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The Journal of Immunology, Vol 158, Issue 1 29-39, Copyright © 1997 by American Association of Immunologists
ARTICLES |
BR Blazar, PA Taylor, A Panoskaltsis-Mortari, J Buhlman, J Xu, RA Flavell, R Korngold, R Noelle and DA Vallera
Department of Pediatrics, University of Minnesota, Minneapolis 55455, USA.
Alloreactive T cells require costimulatory signals via CD40 ligand (CD40L). The tissue-destructive properties of allogeneic CD4+ but not CD8+ T cells were inhibited by anti-CD40L mAb. Fewer CD4+ thoracic duct lymphocytes (TDL) were obtained in mAb-treated recipients. Kinetic studies revealed that CD4+ T cell expansion was reduced or delayed which may account, in part, for the partial graft-vs-host disease protective effect of anti-CD40L mAb. TDL were found to have diminished anti-host-specific proliferative responses. The frequency of donor TDL and splenocytes that expressed the Th1 cytokines IL-2, IL-12 p40, and IFN-gamma mRNA was markedly diminished in mAb-treated recipients, demonstrating that Th1-driven alloresponses were susceptible to CD40L targeting. Perforin mRNA-expressing T cells were undetectable in mAb- treated recipients, consistent with reduced in vivo lethality after the adoptive transfer of allogeneic CD4+ T cells. Similar findings were observed in both B cell-replete or -deficient recipients, indicating that allogeneic T cell expansion and priming can be sustained by a non- B cell, CD40+ host cell population. Mice receiving CD40L-deficient allogeneic CD4+ T cells had survival rates comparable to the rates of those given anti-CD40L mAb treatment. Because anti-CD40L mAb also was found to prevent host anti-donor-mediated marrow allograft rejection, in vivo blockade of CD40L-CD40 interactions may provide a highly beneficial approach to improving the outcome of allogeneic bone marrow transplantation.
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J. E. Buhlmann, M. Gonzalez, B. Ginther, A. Panoskaltsis-Mortari, B. R. Blazar, D. L. Greiner, A. A. Rossini, R. Flavell, and R. J. Noelle Cutting Edge: Sustained Expansion of CD8+ T Cells Requires CD154 Expression by Th Cells in Acute Graft Versus Host Disease J. Immunol., April 15, 1999; 162(8): 4373 - 4376. [Abstract] [Full Text] [PDF]
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A. Panoskaltsis-Mortari, D. L. Lacey, D. A. Vallera, and B. R. Blazar Keratinocyte Growth Factor Administered Before Conditioning Ameliorates Graft-Versus-Host Disease After Allogeneic Bone Marrow Transplantation in Mice Blood, November 15, 1998; 92(10): 3960 - 3967. [Abstract] [Full Text] [PDF]
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B. R. Blazar, P. A. Taylor, A. Panoskaltsis-Mortari, and D. A. Vallera Rapamycin Inhibits the Generation of Graft-Versus-Host Disease- and Graft-Versus-Leukemia-Causing T Cells by Interfering with the Production of Th1 or Th1 Cytotoxic Cytokines J. Immunol., June 1, 1998; 160(11): 5355 - 5365. [Abstract] [Full Text] [PDF]
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K. Saito, J. Sakurai, J. Ohata, T. Kohsaka, H. Hashimoto, K. Okumura, R. Abe, and M. Azuma Involvement of CD40 Ligand-CD40 and CTLA4-B7 Pathways in Murine Acute Graft-Versus-Host Disease Induced by Allogeneic T Cells Lacking CD28 J. Immunol., May 1, 1998; 160(9): 4225 - 4231. [Abstract] [Full Text] [PDF]
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S. L. Kalled, A. H. Cutler, S. K. Datta, and D. W. Thomas Anti-CD40 Ligand Antibody Treatment of SNF1 Mice with Established Nephritis: Preservation of Kidney Function J. Immunol., March 1, 1998; 160(5): 2158 - 2165. [Abstract] [Full Text] [PDF]
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