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The Presence of Infectious Virus but not Conventional Antigen can Exacerbate Graft‐Versus‐Host Reactions
Author(s) -
CRAY C.,
LEVY R. B.
Publication year - 1990
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.1365-3083.1990.tb02907.x
Subject(s) - cytotoxic t cell , virus , antigen , immunology , antibody , immune system , major histocompatibility complex , biology , cd8 , virology , in vitro , biochemistry
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 (even at 100 × 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.