Endogenous retroviruses lead to the expression of a histocompatibility antigen detectable by skin graft rejection.

Colombo, Mario P.; Jaenisch, Rudolf; Wettstein, Peter J.

doi:10.1073/pnas.84.1.189

Cited by 23 publications

(3 citation statements)

References 30 publications

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“…More recent experiments indicate that viral sequences inserted into the mouse genome can code for minor H antigens. This was shown by the classical technique of skin graft rejection and by CTL-reactivity for the SV40 Tgene and for the Moloney mouse leukemia virus (Colombo et al 1987, Wettstein et al 1988). …”

Section: Discussionmentioning

confidence: 95%

Protein-specific cytotoxic T lymphocytes. Recognition of transfectants expressing intracellular, membrane-associated or secreted forms of β-galactosidase

1989

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BALB/c-derived tumor cells were transfected with recombinant Escherichia coli beta-galactosidase (beta-gal) genes which were inserted into IgM heavy chain gene derivatives, leading to expression of the resulting fusion protein in different cellular compartments. A beta-gal-specific, major histocompatibility complex (MHC) class I-restricted CD8+CD4- cytotoxic T lymphocyte (CTL) line of BALB/c origin raised against one transfectant expressing cytoplasmic beta-gal also lysed transfectants expressing beta-gal as membrane-inserted fusion protein, as well as transfectants secreting beta-gal. Our data show that MHC class I-restricted CTL can recognize fragments of nonviral cellular proteins, be they expressed as intracellular, membrane-inserted, or secreted products. The findings confirm and extend a hypothesis on the nature of minor histocompatibility (H) antigens formulated earlier.

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Section: Discussionmentioning

confidence: 95%

Protein-specific cytotoxic T lymphocytes. Recognition of transfectants expressing intracellular, membrane-associated or secreted forms of β-galactosidase

1989

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“…Endogenous peptide presentation by MHC class II molecules is well described [44][45][46]. It is likely there exists a system of minor antigenic peptides in the b 2 m-/-MHC repertoire presented by MHC class II molecules that can be solely responsible for the initiation and maintenance of GVHD in the absence of cell surface intact class I molecules.…”

Section: Discussionmentioning

confidence: 99%

Analysis of graft-versus-host disease (GVHD) and graft rejection using MHC class I-deficient mice

Shenoy

Desch

Duffy³

et al. 1998

Clinical and Experimental Immunology

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GVHD is a major complication in allogeneic bone marrow transplantation (BMT). MHC class I mismatching increases GVHD, but in MHC-matched BMT minor histocompatibility antigens (mH) presented by MHC class I result in significant GVHD. To examine the modification of GVHD in the absence of cell surface MHC class I molecules, beta2-microglobulin-deficient mice (beta2m(-/-)) were used as allogeneic BMT recipients in MHC- and mH-mismatched transplants. Beta2m(-/-) mice accepted MHC class I-expressing BM grafts and developed significant GVHD. MHC (H-2)-mismatched recipients developed acute lethal GVHD. In contrast, animals transplanted across mH barriers developed indolent chronic disease that was eventually fatal. Engrafted splenic T cells in all beta2m(-/-) recipients were predominantly CD3+alphabetaTCR+CD4+ cells (15-20% of all splenocytes). In contrast, CD8+ cells engrafted in very small numbers (1-5%) irrespective of the degree of MHC mismatching. T cells proliferated against recipient strain antigens and recognized recipient strain targets in cytolytic assays. Cytolysis was blocked by anti-MHC class II but not anti-CD8 or anti-MHC class I monoclonal antibodies (MoAbs). Cytolytic CD4+ T cells induced and maintained GVHD in mH-mismatched beta2m(-/-) mice, supporting endogenous mH presentation solely by MHC class II. Conversely, haematopoietic beta2m(-/-) cells were unable to engraft in normal MHC-matched recipients, presumably due to natural killer (NK)-mediated rejection of class I-negative cells. Donor-derived lymphokine-activated killer cells (LAK) were unable to overcome graft rejection (GR) and support engraftment.

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“…Endogenous retroviral sequences can encode antigens capable of stimulating both skin graft rejection and CTL (Colombo et al 1987b), and many minor histocompatibility antigens show fight linkage to endogenous proviruses and the antigens (Meruelo et al 1983;Rossomando and Meruelo 1986). Although none of the Table 2.…”

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confidence: 99%

Immunodominance in the T-cell response to multiple non-H-2 histocompatibility antigens. V. Chromosomal mapping of the immunodominant cytotoxic T-cell target-1 (CTT-1)

et al. 1993

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Endogenous retroviruses lead to the expression of a histocompatibility antigen detectable by skin graft rejection.

Abstract: Mov mouse strains differ from their respec-

Cited by 23 publications

References 30 publications

Protein-specific cytotoxic T lymphocytes. Recognition of transfectants expressing intracellular, membrane-associated or secreted forms of β-galactosidase

Protein-specific cytotoxic T lymphocytes. Recognition of transfectants expressing intracellular, membrane-associated or secreted forms of β-galactosidase

Analysis of graft-versus-host disease (GVHD) and graft rejection using MHC class I-deficient mice

Immunodominance in the T-cell response to multiple non-H-2 histocompatibility antigens. V. Chromosomal mapping of the immunodominant cytotoxic T-cell target-1 (CTT-1)

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