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)

Human and rabbit antibodies to trophoblast-lymphocyte cross-reactive (TLX) antigens were employed in an enzyme-linked immunosorbent assay (ELISA) to identify and characterize the TLX alloantigen system on human platelets. Neither washing nor extraction in chaotrope or acid altered platelet TLX. The antigen was significantly changed by pronase and trypsin digestion, but Folch extraction yielded antigen in the hydrophilic interface, suggesting carbohydrate. Rabbit antibodies prepared to HLA-negative human syncytiotrophoblast TLX antigens were shown by platelet ELISA to have the same specificity and similar allotypy as anti-TLX antibodies from secondary (2 degrees) spontaneously aborting women. Patients with normal pregnancies before becoming 2 degrees aborters had both IgG and IgM antibodies to TLX. Anti-TLX in patients who never had a normal pregnancy were predominantly IgG. ELISA reactions performed with different concentrations of protein in the buffers detected anti-TLX activity in buffers containing high protein concentrations. This has been observed in studies of blocking antibodies in graft-versus-host disease and immune responses to tumor cells. Platelet TLX offers a new genetic and immunological approach to study similarities of the host-parasite relationships in pregnancy, transplantation, and cancer.
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PMID:Antigens of human trophoblast: trophoblast-lymphocyte cross-reactive antigens on platelets. 367 62

The studies presented herein were designed to directly evaluate the effects of a transient GVH reaction on T lymphocyte functions. To this end, we have shown that generation of carrier-specific helper cell function can be significantly influenced by the allogeneic effect. Thus, carrier-primed helper cells derived from CAF(1) donor mice were generally much more active in specifically cooperating with syngeneic 2,4-dinitrophenyl (DNP)-primed B cells in adoptive recipients when parental A strain lymphocytes had been administered at some time during the priming regimen. This was true when allogeneic cells were administered concomitantly with the initial priming dose of carrier protein as well as when the GVH was induced in animals that had been exposed to antigen several days previously. This indicates that the allogeneic enhancing effects can be manifested on either primed or unprimed T cell populations. The ultimate effect of the GVH reaction on the development of helper T cell activity was found to be related to the number of allogeneic cells employed and the duration of the resultant GVH reaction in the carrier-primed host animal. Hence, allogeneic stimulation of slightly greater magnitude and/or longer duration resulted in marked suppression rather than enhancement of helper cell function in such donor mice. These findings may have general relevance to problems in autoimmune diseases and tumor immunity.
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PMID:The allogeneic effect in inbred mice. IV. Regulatory influences of graft-vs.-host reactions on host T lymphocyte functions. 412 47

Under in vitro conditions spleen cells from nonirradiated F(1) hybrids, in which a (graft-vs.-host) (GVH) reaction had been induced with lymphoid cells of parental origin, lysed nonspecifically target cells, i.e., cells syngeneic or allogeneic to the parental genotypes. Furthermore, tumor cells exposed in vitro to spleen cells of F(1) hybrid mice undergoing GVH reaction had markedly decreased ability to grow in syngeneic recipients. Experiments involving inhibition of cytotoxicity with alloantisera indicated that this nonspecific effect was due to host cells. By contrast, spleen cells of lethally irradiated F(1) hybrids undergoing GVH reaction lysed specifically the target cells of the genotype against which the parental (donor) cells had been sensitized; this finding further supports the contribution of host cells to the nonspecific cytotoxic effects in GVH reaction. From these results it was deduced that the cytotoxic effects during GVH reaction involve at least two processes: (a) sensitization of the donor cells to the antigens of the recipient resulting in the activation of their potential to lyse specifically the recipient's cells, and (b) activation of the host's cells into a state of nonspecific cytotoxicity, as a consequence of the immunologically specific attack of the donor cells.
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PMID:Cytotoxicity in graft-versus-host reaction. I. Role of donor and host spleen cells. 440 94

