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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)

A severe, antigen-nonspecific, and long-lasting immune-deficient state can be induced in healthy, adult immune-competent F1 hybrid mice by a single i.v. injection of parental T lymphocytes. The present report demonstrates that this graft-vs-host-induced immune deficiency (GVHID) can be prevented in an antigen-specific way by immunization of the F1 mice with allogeneic cells before induction of GVHID. Thus, spleen cells from (A X B)F1 mice primed with allogeneic cells from strain C and then injected with parental spleen cells from A did not generate cytotoxic T lymphocyte responses to trinitophenyl-modified self cells or to allogeneic cells from third party strains D or E. However, spleen cells from the same mice generated normal levels of cytotoxic T lymphocyte activity to allogeneic cells from C, the strain used for immunization. Furthermore, mice exposed to murine cytomegalovirus before induction of GVHID were resistant to a subsequent challenge with murine cytomegalovirus, whereas GVHID mice that received only the murine cytomegalovirus challenge all died. These findings are discussed with respect to the possibilities that primed and unprimed T helper cells may be differentially susceptible to the suppressive effects of GVH.
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PMID:Antigen-specific protection against graft-vs-host induced immune deficiency. 303 9

Nowadays the application of blood cell concentrates corresponding to indication is in nearly all cases superior to the whole-blood transfusion. For the substitution of erythrocytes are to be recommended buffy coat-free concentrates, for special indications also cryopreserved ones in order to avoid complications (sensitization, transmission of viruses). Concentrates of thrombocytes are to be administered nearly exclusively in disturbances of formation and may be used for the short-term application as pooled randomized preparations, in a medium period better may be used as individual donor preparation. In order to avoid sensitizations, but always when HLA-antibodies occur, HLA-compatible individual donor concentrates must be used. Particularly in the patient with immune deficiency the possible transmission and the growth of stem cells with subsequent graft-versus-host disease (therefore the concentrates should be irradiated with 15-30 Gy) and the transmission of cytomegaly viruses (CMV), respectively, which can be minimized using CMV-negative donors, is to be taken into consideration. Prophylactically applied concentrates of thrombocytes evidently co-determine the therapeutic success of the highly aggressive chemotherapy; transplantation of bone marrow could not be performed without them. On account of the danger of the transmission of CMV concentrates of granulocytes are administered only strongly therapeutically in life-threatening infections, when the patient shows a decrease of the number of granulocytes below 0.5 Gpt/l. However, the substitution must be performed consequently over at least 3 days and up to the proof of clinical effectiveness, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Blood cell substitution within the scope of hematologic intensive therapy for supportive hemotherapy with erythrocyte, thrombocyte and granulocyte concentrates]. 306 34

Lethally irradiated F1 mice, heterozygous at the hematopoietic histocompatibility locus Hh-1, which is linked with H-2Db, reject bone marrow grafts from H-2b parents. This hybrid resistance (HR) is reduced by prior injection of H-2b parental spleen cells. Because injection of parental spleen cells produces a profound suppression of F1 immune functions, we investigated whether parental-induced abrogation of HR was due to graft-vs-host-induced immune deficiency (GVHID). HR was assessed by quantifying engraftment of H-2b bone marrow in F1 mice with the use of splenic [125I]IUdR uptake; GVHID, by the ability of F1 spleen cells to generate cytotoxic T lymphocytes (CTL) in vitro. We observed a correlation in the time course and spleen cell dose dependence between loss of HR and GVHID. Both GVHID and loss of HR were dependent on injection of parental T cells; nude or T-depleted spleen cells were ineffective. The injection of B10 recombinant congenic spleens into (B10 X B10.A)F1 mice, before grafting with B10 marrow, demonstrated that only those disparities in major histocompatibility antigens that generated GVH would result in loss of HR. Thus, spleens from (B10 X B10.A(2R]F1 mice (Class I disparity only) did not induce GVHID or affect HR, whereas (B10 X B10.A(5R))F1 spleens (Class I and II disparity) abrogated CTL generation and HR completely. GVHID produced by a class II only disparity, as in (B10 X B10.A(5R))F1 spleens injected into (B6bm12 X B10.A(5R))F1 mice, was also sufficient to markedly reduce HR to B10 bone marrow. This evidence that GVHID can modulate hematopoietic graft rejection may be relevant to the mechanisms of natural resistance to marrow grafts in man.
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PMID:Abrogation of hybrid resistance to bone marrow engraftment by graft-vs-host-induced immune deficiency. 309 24

Graft-versus-host disease (GVHD) classically involves the skin, intestines, liver, esophagus, and tongue. clinically apparent disease involving the heart, lungs, kidneys, and central nervous system (CNS) is frequently secondary to other complicating factors. This report describes a case of an infant with severe combined immune deficiency (SCID) who developed unusual manifestations of GVHD following a bone marrow transplant (BMT). These were complete heart block and respiratory insufficiency in the absence of significant pulmonary disease. He lived 133 days post-transplantation. At autopsy, the brain showed focal lymphohistiocytic aggregates which may represent a hitherto unreported lesion of GVHD.
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PMID:Graft-versus-host disease in the central nervous system. A real entity? 905 93

The factors that impact upon successful bone marrow transplantation leading to immunologic reconstitution in severe combined immune deficiency (SCID). Wiskott-Aldrich syndrome, and in other lethal congenital immunodeficiencies are reviewed. Evidence is presented that graft-versus-host disease (GVHD) can be abrogated by the depletion of T cells, even from histoincompatible marrow grafts. However, graft resistance or restricted immune reconstitution has been observed with significant frequency. The bases for T cell reconstitution and limitations in B cell humoral immune recovery in the postgrafting period are reviewed, together with emerging evidence that pretransplant cytoreduction might obviate some of these problems.
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PMID:Evaluation of HLA-haplotype disparate parental marrow grafts depleted of T lymphocytes by differential agglutination with a soybean lectin and E-rosette depletion for the treatment of severe combined immunodeficiency. 353 40

