TY - JOUR
T1 - The Presence of Infectious Virus but not Conventional Antigen can Exacerbate Graft‐Versus‐Host Reactions
AU - CRAY, C.
AU - LEVY, R. B.
PY - 1990/8
Y1 - 1990/8
N2 - Previous reports have demonstrated that the introduction of virus (MCMV, HSV-1) concurrent with a graft-versus-host reaction (GvHR) limited to a class I MHC disparity can result in the enhancement of GvHR-associated phenotypic (changes in CD4/CD8 ratio) and functional (inability to produce secondary antibody responses) alterations including the augmentation of in situ natural killer (NK) and donor anti-host cytotoxic T-cell activity. In the present study, we investigated whether immunogens other than infectious virus may be capable of enhancing GvHR. Mice receiving donor cells and the T-dependent antigen dinitrophenyl-bovine serum albumin (DNP-BSA) did not display exacerbated GvHR as evidenced by the absence of phenotypic alterations and the absence of elevated NK activity and the lack of donor anti-host cytotoxic activity. Furthermore, these recipients produced normal levels of IgM and IgG anti-DNP antibody. In addition, mice which received ultraviolet light (UV)-inactivated virus (event at 100 x dosage) together with donor cells also did not exhibit exacerbated GvHR. In total, these findings illustrate a novel ability of infectious virus to exacerbate GvH reactions and are consistent with the hypothesis that viral-induced immune responses may be important in the ability of a pathogen to induce the development of severe GvHR.
AB - Previous reports have demonstrated that the introduction of virus (MCMV, HSV-1) concurrent with a graft-versus-host reaction (GvHR) limited to a class I MHC disparity can result in the enhancement of GvHR-associated phenotypic (changes in CD4/CD8 ratio) and functional (inability to produce secondary antibody responses) alterations including the augmentation of in situ natural killer (NK) and donor anti-host cytotoxic T-cell activity. In the present study, we investigated whether immunogens other than infectious virus may be capable of enhancing GvHR. Mice receiving donor cells and the T-dependent antigen dinitrophenyl-bovine serum albumin (DNP-BSA) did not display exacerbated GvHR as evidenced by the absence of phenotypic alterations and the absence of elevated NK activity and the lack of donor anti-host cytotoxic activity. Furthermore, these recipients produced normal levels of IgM and IgG anti-DNP antibody. In addition, mice which received ultraviolet light (UV)-inactivated virus (event at 100 x dosage) together with donor cells also did not exhibit exacerbated GvHR. In total, these findings illustrate a novel ability of infectious virus to exacerbate GvH reactions and are consistent with the hypothesis that viral-induced immune responses may be important in the ability of a pathogen to induce the development of severe GvHR.
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U2 - 10.1111/j.1365-3083.1990.tb02907.x
DO - 10.1111/j.1365-3083.1990.tb02907.x
M3 - Article
C2 - 1975119
AN - SCOPUS:0025359974
VL - 32
SP - 177
EP - 182
JO - Scandinavian Journal of Immunology
JF - Scandinavian Journal of Immunology
SN - 0300-9475
IS - 2
ER -