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)

We examined the kinetics of intestinal intraepithelial lymphocytes (IEL) and the incidence of apoptosis at villus or crypt sites during the development of non-irradiated acute graft-versus-host disease (GVHD). The first IEL to increase were host-origin on day 3 and the donor-derived IEL appeared first on day 12 after GVHD induction. Unique CD3+CD4+CD8 alpha/alpha+ IEL were significantly increased on day 6 and an appreciable number of IEL bearing T cell receptor V beta capable of recognizing self-superantigen were detected on day 9. The sudden appearance of apoptosis and reduction of mitotic activity occurred on day 12, accompanied by a dramatic decrease of CD3+CD4-CD8 alpha/alpha+ IEL of host origin. CD8 alpha/alpha+ IEL of host origin, which expand and then decrease by apoptosis at the early stage of acute GVHD, may be associated with pathogenesis of the enteropathy occurring during acute GVHD.
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PMID:Kinetics of intestinal intraepithelial lymphocytes during acute graft-versus-host disease in mice. 790 97

In the present study, we examined changes in the expression of CD45RA, CD31, and CD29 on total CD4 and CD8 lymphocytes in patients who had received CD6 T cell-depleted allogeneic marrow and received no immune suppressive drugs after engraftment in order to identify defects in reconstitution of immunoregulatory T cells after allogeneic BMT. Results following allo-BMT were compared with normal controls and patients following autologous BMT. We showed that CD4+CD45RA+, CD4+CD29+ (CD29high), and CD4+CD31+ cells were markedly decreased during the first 24 months after allo- and auto-BMT. CD8+CD45RA+ cells recovered to normal levels within the first month after auto-BMT, while after allo-BMT, the CD8+CD45RA+ cells were at slightly low levels during the first month, but gradually increased to normal levels by 12 months post-BMT. CD8+CD29+ cells were increased during the first 12 months both after allo- and auto-BMT although during the first month, a decreased percentage of CD8+CD29+ cells was observed in allo-BMT patients. More important, CD4+CD29+, CD8+CD29+, and CD8+S6F1+ cells were significantly increased in patients with moderate-to-severe acute GVHD (grades II-IV) compared with those with or without mild acute GVHD (grade I), suggesting that CD4 helper-inducer (CD4+CD29high) and CD8 killer-effector (CD8+CD29highS6F1+) cells play an important role in the pathophysiology of acute GVHD.
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PMID:The phenotype and reconstitution of immunoregulatory T cell subsets after T cell-depleted allogeneic and autologous bone marrow transplantation. 791 Sep 87

Roles of CD8+ and CD4+ cells on lethal graft-versus-host disease (GVHD) were investigated. Injection of spleen cells from C57BL/6 (B6) female mice into (BALB/c x B6)F1 nu/nu female mice caused subacute lethal GVHD (survival: 10-50 days). Injection of anti-Lyt-2.2 (CD8) monoclonal antibody (mAb) on days zero, four and 14 into recipient mice prolonged their survival for at least the 200-day observation period. Injection of anti-L3T4 (CD4) mAb also prolonged survival of the mice for more than 70 days, but they eventually died by 150 days. Pretreatment of the donor B6 spleen cells with anti-Lyt-2.2 (CD8) mAb and complement (C) prevented the development of GVHD, and their pretreatment with anti-L3T4 (CD4) mAb and C markedly prolonged the survival of recipient mice. Injection of a mixture of donor spleen cells pretreated with anti-Lyt-2.2 (CD8) mAb and C and those pretreated with anti-L3T4 (CD4) mAb and C induced subacute lethal GVHD. Injection of anti-L3T4 (CD4) mAb, but not anti-Lyt-2.2 (CD8) mAb on days five, nine and 14 prolonged survival of the recipient mice. These results indicated that the collaboration of CD8+ cells and CD4+ cells was necessary for induction of subacute lethal GVHD. CD4+ cells but not CD8+ cells were involved in mediating subacute GVHD from the onset of the disease. CD8+ cells were, however, capable of inducing late-onset lethal GVHD. Direct phenotyping of T cells in the recipient mice revealed that the CD4+ cells were incapable of repopulating without CD8+ cells, but that CD8+ cells were capable of repopulating without CD4+ cells.
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PMID:Roles of CD8+ and CD4+ cells on lethal graft-versus-host disease in nude mice. 791 51

