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)

AFP is one of several oncofetal proteins synthesized in large amounts by the fetus. Although synthesis drops markedly shortly after birth, small amounts of AFP continue to be produced in the adult. The function of AFP is unknown, but recent studies suggest the possibility that it may have immunoregulatory properties and/or may influence cell proliferation and growth. The high affinity of AFP for estrogen could have important biological functions, although the significance of this binding has not yet been clearly defined. Elevated levels of AFP are seen in a variety of clinical situations, including pregnancy; hepatic disorders, especially chronic hepatitis; and various malignancies, particularly hepatomas, teratomas, and those of primitive gut origin. It is also produced in murine GVH reactions and in lymphomas, both in mice and humans. In human and murine lymphomas, and murine GVH reactions, the presence of AFP-positive cells and immune suppression are highly correlated, but the role of these in the pathogenesis of the diseases is as yet unclear. It appears, however, that AFP may be produced locally in lymphoid tissues involved in GVH and lymphomatous disease without elevations in serum AFP levels. It is speculated that the local production of AFP in these situations may result from blastogenesis of lymphoid cells directed against foreign tumor or viral antigens. AFP could promote the development of tumors either by suppressing immune surveillance and/or immunity to oncogenic viruses, although this is speculative. Finally, the AFP elevations in maternal serum and amniotic fluid are valuable diagnostically in the detection of fetal abnormalities, particularly neural-tube defects.
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PMID:Structure and function of alpha-fetoprotein. 6 21

Fetal liver transplantation was attempted in 7 patients with aplastic anemia. 4 of these patients showed a partial response as evidenced by decrease in blood transfusion requirements and increase in the peripheral blood counts and hematopoietic cells in the bone marrow. Bone marrow culture studies revealed evidence of a temporary mixed lymphoid chimerism (cases 1 and 3). While case 1 lived for 16 months, case 3 is surviving at 17 months. None of the patients showed apparent graft-versus-host disease. Increased incidence of infections was noticed. Possible causes for the same are discussed. 3 patients failed to respond. Fetal liver transplant may be of therapeutic value in management of aplastic anemia.
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PMID:Fetal liver transplantation in aplastic anemia. 11 10

Lewis rats given total lymphoid irradiation (TLI) accepted bone marrow allografts from AgB-incompatible donors. The chimeras showed no clinical signs of graft-versus-host disease. Skin allografts from the marrow donor strain survived for more than 150 days on the chimeras. However, third-party skin grafts were rejected promptly. Although heart allografts survived more than 300 days in Lewis recipients given TLI and bone marrow allografts, detectable levels of chimerism were not required for permanent survival.
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PMID:Transplantation tolerance in adult rats using total lymphoid irradiation: permanent survival of skin, heart, and marrow allografts. 14 1

The effect of dietary protein restriction in mice on the capacity of their lymphoid cells to induce graft-vs.-host responses (GVHR) was studied. Mice were fed diets containing 4% or 20% protein ad libitum. The GVHR capacity of cells from all lymphoid organs of deprived mice was increased on a cell-for-cell basis over that of their normally fed counterparts. The slope of the dose-response curves did not change for spleen and mesenteric lymph node cells although their reactivity was increased by fourfold, and 50% respectively. The slope of the curves for thymus and Peyer's patches was changed indicating fundamental changes in the reactive cellular populations of these organs. Changes in GVH reactivity of cell populations from deprived mice were not mediated by increased corticosteroid production as adrenalectomy did not reduce their GVH responses. An explanation for the results was sought in a general decrease in production of short-lived cells with a rapid turnover such as most B cells. Long-lived T cells appear to persist and retain their reactivity for quite long periods in the face of nutritional insults.
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PMID:Influence of dietary protein restriction on immune competence. I. Effect on the capacity of cells from various lymphoid organs to induce graft-vs.-host reactions. 23 2

Graft-versus-host reactions were induced in adult F1 hybrid animals by injecting parental spleen cells. Adenylate cyclase activity was determined in the washed cell particles of the lymphoid tissues. During a time course study of the regional GVH reaction an increase in lymph node weight was apparent at day 2, whereas the adenylate cyclase activity increased at day 4 after the injection. Maximal lymph node hypertrophy and adenylate cyclase activation were observed 8 to 10 days after initiation of the GVH response. Adenylate cyclase stimulation by epinephrine of the GVH response. Adenylate cyclase stimulation by epinephrine and glucagon in experimental preparations was less than in the control. NaF was stimulatory only in the control preparations. Ca-2+ in concentrations up to 8 mM had no inhibitory effects on the control or experimental preparations. The pattern of responses of the experimental preparations to Zn-2+ and Cu-2+ was different than the control; however, in high concentrations both of these cations had marked inhibitory effects. An increase in the adenylate cyclase activity was also direct relationship between the adenylate cyclase activity and the cytolytic activity of spleen cells from mice undergoing systemic GVH reaction. These results can be explained on the basis of alterations in the cell membranes, and it is suggested that such changes play an important role in the pathogenesis of GVH disease.
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PMID:Adenylate cyclase activation in lymphoid tissues during graft-versus-host reaction. 23 44

