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Biomedical subjects

G T Stelzer

Publications and source records attributed to G T Stelzer.

31 records · Page 2Linked to original sources
PubMed1985

Alterations in serum antibody and peripheral T-lymphocyte subsets resulting from treatment of murine immune complex glomerulonephritis with PGE2.

The effects of treatment with 16,16-dimethyl prostaglandin E2 (DMPGE2) on histologic damage, glomerular immune complex deposition, serum total IgG subclass levels, anti-apoferritin IgG levels, and peripheral blood T-lymphocyte subsets were determined in apoferritin-induced immune complex glomerulonephritis of mice. The results demonstrate that doses of DMPGE2 ranging from 2.5 to 10 micrograms twice daily significantly reduced the degree of glomerular damage in a dose-dependent manner. Similarly, these doses of DMPGE2 reduced the amount of immunoglobulin deposition along peripheral capillary loops. Total IgM, IgG1, IgG2a, and IgG2b were unaffected by DMPGE2 administration. Serum anti-apoferritin IgG levels were significantly reduced in mice receiving DMPGE2 at doses of 5 and 10 micrograms twice daily. Nephrotic mice had significantly reduced peripheral blood total T lymphocytes (Lyt-1+) and a reduction of T-suppressor (Lyt-2+) cells. Administration of DMPGE2 at doses of 5 and 10 micrograms twice daily prevented these T-lymphocyte alterations. These studies indicate that treatment of mice receiving apoferritin with DMPGE2 may prevent glomerulonephritis by altering both cellular and humoral immune responses.

16,16-Dimethylprostaglandin E2↗
PubMed1985

Human histocompatibility antigen associations in patients with chronic cutaneous lupus erythematosus.

Increased frequency of certain human leukocyte antigens (HLA) has been reported in various subsets of patients with lupus erythematosus (LE). Specifically, HLA-B8 and HLA-DR3 have been associated with subacute cutaneous LE; HLA-DR3 or HLA-DR2 is found in mothers of infants with neonatal LE; and HLA-A1, HLA-B8, HLA-B15, and HLA-DR2 occur in patients with systemic LE. We typed twenty-two white and nineteen black patients with chronic cutaneous (discoid) LE (DLE) for the A, B, and DR loci of the HLA antigens. HLA-DRw6 was found in an increased proportion of our patients of both races compared with controls. HLA-B8 was found more frequently in white DLE patients than in white control subjects. Thus a genetic predisposition may be a factor that explains the variation in disease expression.

Black People↗
PubMed1985

Serial changes in humoral and cellular immunity induced by prostaglandin E2 treatment of murine immune complex glomerulonephritis.

To examine the mechanism by which prostaglandin E2 (PGE2) inhibits the development of apoferritin (HAF)-induced immune complex glomerulonephritis (ICGN), weekly determinations of glomerular histologic conditions, blood urea nitrogen (BUN), total immunoglobulin levels, anti-HAF antibody, peripheral blood and splenic T cell subsets, and splenic suppressor cell activity were compared between mice receiving HAF and mice additionally treated with PGE2. PGE2 therapy prevented the development of glomerular hypercellularity and the increase in BUN concentration. Administration of PGE2 reduced anti-HAF IgG levels, but total IgM and IgG1, IgG2a, and IgG2b levels were unchanged. Mice receiving HAF alone demonstrated serial reductions in phenotypically identified peripheral blood pan-T cells and suppressor-cytotoxic T cells. PGE2-treated mice maintained normal levels of peripheral blood T cell subsets. Significant reductions in splenic total T cells and suppressor-cytotoxic cells occurred in mice receiving HAF as compared with normal mice. This reduction was offset by an increase in splenic B cells. PGE2 therapy prevented the decrease in splenic T cells at week 1, but not at week 4. Nonspecific suppressor cell activity, as measured by the ability of spleen cells from experimental mice to suppress a mixed lymphocyte reaction (MLR) or to suppress MLR-induced polyclonal IgG synthesis, was not different between the two groups. We conclude that prevention of HAF-ICGN by PGE2 is associated with a reduction in nephritogenic antibody production without an alteration in total immunoglobulin synthesis or the generation of nonspecific suppressor T cells. Changes in the percent of peripheral blood and splenic T cells and B cells may represent an effect of PGE2 on antigen-stimulated B cell proliferation.

Animals↗
PubMed1984

Alterations in T lymphocyte subpopulations associated with renal allograft rejection.

The peripheral blood OKT3 (total T), OKT4 (T helper/inducer), and OKT8 (T suppressor/cytotoxic) cells were determined by flow cytometry on twenty consecutive recipients of HLA-nonidentical cadaveric renal allografts. The absolute number of cells in all three populations decreased significantly posttransplantation, but no differences were found between patients experiencing rejection and those in quiescence. An OKT4/OKT8 ratio of greater than or equal to 1.7, either pretransplant or posttransplant, uniformly identified patients who subsequently experienced rejection. However, an OKT4/OKT8 ratio of less than 1.7 did not identify patients with a low risk of rejection. Pretransplant splenectomy was performed in 6 of 7 patients who rejected despite a low ratio. Serial monitoring of the OKT4/OKT8 ratio posttransplantation determined that an increase in the ratio of greater than or equal to 0.5 was a sensitive (81%) and specific (91%) indicator of a rejection episode. Graft survival was improved in patients with a high posttransplant OKT4/OKT8 ratio. These results indicate that the balance of helper and suppressor cell function may be of critical importance to the fate of an allograft, and that the alterations in this balance can be used to assist in the clinical management of allograft recipients.