Spleen cells from BALB/c or CAF(1) mice released little or no detectable leukemia virus when cultured 2-7 days in vitro. In contrast, spleen cells of CAF(1) mice previously inoculated with parental BALB/c spleen cells released leukemia viruses in 10 of 11 cases studied. Cultures of a mixture of spleen cells from normal BALB/c and CAF(1) mice also contained leukemia viruses. Phytohemagglutinin induced the transformation of lymphocytes in cultures of CAF(1) or BALB/c spleen cells, but this transformation did not activate leukemia viruses. It is concluded that mixed lymphocyte cultures in vitro, just as graft-versus-host reactions in vivo, can activate leukemia viruses that are normally present in a repressed form. This activation is not solely a function of lymphocyte transformation. The activated mouse leukemia virus may subsequently account for the observed high incidence of neoplasia in graft-versus-host disease.
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PMID:Activation of leukemia viruses by graft-versus-host and mixed lymphocyte reactions in vitro. 440 35

We have previously reported that the elimination of T-lymphocytes (greater than 99%) from the donor bone marrow prevents significant graft versus host disease (GvHD). This has been confirmed by other centres. Many of these groups have applied monoclonal antibodies with cytolytic rabbit complement. In some of these studies mostly patients with fully matched sibling donors have been studied and no further immunosuppression has been given during the regeneration period. The experience here shows that the haemopoietic regeneration (to recover a total leucocyte count of 1.0 X 10(9)/l) has only been minimally delayed (mean 25 days) when compared to patients receiving standard methotrexate (Mtx) GvHD prophylaxis (22 days). The incidence of cytomegalovirus (CMV) infections (14%; none fatal) was lower than that in our previous 54 patients (43% CMV infections, 13% fatal). Furthermore, no fatal pneumonitis was seen. The regeneration of T-cells in our patients has shown normal values of T8-positive cells in the circulation from 45 to 50 days onwards, as opposed to the previous groups of patients whose T8-positive cells regenerated to 3-4 times higher than normal values. These observations indicate that T-cell depletion with monoclonal antibodies is an effective method for preventing GvHD, but further studies are necessary to investigate the cause(s) of a new occasional complication, the rejection of the newly established bone marrow.
Med Oncol Tumor Pharmacother 1984
PMID:The role of monoclonal antibodies in the prevention of graft versus host disease. 610 May 58

Ocular inflammatory diseases and ocular adnexal lymphoid tumors have become less obscure and intimidating by virtue of our ability to study the infiltrates in these various diseases for their B-lymphocyte and T-lymphocyte composition. Comparisons are also possible between lymphocytic profiles in the peripheral blood and the precise composition of the in situ infiltrates within the ocular tissue themselves. The availability of monoclonal antibodies, which can determine T-lymphocytic subsets such as T-helper cells and T-suppressor/cytotoxic cells, natural killer cells, and monocytes-histiocytes, has provided a powerful technology for the delineation of the distinctive immune composition of the inflammatory infiltrates, as well as any possible disturbances in T-cell immunoregulation. B-lymphocytes produce immunoglobulins, which may be misdirected as autoantibodies in local or systemic autoimmune diseases. Immunoglobulin-mediated and therefore B-cell derived conditions include vasculitis, progressive cicatricial ocular pemphigoid, Mooren's corneal ulcer, scleritis, and hay fever and vernal conjunctivitis. Other diseases in which B-lymphocytes, their immunoglobulin products or immune complexes formed with presently unknown antigens are potentially at fault are chronic non-specific uveitis; iridocyclitis in Behcet's syndrome; Fuch's heterochromic syndrome, ankylosing spondylitis, and Reiter's syndrome; Graves' disease; and idiopathic inflammatory orbital pseudotumor and myositis. T-cells do not produce immunoglobins, but rather secrete lymphokines or interact directly with receptors or determinants on viruses or target tissues (eg. immunosurveillance against neoplasia); it is possible that some autoimmune diseases are the result of neo-antigens on the surfaces of host tissues that have been coded for by a cryptic inciting virus. T-cell diseases include phlyctenulosis graft rejections, graft versus host disease, and possibly sympathetic ophthalmia and temporal arteritis. Natural killer cells are involved in many of the same diseases as cytotoxic T-cells, except that the former require no period of sensitization (natural immunity), whereas cytotoxic T-cells must undergo an antigen-specific blast transformation (acquired immunity of the delayed hypersensitivity type). In many diseases in which B-cell derived auto-antibodies are at fault, there may be local tissue or systemic T-cell imbalances, with a reduction in T-suppressor cells and a relative augmentation in T-helper cells, thereby facilitating production of misdirected auto-antibodies.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:B- and T-lymphocytes in ocular disease. 623 70