An infant with severe immune deficiency received bone marrow from an HLA-A, -B, -DR matched, mixed leucocyte reaction non-reactive first cousin. The donor marrow was fractionated on a discontinuous Percoll gradient and before infusion was treated with the anti-human T lymphocyte antibody, HuLy-m1, and rabbit serum as a source of complement. Methotrexate was given during the following two weeks. A rise in the peripheral blood lymphocyte count, indicating engraftment, occurred six weeks after transplantation. There was no clinical evidence of graft versus host disease (GVHD). Engraftment has been sustained for one year and the patient is in normal health and has normal in vitro immunological function. In vitro treatment of human marrow with HuLy-m1 allows stable engraftment and may be useful in attempting to diminish or prevent GVHD.
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PMID:Immunological reconstitution in a patient with severe combined immune deficiency using non-sibling bone marrow depleted of T cells with HuLy-m1. 353 67

A chronic GVH reaction (detected by T cell immune deficiency) was induced in unirradiated, adult (C57BL/10 X B10.A)F1 mice by injecting them i.v. with 3 X 10(7) B10.A parental spleen cells. Thirty-four days later, attempts were made to reconstitute the GVH immune-deficient mice by whole-body irradiation and repopulation with bone marrow cells from normal syngeneic F1 mice. The reconstituted mice were tested for CTL responses 147 and 272 days after repopulation with normal F1 bone marrow. These GVH/chimera mice remained immunoincompetent for at least 272 days for CTL responses to hapten-self and H-2 allogeneic antigens.
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PMID:Failure of bone marrow cells to reconstitute T cell immunity in graft-vs-host mice. 388 28

The current use of allogeneic bone marrow transplantation in various hematologic diseases is reviewed. Bone marrow transplantation (BMT) involves infusion of bone marrow from a suitable donor into a properly conditioned recipient. Most BMT is allogeneic, in which the donor is genetically dissimilar but shares some common tissue antigens with the recipient. Almost all patients undergoing allogeneic BMT must be "prepared" with high-dose cyclophosphamide to prevent graft rejection. Most patients with hematologic malignancy also receive total body irradiation to eradicate malignant cells located in areas inaccessible to the systemic circulation. Bone marrow transplantation is the treatment of choice for severe aplastic anemia. In acute myelogenous leukemia, the best results are observed in young patients undergoing BMT in first remission. In acute lymphoblastic leukemia, BMT is usually reserved for patients in second or subsequent remission. Early results are promising in patients with chronic myelogenous leukemia who receive BMT before the accelerated phase or blast crisis of this disease. Allogeneic BMT offers an opportunity for cure in some patients with relapses of Hodgkin's disease or those with certain subtypes of non-Hodgkin's lymphoma. Other diseases for which BMT has been used include severe combined immune deficiency disease, Fanconi's anemia, and multiple myeloma. Complications of BMT include graft failure or rejection, acute and chronic graft-versus-host disease, and infectious complications; late complications, such as restrictive and obstructive pulmonary disease, cataracts, sterility, and secondary malignancies, may also occur. Bone marrow transplantation has become an important treatment for many hematologic diseases, but it will probably remain a treatment reserved for only a few highly specialized centers. If morbidity and mortality caused by transplant-related complications can be reduced, BMT may be offered to older patients and those without HLA-identical sibling donors.
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PMID:Allogeneic bone marrow transplantation in the treatment of hematologic diseases. 388 73

Immunologic evaluation of two unrelated male infants with clinical and laboratory evidence of severe combined immunodeficiency (SCID) revealed T cells with a mature phenotype in the peripheral circulation of both patients although both had biopsy evidence of thymic alymphoplasia. Both had a normal number of T cells with a cytotoxic/suppressor surface marker (OKT8) but very few T helper cells (OKT4). Lymphocyte stimulation with the mitogens PHA, Con A, and pokeweed or with allogeneic cells resulted in no proliferation. However, addition of T cell growth factor, plus the phorbol ester TPA, to lymphocytes cultured with the T cell mitogen PHA did result in some proliferation of T cells. In both cases these T cells demonstrated an XX female karyotype and were probably of maternal origin. In contrast, proliferating B cells stimulated with Epstein-Barr virus demonstrated a normal XY male karyotype. The possibility that severe combined immune deficiency in these patients was the result of graft-versus-host disease induced by maternal lymphocytes is discussed.
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PMID:XX T cells and XY B cells in two patients with severe combined immune deficiency. 660 7

Graft versus host disease (GVHD) is a well recognized entity following bone marrow transplantation. Similar syndromes have been described after blood product transfusions, notably in patients with primary immunodeficiency syndromes and in patients with malignancies associated with immune deficiency or under immunosuppressive treatment. Review of the literature shows that posttransfusion GVHD is characterized by maculopapular skin rash, gastro-intestinal symptoms, liver disease, severe pancytopenia and, in some cases, hepatosplenomegaly and lymphadenopathy. The time to onset and the duration of the disease are short (10 days) and the mortality approaches 90%. The clinical features of this rare disorder are presented in the hope that, with increased awareness of this complication, clinicians will take preventive measures in patients at risk because no satisfactory therapy yet exists.
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PMID:[Clinical characteristics and evaluation of risk in the graft versus host reaction following transfusion]. 663 42


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