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

Graft-versus-host disease across minor histocompatibility barriers was induced in two different models by transplanting allogeneic bone marrow and spleen cells into irradiated H-2-compatible recipient mice. In this report, we show that administration of peptides with high binding affinity for the respective class II major histocompatibility complex molecules after transplantation is capable of preventing the development of graft-versus-host disease in two different murine models. The peptides used were myelin basic protein residues 1 through 11 with alanine at position 4 (Ac 1-11[4A]) for I-Au (A alpha uA beta u), and the antigenic core sequence 323 through 339 of ovalbumin with lysine and methionine extension (KM core) for I-As (A alpha sA beta s). In both systems, the mechanism of prevention was found to be major histocompatibility complex-associated, because nonbinding control peptides did not have any effect. Engraftment of allogeneic bone marrow cells was shown by polymerase chain reaction analysis of DNA polymorphisms in a microsatellite region within the murine interleukin-5 gene.
 ...
PMID:Prevention of graft-versus-host disease by peptides binding to class II major histocompatibility complex molecules. 752 44

Intracisternal (IC) transfer of cerebrospinal fluid (CSF) mononuclear cells from multiple sclerosis (MS) patients has been reported by others to induce an 'MS-like pathology' in severe combined immunodeficient (SCID) mice. We injected cells from several sources intracisternally into SCID mice and assessed the recipients for clinical and histological disease. CSF cells and myelin basic protein (BP)-specific T lymphocytes from MS patients failed to induce clinical or histological disease following IC injection in SCID mice. Similarly, encephalitogenic BP-specific T cells from Lewis rats were unable to induce disease after IC injection in either SCID mice or Lewis rats, even at cell numbers which induced experimental autoimmune encephalomyelitis in Lewis rats following intraperitoneal (IP) injection. In contrast, naive Lewis rat splenocytes, which were capable of inducing lethal graft-versus-host (GVH) disease following IP transfer in SCID mice, induced paralysis and histopathological changes following IC transfer in SCID mice. We conclude that MS CSF cells do not typically transfer disease into SCID mice following IC injection. Furthermore, it appears likely that neuropathological disease following IC transfer of cells reflects the potential of the transferred cells for inducing GVH disease. Specific recognition of neuroantigens by T cells, as occurs in EAE, is probably not involved in the transfer of paralytic disease by IC transferred MS patient CSF cells.
 ...
PMID:T cells with encephalitogenic potential from multiple sclerosis patients and Lewis rats fail to induce disease in SCID mice following intracisternal injection. 786 Jul 7

The OX-40 protein was selectively upregulated on encephalitogenic myelin basic protein (MBP)-specific T cells at the site of inflammation during the onset of experimental autoimmune encephalomyelitis (EAE). An OX-40 immunotoxin was used to target and eliminate MBP-specific T cells within the central nervous system without affecting peripheral T cells. When injected in vivo, the OX-40 immunotoxin bound exclusively to myelin-reactive T cells isolated from the CNS, which resulted in amelioration of EAE. Expression of the human OX-40 antigen was also found in peripheral blood of patients with acute graft-versus-host disease and the synovia of patients with rheumatoid arthritis during active disease. The unique expression of the OX-40 molecule may provide a novel therapeutic strategy for eliminating autoreactive CD4+T cells that does not require prior knowledge of the pathogenic autoantigen.
 ...
PMID:Selective depletion of myelin-reactive T cells with the anti-OX-40 antibody ameliorates autoimmune encephalomyelitis. 857 63

We experienced a case of demyelinating, inflammatory cervical myelopathy after bone marrow transplantation for chronic myelocytic leukemia (CML). A 28 years-old man who had been having skin and liver graft versus host disease (GVHD), developed paresthesia in the legs, and then, difficulty in walking. At the time of admission, weakness of the hands also appeared. There was no evidence of CML recurrence after bone marrow transplantation. The myelopathy was characterized by multiple abnormal spotty signal intensities in the cervical spinal cord on MRI and these were in part Gd-enhanced. A course of pulse-dose methylprednisolone was given, followed by prednisolone. The neurological deficits were improved to the degree of full recovery. The inflammatory myelopathy together with a plaque in the cerebral hemisphere, moderately delayed p-100 latency of VEP and elevation of myelin basic protein of the spinal fluid, is difficult to distinguish from that of multiple sclerosis. Although the precise mechanism of GVHD-myelopathy is not known, it is likely that the donor myelin-reactive T-lymphocytes were non-specifically activated with GVHD reaction and directed to a central nervous system. Tacrolimus might have precipitated the focal immune reaction by way of cytotoxic effects on brain capillaries. The "GVHD-myelopathy" presented here may thus be akin to multiple sclerosis in its immune mechanism.
 ...
PMID:[A case of inflammatory demyelinative myelopathy after bone marrow transplantation]. 1108 92