Mice from which a MCA-induced sarcoma has been removed and which are exposed to repeated (every three months) tumoral cell transplants, gradually lose their protection against a certain threshold number of cells. Although the survival period after each transplant is longer than in non-protected animals (those that never received a primary tumor) it is seen that while some of them survive for three months (these are the ones to be re-inoculated with tumoral cells) others die. The proportion of mice which die rises with the number of inoculations received; and among those which die, the proportion of mice without localized tumor or neoplastic dissemination is also progressively higher. We do not know why these mice die at a later and cachectic stage without tumor but in a situation resembling a GVH (graft versus host) reaction. Repeated challenge through re-inoculation induces "bradyphylaxis" (progressively diminishing protection). On histopathological examination intense congestion is found, with haemorrhages in the lungs, liver, spleen and kidneys.
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PMID:[Gradually diminishing tumor protection caused by reimplants]. 654 10

Equitoxic doses of 5-(3-3-dimethyl-1-triazeno)imidazole-4-carboxamide (DTIC) and aryl-triazene derivatives (compounds all capable of inducing a marked increase in murine tumor cell immunogenicity) were studied for their effects on the host immune system. At different times after drug exposure the animals were tested for allograft responses, competence in producing lymphocytes active in lethal graft-versus-host disease, delayed-type hypersensitivity, humoral antibody production, and mitogen responsiveness. While some of the aryl-triazenes tested (DM-COOK DM-NO2) showed a pattern of immunodepression similar to that of DTIC, others were less (MIC, MM-COOK, MM-Cl) or far less (DM-Cl, MM-NO2) active than DTIC in impairing host immunocompetence, although all retained or even augmented their ability to induce chemical xenogenization.
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PMID:Chemical xenogenization of murine lymphoma cells with triazene derivatives: immunotoxicological studies. 656 3

Bone marrow transplantation offers two potential therapeutic advantages over more conventional therapy of leukemia. It allows more intensive treatment to be given without regard to marrow toxicity and allows in the case of allogeneic marrow an additional immunotherapeutic effect through graft-versus-host disease (GVHD). Initially, allogeneic transplants in HLA matched sibling donors were only employed in end-stage patients. Although there were encouraging results in terms of long-term therapeutic effects, the overall mortality was prohibitive. Subsequently, patients were transplanted in remission with a marked improvement in overall survival in both acute lymphocytic leukemia and acute non-lymphocytic leukemia. The major obstacles to further improvement in the therapeutic effects of this procedure have been identified (i.e., GVHD, viral infection, and relapse in ALL) and are subject to intensive investigations that already show encouraging results. Syngeneic marrow transplantation is limited for obvious reasons, but early results have shown significant therapeutic effects, in particular, in chronic myelogenous leukemia. These results have encouraged others to use autologous bone marrow. Marrow contamination with unseen tumor cells is being approached by pharmacologic and immunologic techniques designed to "purge" marrow of tumor cells. Animal and initial clinical studies have been encouraging.
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PMID:Bone marrow transplantation: current results in leukemia. 676 16

Two allospecific uncloned T cell lines, C.C3.11.75 (H-2d anti-H-2k) and B6-C.7.76 (H-2b anti-H-2d), were assayed for their ability to elicit a DTH reaction in vivo. It was shown that both cell lines, C.C3.11.75 being cytolytic and B6-C.7.76 being noncytolytic, evoke a strong DTH reaction. The reaction was in tempo and histology typical for a DTH reaction and could not be distinguished from a DTH reaction elicited by in vivo generated T cells active in a GVH reaction. Both cell lines recognize a private specificity encoded in the H-2 IA subregion. Cell proliferation of the responder cells did not appear to be critical in the reaction nor are T cells from the host recruited during the reaction. The DTH reaction can be assayed in allogeneic hosts demonstrating a complete lack of H-2 restriction in the reaction even when presumably antigen presenting macrophages are removed from the stimulator cell population. Furthermore, tumor cells expressing IA antigens could be employed to cause the reaction in both syngeneic and allogeneic recipients. Cloned sublines of one of the lines are also active in the reaction.
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PMID:T cell lines active in the delayed-type hypersensitivity reaction (DTH). 697 19


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