Two cases of graft versus host disease (GVHD) were reported. Case 1: A 74-year-old man noticed erythematous rash with high fever in fourteen days after blood transfusion. Skin rash spread gradually and resulted in toxic epidermal necrolysis (TEN) in accompany with diarrhea, liver dysfunction and pancytopenia. Case 2: A 24-year-old man with acute lymphocytic leukemia treated with allogeneic bone marrow transplantation, developed macular erythema diffusely and he had received transfusion of peripheral buffy coat cells from his brother. Histological findings revealed eosinophilic necrotic keratinocytes and infiltrating cells which consisted of CD4 and CD8(+) T cells. The both cases were diagnosed as GVHD caused by blood transfusion, though in case 1, differentiation from toxic eruption was needed. We described clinical and histopathological findings of the cutaneous manifestations of GVHD and distinction from some cutaneous lesions caused by drug toxicity and collagen disease.
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PMID:Exanthema and enanthema in graft versus host disease (GVHD). 792 32

Attempts to identify an early and discriminating marker of acute graft-versus-host disease (aGvHD) have been unsuccessful. The levels of soluble CD4 and soluble CD8 in serum correlate with T cell subset activation and may be important in monitoring and characterizing immunological processes. We determined serum soluble CD4 (sCD4) and sCD8 levels with a two-site sandwich enzyme immunoassay on patients' serum samples collected prior to bone marrow transplantation and weekly after transplantation until day +28. No significant increment of sCD4 was documented in each determination. sCD8 rose significantly before diagnosis or development of maximal clinical symptoms in patients with grade II-III aGvHD than grade 0-I aGvHD [at day +21--median value 447 IU/ml; range 94-713; versus 1136 IU/ml, range 790-1416 (P = 0.002); at day +28--median value 443 IU/ml, range 73-992, versus 1164 IU/ml, range 625-1960 (P = 0.005)]. On the day of marrow infusion the sCD8 levels were significantly higher in patients who subsequently developed grade II-III than in patients with grade 0-I aGvHD (median value 155 IU/ml, range 10-332, versus 350 IU/ml, range 283-830; P = 0.003). Careful monitoring of sCD8 is a useful tool for a prompt aGvHD diagnosis and may be used in a clinical bone marrow transplantation setting.
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PMID:CD8 serum levels in acute graft-versus-host disease diagnosis. 792 96

Forty-eight adult leukemic recipients of HLA-identical sibling marrow were randomized to T cell depletion using anti-CD8 and anti-CD6 antibodies plus complement (n = 28) or prophylaxis with methotrexate (MTX) and cyclosporine (CsA) (n = 25). Patient characteristics were comparable in the two groups. The median observation time was 5 1/2 years. Transfusions, infections, and acute GVHD did not differ between the groups. Chronic GVHD occurred in 52% of patients receiving T cell-depleted marrow and 23% of those receiving MTX + CsA (P = 0.06). Overall probability of relapse was similar in both groups and actuarial leukemia-free survivals at 5 years were 39% and 35% in the two groups, respectively. Among patients with chronic myeloid leukemia (CML), leukemia-free survival at 5 years was 25% in patients receiving T cell-depleted marrow compared with 51% in those given MTX + CsA (P = 0.09). In patients with acute leukemia the probability of relapse was 24% in the group receiving T cell-depleted marrow compared with 73% in those treated with MTX + CsA (P = 0.06). Leukemia-free survival was 55% and 21% in the two groups, respectively (NS). CML patients tended to have a poorer prognosis and those with acute-leukemia better outcome with T cell depletion than with combined MTX + CsA. It is concluded that T cell depletion is unsuitable for patients with CML, but may be considered in patients with acute leukemia.
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PMID:Long-term follow-up of a randomized trial comparing T cell depletion with a combination of methotrexate and cyclosporine in adult leukemic marrow transplant recipients. 794 Jul 31

Gastrointestinal (GI) disease is frequent in all types of immunocompromised patients but occurs with greatest frequency in patients with acquired immunodeficiency syndrome (AIDS). Thus, much of this review deals with human immunodeficiency virus (HIV)-related GI diseases. Gastrointestinal diseases in other immunocompromised patients are compared with those in patients with AIDS. Conditions unique to transplant recipients, such as graft-versus-host disease (GVHD) and posttransplant lymphoproliferative disorders (PTLDs), are discussed separately. We have divided these GI diseases into four main categories: (1) HIV-related inflammatory conditions other than opportunistic infections (HIV-related enteropathy, proctocolitis, and CD8 lymphocytosis); (2) inflammatory conditions unrelated to HIV or opportunistic infections (neutropenic enterocolitis, regional enteritislike enteropathy, and GVHD); (3) opportunistic infections (illnesses caused by herpesvirus, cytomegalovirus, and miscellaneous other viruses; Mycobacterium, Candida, Histoplasma, Cryptococcus, Cryptosporidium, Microsporida, Isospora, Leishmania, Toxoplasma and Strongyloides organisms as well as Pneumocystitis carinii; and (4) neoplasias (Kaposi's sarcoma [KS], AIDS-related non-Hodgkin's lymphoma [NHL], HIV-related Hodgkin's disease [HD], PTLDs, and miscellaneous neoplasms). The prevalence, pathogenesis, clinical manifestations, gross pathological findings, and microscopic features of each disease entity are discussed.
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PMID:Gastrointestinal disease in the immunocompromised patient. 795 57

