Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018133 (graft-versus-host disease)
 18,032 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Using histocompatible chicken strains B14 and B19, we demonstrate that the capacity to induce a GVH-R in an embryo could be induced precociously by the reaction itself. While naive chickens display this capacity around 3 to 4 weeks posthatching, embryos engrafted with adult allogeneic cells at E13 or E8 became endowed with this capacity at E20 and E15, respectively. Furthermore, this acceleration could be obtained by serial transfer of splenic cells through a sequence of three embryos undergoing the GVH-R. The highest efficiency in transfer was realized by regularly alternating the MHC haplotype at each transfer. It is concluded that the original cells from the adult donor may be partially responsible for the transfer, but that cells from the successive embryos are also certainly involved. Thus, maturation of the embryonic immune system appears accelerated by a GVH-R.
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PMID:Serial transfer of GVH-R splenomegaly in chicken embryos. 177 58

The relationship between the incidence of graft-versus-host disease (GVHD) and human leukocyte antigens (HLA) was analyzed in HLA-identical sibling bone marrow transplantation donor/recipient pairs from the two major populations in Israel: Jewish and Arabic. HLA phenotypes were significantly different, in both groups, between patients and healthy controls. Among Jews, a higher incidence of GVHD was found with A28, CW3, CW6 of class I and DR7, DQ2 of class II; a lower incidence was found with A2, A26, B14. Among Arabs, a higher incidence of GVHD was found with B41, CW7 of class I, and DR2, DR13 of class II. The development of GVHD is apparently associated with HLA phenotypes specific to each population.
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PMID:HLA and graft-versus-host disease: a population-based study of HLA phenotypes of Jewish and Arabic bone marrow transplanted patients in Israel. 911 27

In the present report, cytotoxic T lymphocyte (CTL) clones are described that display dual specificity for one of two common human leukocyte antigens (HLA B14 or B35) as alloantigens, and an immunodominant epitope (FLRGRAYGL) from Epstein-Barr virus (EBV) that binds to HLA B8. These T cell clonotypes were isolated from several unrelated HLA B8+, EBV-exposed individuals, and each distinct cross-reactivity pattern was associated with a common, public T cell receptor (TCR). In some individuals, CTL cross-reactive with these alloantigens completely dominated the memory response to this EBV epitope. Moreover, these memory T cells to EBV could be reactivated as a significant component of the repertoire of CTL responding to allogeneic stimulator cells expressing either HLA B14 or B35. These data illustrate how a history of infection with an immunogenic virus such as EBV can augment responsiveness to particular alloantigens; such influences may underlie the observed clinical association between herpesvirus infection and both allograft rejection and graft-versus-host disease. We have also explored the molecular basis for T cell cross-reactivity with alloantigens using the HLA B35 allo-reactive CTL clonotype. To elucidate the structural features of peptides that may be cross-recognized by these T cells, mono-substituted analogs of the viral epitope were screened for recognition, revealing broad specificity for major histocompatibility complex (MHC)-bound peptide. Based on the particular amino acid changes tolerated by the CTL at each peptide position, the human protein sequence database was searched for possible sequences that were recognized in association with HLA B35. Four peptides were identified (MPEATVYGL, IPIAPVYGM, KPSPPYFGL, and KPIVVLHGY) that were powerful activating ligands for the CTL when presented on HLA B35 but not B8. Thus, equivalent epitopes, capable of fully activating a single TCR, were formed by peptides with minimal obvious sequence homology bound to either HLA B8 or B35. These data indicate that degenerate peptide recognition by TCR may play an important role in the vigorous response of self-MHC-restricted T cells to alloantigens.
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PMID:Cross-reactive memory T cells for Epstein-Barr virus augment the alloresponse to common human leukocyte antigens: degenerate recognition of major histocompatibility complex-bound peptide by T cells and its role in alloreactivity. 924 84