Experimental animal models of the two forms of toxic epidermal necrolysis have been reviewed: a murine model of staphylococcal-induced epidermolysis and a hamster model of graft-versus-host disease. In the former, a protein exotoxin, epidermolysin, has been purified and characterized. The exotoxin has a molecular weight of approximately 30,000 and causes a split beneath the granular layer. It is effective at 3 times 10(-12) moles. Epidermolysin does not require an intact complement system for its action since B10D2 mice deficient in C5 or mice injected with the decomplementing agent in cobra venom factor were susceptible to its epidermolytic effects. Neither are immunocompetent thymocytes required for the action of the toxin since hairless, athymic adult (nu/nu) mice are susceptible. A few reports of epidermolysis due to an exotoxin of group I Staphylococcus aureus have appeared. This toxin is antigenically different from the exotoxin of group II organisms. A model of drug-induced toxic epidermal necrolysis has been described in hamsters, but the toxic principle released from sensitized lymphoid cells has not yet been characterized.
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PMID:Studies of the mechanism of epidermal injury by a Staphylococcal epidermolytic toxin. 23 71

Lymphocytes from mice of strain CBA are strongly MLC-responsive to lymphocytes from the H-2-compatible but M-antigen-incompatible strain C3H. This strong reactivity disappears after infusion of CBA mice with C3H lymphocytes. This study shows that the host-versus-graft reactivity (swelling of local lymph node after antigen injection) is specifically reduced after injection of CBA mice with C3H times CBA spleen cells. However, lymphocytes from such mice showed a specifically increased GVH reactivity (inhibition of erythroid cell growth) compared with lymphocytes from unimmunized mice. Lymphocytes from normal CBA mice showed a high proliferative rate in the spleens of irradiated C3H times CBA mice. Such 'educated' cells showed strongly increased specific GVH reactivity. Lymphocytes from CBA mice previously injected with C3H times CBA cells showed reduced capacity to proliferate when injected into irradiated C3H times CBA hybrids and a poor capacity to develop new 'effector' cells reactive against C3H times CBA bone marrow target cells. The results indicate that the presence of specifically 'MLC-responsive' lymphocytes in a lymphoid cell population is a prerequisite of its production of 'effector' cells able to respond in this GVH assay.
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PMID:Reduced capacity to produce specific 'effector' cells after injection of CBA mice with C3H cells. 24 Nov 16

The mechanism of prolongation of skin allograft survival in rats treated with specific antigen and hydrocortisone was studied in the strain combination with the strong (H-1 + non-H-1) and weak (non-H-1) antigenic difference. The grafts differing from the recipients at the weak non-H-1 loci only showed the longest survival although unresponsiveness to the strong (H-1) antigens of the donor type had already disappeared. In both strain combinations, immunological reactivity of lymphoid cells from treated animals was demonstrated in local GVH reactions at the end of the treatment (i.e., 12 days after transplantation). Lymphoid cells isolated from long surviving (100 days) AVN recipients of non-H-1 different grafts did not react in the GVH test. Attempts to obtain prolongation of skin allograft survival by passive transfer of serum removed after termination of immunization with strong (H-1 + non-H-1) or only weak (non-H-1) antigens were not successful.
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PMID:Prolonged survival of skin allografts in rats treated with antigen and hydrocortisone and the trend in graft-versus-host reactions. 24 69

The cells in mouse bone marrow (BM) capable of responding to phytohemagglutinin (PHA) were shown to be precursor T cells in experiments employing athymic mice, immunofluorescence, and specific lysis of T or B cells with cytotoxic antisera + complement. In contrast, the responses of lymph node (LN) and spleen (Spl) cells to this mitogen were shown by the same techniques to rely upon resident populations of mature T lymphocytes in these peripheral lymphoid organs. Cytolysis of T cells with anti-theta (anti-Thy 1), anti-thymocyte, or anti-brain antisera abolished the PHA responses of LN and Spl, but had no appreciable effect on the BM PHA response. Lysis of B cells with anti-mouse gamma globulin or anti-mouse IgM antisera had no significant effect on either Spl or BM blastogenesis in response to this lectin. Immunofluorescent studies with fluoresceinated anti-brain sera demonstrated acquisition of T-cell surface antigens by BM null lymphocytes during the blastogenic response of this tissue to PHA. The results of these immunofluorescence experiments were reproducible even when marrow obtained from nude mice and pretreated with anti-brain serum plus complement was employed. The implications of these findings with regard to prophylaxis against graft versus host disease in BM transplant recipients are discussed.
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PMID:Phytohemagglutinin-induced differentiation and blastogenesis of precursor T cells from mouse bone marrow. 33 Jul 90

Two patients with the Wiskott-Aldrich syndrome had complete donor lymphoid and hematopoietic engraftment after successful allogeneic bone-marrow transplantation. One patient had had only a temporary donor T-lymphocyte graft after a previous transplantation, for which he had been prepared with cytarabine and cyclophosphamide; the patient's own T lymphocytes returned six months later. A repeat transplant, for which the patient was prepared with anti-human thymocyte serum, total-body irradiation and procarbazine, resulted in complete donor engraftment. The second patient underwent a successful transplantation after similar preparation, except that procarbazine was omitted. At 11 and five months after transplantation both had normal hematopoiesis and no evidence of graft-versus-host disease. This treatment of the Wiskott-Aldrich syndrome may be a model for the correction of other genetically determined immune and hematologic bone-marrow disorders.
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PMID:Complete correction of the Wiskott-Aldrich syndrome by allogeneic bone-marrow transplantation. 34 89


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