We report a case of cyclosporin- and methylprednisolone-resistant intestinal acute graft-versus-host disease (GVHD) after allogeneic bone marrow transplantation which responded to a new immunosuppressant, 15-deoxyspergualin (DSG). Endoscopy showed lymphoid hyperplasia with CD3+, CD4+, CD8- lymphocyte infiltration into the submucosa of the jejunum and colon. DSG effectively suppressed this intestinal acute GVHD.
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PMID:15-Deoxyspergualin controls cyclosporin- and steroid-resistant intestinal acute graft-versus-host disease after allogeneic bone marrow transplantation. 799 48

The number and types of mononuclear cells obtained by bronchoalveolar lavage from 105 marrow transplant patients with and without cytomegalovirus pneumonia were studied to determine whether: (1) CMV pneumonia was associated with local recruitment of lymphocytes and lymphocytes of particular subtypes to the lung, and (2) whether local recruitment was affected by the known risk factors for the development of CMV pneumonia, namely acute graft-versus-host disease and total body irradiation. Results showed a significant increase in the number of lymphocytes (P = 0.014) and in the number of lymphocytes marking for CD8 (P = 0.0045) and CD16 (P = 0.052) in BAL from all patients compared with BAL from normal subjects. However, no significant differences were observed in BAL cellular characteristics between patients with and without pneumonia nor between patients with CMV or other etiologies of pneumonia. There were also no significant differences in BAL characteristics when patients were analyzed for the presence of acute GVHD, the use of TBI, or the type of transplant. These results do not provide evidence for local recruitment of lymphocytes to the lung unique of patients with CMV pneumonia nor to patients with GVHD and CMV pneumonia, in contrast to what is observed in murine CMV pneumonia.
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PMID:Mononuclear cell reconstitution in the lung after marrow transplantation. Lack of influence of cytomegalovirus pneumonia, irradiation, and graft-versus-host disease. 809 99

Treatment of lethally irradiated mice with a short course of high-dose interleukin (IL)-2 markedly inhibits acute and chronic graft-versus-host disease (GVHD), while preserving a graft-versus-leukemia (GVL) effect of allogeneic T-cells. We recently demonstrated that this GVL effect, observed with the EL4 leukemia/lymphoma in the A/J-->B10 strain combination, was mediated by CD8+ A/J T-cells in a CD4-independent fashion. IL-2 inhibited only the activity of CD4+ cells, and not that of CD4-independent CD8+ T-cells in A/J spleen cell inocula. This inhibition of CD4 function was sufficient to markedly inhibit GVHD, thus explaining the dissociation of GVHD and GVL in IL-2-treated mice. We have now performed studies to determine the capacity of IL-2 to inhibit GVHD induced across a variety of different histocompatibility barriers. IL-2 significantly delayed GVHD mortality in three of four additional fully major histocompatibility complex (MHC) plus minor-disparate strain combinations when CD4+ T-cells were given. Numbers of CD8+ T-cells comparable to those that might contaminate human marrow demonstrated a relatively poor capacity to produce acute GVHD when given without CD4+ cells in all of three additional strain combinations evaluated. In one of these strain combinations (B10-->BALB/c), IL-2 protected against acute but not chronic GVHD mortality when CD4+ cells were given with or without CD8+ cells. In one fully allogenic strain combination, B10-->A/J, IL-2 did not inhibit the GVHD produced by CD4+ cells given with or without CD8+ cells. IL-2 was unable to inhibit CD8-mediated GVHD in strain combinations differing at isolated class I MHC loci. In a strain combination differing only at multiple minor histocompatibility antigen (HA) loci, B10-->C3H.SW, GVHD was largely CD8-dependent, but IL-2 did not inhibit the small CD4-mediated component of GVHD. Together, these results suggest that IL-2 inhibits a restricted subset of CD4 cells or functions, and that the type of CD4 activities mediating GVHD is determined by the particular histoincompatibilities between donor and host.
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PMID:Strain dependence of interleukin-2-induced graft-versus-host disease protection: evidence that interleukin-2 inhibits selected CD4 functions. 811 Jul 26


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