases J. Immunol., November 1, 2001; 167(9): 4981 - 4986. [Abstract] [Full Text] [PDF]
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J. L. Cannons, P. Lau, B. Ghumman, M. A. DeBenedette, H. Yagita, K. Okumura, and T. H. Watts 4-1BB Ligand Induces Cell Division, Sustains Survival, and Enhances Effector Function of CD4 and CD8 T Cells with Similar Efficacy J. Immunol., August 1, 2001; 167(3): 1313 - 1324. [Abstract] [Full Text] [PDF]
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