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Biomedical subjects

G Opelz

Publications and source records attributed to G Opelz.

At least 217 records · Page 12Linked to original sources

A B cell-suppressive IgG-antiimmunoglobulin antibody induced by alloimmunization.

This study is an extension of our previous report that alloimmunization produces a serum factor that suppresses the lymphocytotoxic antibody response. The experiments presented herein show that: (1) serum and IgG of pretreated rats contain an antibody directed against the constant region of IgG; (2) the anti-IgG has strong anti-Fc-gamma and weak anti-Fab activity; (3) the antibody also reacts with IgM; (4) the antiimmunoglobulin is an autoantibody; and (5) the antiimmunoglobulin suppresses the primary B cell response in vitro.

Animals↗

Comparison of RFLP-DR beta and serological HLA-DR typing in 1500 individuals.

A group of 1522 individuals were HLA-DR-typed both by the standard serological technique and by the RFLP method. Whereas 11% (n = 164) of the serological typings were technically unsuccessful or doubtful, all typings were successful by RFLP. The results of the remaining 1358 typings revealed a serological error rate of 25%. In 16% a serological "blank" turned out to be a definable allele by RFLP, while in 9% an allele was incorrectly interpreted by serology. Of the individuals tested, 11% were HLA-DR homozygous by RFLP. Our results demonstrate an important clinical potential of RFLP typing for the typing of bone marrow transplant candidates in whom serology often fails, and for kidney transplant candidates with "blanks" or serologically "difficult" HLA antigens.

Alleles↗

An experimental model for preventing alloimmunization against platelet transfusions by pretreatment with antibody-coated cells.

The pretreatment of LEW (RT-1l) rat recipients with antibody-coated BN (RT-1n) blood cells resulted in the suppression of the LEW antibody response against subsequent BN platelet and leukocyte transfusions. Both coating with homologous LEW-anti-BN serum or heterologous rabbit-anti-rat lymphocyte serum was effective. Repeated boosting with uncoated platelets or leukocytes did not abrogate the suppression. The degree of suppression was dependent on the amount of antibody used for cell coating. The induced suppression was also extended to uncoated antigens and unrelated third-party cells. The serum-IgG fraction of pretreated rats was strongly immunosuppressive, suggesting that the mechanism of suppression was related to the induction of a broadly reactive regulatory IgG.

Animals↗

Influence of HLA matching on survival of second kidney transplants in cyclosporine-treated recipients.

In an analysis of over 4000 cyclosporine-treated recipients of second kidney transplants we observed a strong effect of HLA matching in living-related and cadaver transplants. In contrast to the results obtained in first cadaver transplants, second cadaver transplants benefited substantially from matching for HLA-A locus antigens. The strongest effect of matching was found when HLA-A, HLA-B, and HLA-DR antigens were analyzed together: 214 second grafts with no mismatch had a survival rate of 82 +/- 3% at two years in contrast to a 49 +/- 4% rate in 149 grafts with 6 mismatches (P less than 0.0001, log rank). Patients whose first graft functioned for more than 1 year had a significantly higher second graft survival rate than patients with shorter first graft duration. Because the effect of HLA matching is particularly strong in patients with less than 1 year first graft duration, it is suggested that HLA well-matched kidneys should be allocated to them with priority.

Cyclosporins↗

Autoantibodies against CD4- and CD8-positive T lymphocytes in HIV-infected hemophilia patients.

The presence of IgG, IgM, C3d, or gp120 on the surface of T lymphocytes was analyzed by flow cytometry in blood samples from 73 hemophilia patients and 56 healthy controls. IgG and IgM autoantibodies against CD4+ lymphocytes were found in HIV + patients but not in HIV-patients or healthy controls (p less than 0.001). IgM autoantibodies were more frequent than IgG autoantibodies. Autoantibody formation increased with disease progression. However, within the same disease risk category, patients with autoantibodies were not "more immunologically abnormal' than patients without autoantibodies. HIV + patients who possessed autoantibodies had similar CD4+ and CD8+ lymphocyte counts as HIV + patients without autoantibodies. There was no significant difference in the number of patients with abnormal CD4/CD8 ratios, serum neopterin levels, or in vitro responses to allogeneic stimulator cells or mitogens between autoantibody-positive or -negative patients of the same risk category. Our data suggest that autoantibodies against CD4+ lymphocytes may be helpful as indicators of disease progression, however, their immunopathogenetic role remains unclear.

AIDS-Related Complex↗

Helper and suppressor T-cell function in HIV-infected hemophilia patients.

T-lymphocyte helper and suppressor functions were assessed in 61 hemophilia patients. Twenty one patients were HIV-negative (Group 1), 27 were HIV-positive without having AIDS-related complex (ARC)/AIDS (Group 2), and 13 had ARC/AIDS (Group 3). T, CD4-positive, or CD8-positive T lymphocytes were cocultured with B lymphocytes and pokeweed mitogen for 6 days and immunoglobulin producing cells were assessed in a reverse hemolytic plaque assay. In HIV-infected patients, T cells as well as the CD4-positive T cell subset exhibited reduced helper (P less than .01, Group 2; P less than .0005, Group 3) and elevated suppressor activity (P less than .02, Group 2; P less than .005, Group 3), whereas no significant difference was found between HIV-negative patients and controls. The number of CD4-positive cells was not correlated with CD4 cell function. CD4-positive cells showed no helper activity (less than 10% of control T cells) in 8/11 (73%), but an excessive suppressor activity (greater than 80% suppression of plaque formation) in 6/11 (55%) Group 3 patients. Our results show that defective helper and elevated suppressor functions of T cells in HIV-infected patients are caused not only by a change in the CD4/CD8 cell counts but also by functional abnormalities of the CD4-positive T-cell subset. These abnormal helper and suppressor functions may play a role in the development of the immunodeficiency state of AIDS patients.

Acquired Immunodeficiency Syndrome↗

B lymphocyte response as an indicator of acute renal transplant rejection. I. Immunoglobulin-secreting cells in peripheral blood.

Monitoring of immunoglobulin-secreting cells in peripheral blood was performed in 88 renal transplant recipients using a reverse hemolytic plaque-forming cell assay. Comparison with other in vitro tests for rejection (plasma neopterin, CD4/CD8 ratio) demonstrated that the number of immunoglobulin-secreting cells in peripheral blood provides a highly sensitive rejection marker. Evidence of rejection was obtained 1.7 +/- 0.4 (mean +/- SEM) days before a rise in creatinine, with a significant PFC rise in 95% (73/77) of rejection episodes. The PFC response was not influenced by HLA matching, number of preoperative blood transfusions, acute tubular necrosis, or uremia. A significant PFC rise in the absence of an ongoing rejection episode occurred in the presence of bacterial or viral infections, in case of posttransplant surgical complications, and regularly during the early posttransplant period (days 4-9). However, even early posttransplant the PFC peak was significantly higher in patients with an ongoing rejection episode than in patients without rejection (P less than 0.001).

Antibody-Producing Cells↗