Antibodies, Monoclonal↗
PubMed1984

The early posttransplant prognosis of acute renal allograft rejection as determined by detection of cytotoxic antibodies to lymphoid B cell lines.

We have studied serial samples of pretransplant and posttransplant sera for cytotoxic antibodies to lymphoid B cell lines (LCL) in 45 renal allograft recipients. A total of 48 rejection reactions occurred in 31 patients. A comparison of each patient's most reactive posttransplant serum showed a significantly higher reactivity in the ten patients with early allograft failure when compared with the 21 patients with reversible rejections and the 14 patients who had no rejections. Rejection reactions were easily differentiated by comparing the change in cytotoxic reactivity to LCL of recipients' sera drawn at the time of a rejection episode with the reactivity of their pretransplant sera. In 32 rejections considered non-antibody-associated cytotoxic reactivity of recipients' sera to LCL either decreased or remained essentially unchanged during the rejection. In 16 rejections considered antibody-associated the recipients' sera drawn during the rejection episode showed an increase in cytotoxic reactivity ranging from 40% to 100%. Response to antirejection therapy and three month graft survival had a significant correlation with changes in LCL antibody reactivity during a rejection. Only two of the 32 rejections considered non-antibody-associated failed to reverse compared with eight of the 16 antibody-associated rejections (P less than .001). Graft survival at three months in patients with non-antibody-associated rejections was 90% compared with 27% in the 11 patients who had antibody-associated rejections (P less than .001) Other parameters possibly related to the severity of a rejection reaction or to early allograft prognosis did not differ appreciably between the two types of rejections. This included the time posttransplant to the first rejection episode, the number of patients with multiple rejections in the first three months, and rejections requiring dialysis therapy. Determination of a change in cytotoxic reactivity to LCL during a rejection reaction enables one to predict the response to antirejection therapy and early allograft prognosis. This may ultimately be useful in selecting different types of antirejection therapy for individual patients.

Acute Disease↗
PubMed1983

Treatment of murine immune complex glomerulonephritis with prostaglandin E2: dose--response of immune complex deposition, antibody synthesis, and glomerular damage.

A model of immune complex glomerulonephritis (ICGN) produced in mice by the daily injection of apoferritin was employed to study the effect of treatment with various doses of prostaglandin E2 (PGE2) on glomerular damage, immune complex deposition, proteinuria, and serum anti-apoferritin antibody. Administration of PGE2, 200 micrograms twice daily, resulted in a significant decrease in glomerular damage and immune complex deposition, prevented the development of proteinuria, and significantly reduced serum levels of anti-apoferritin antibody. PGE2, 100 micrograms twice daily, resulted in a decrease in immune complex deposition as assessed by immunofluorescence microscopy, but this dosage did not significantly alter glomerular damage, proteinuria, or antibody levels. PGE2 dosages of 50 and 25 micrograms twice daily had no effect on any of these parameters. The protective effect of PGE2 on the development of ICGN occurred only at dosages that were associated with decreased anti-apoferritin antibody.

Animals↗
PubMed1983

Phenotype of the hairy cells of leukemic reticuloendotheliosis defined by monoclonal antibodies.

Hairy cell populations of greater than 90 purity were prepared from six samples obtained from four patients with leukemic reticuloendotheliosis (LRE). These then were analyzed for surface immunoglobulin (SIg) and antigens specified by a panel of monoclonal antibodies. The hairy cells from all patients displayed SIg and antigens reactive with OKIa-1 and OKM-1 antibodies; these markers often were expressed simultaneously. T-cell-specific antigens were not displayed on the surface of hairy cells. The simultaneous expression of SIg and OKM-1 which ordinarily are unique for B cells or myeloid cells, respectively, suggests that hairy cells may represent an aberrant form of either cell type with defective regulation of antigen expression. It alternatively suggests the possibility that B cells and myeloid elements develop along a common pathway and that the hairy cell is a component of such a pathway.

Adult↗
PubMed1980

Characterization of suppressor cells in mice with a transplantable malignant melanoma.

C57BL/6 mice with progressive B-16 melanoma develop a generalized immunosuppression, as measured by their lack of response to SRBC in vivo and in vitro. The severity of immunosuppression increases with the progress of the tumor, and is due to the generation of an antigen-nonspecific suppressor cell. Suppressor cells were first demonstrable 15 days after the appearance of the tumor, and their appearance correlated with the induction of immunosuppression in vivo. The suppressor cell generated by the growth of B-16 melanoma was a T lymphocyte since it was nonadherent to plastic and nylon wool, unaffected by passage through Sephadex G-10, and sensitive to treatment with rabbit antimouse brain serum and complement.

Animals↗
PubMed1980

The influence of cigarette tobacco smoke products on the immune response. The cellular basis of immunosuppression by a water-soluble condensate of tobacco smoke.

The immunosuppression exhibited by a water-soluble condensate of tobacco smoke (WSC) has been studied in vivo and in vitro. When multiple sublethal doses of WSC were injected into C57Bl/6 mice, their ability to respond to immunization with sheep erythrocytes by the formation of plaque-forming cells was severely inhibited. In addition, spleen cells from WSC-treated mice were unable to mount a primary response to SRBC in vitro. Studies on the cellular basis of the immunosuppression induced by WSC showed a decrease in T lymphocytes in the spleens of WSC-treated mice. Additional experiments were conducted in which isolated populations of T cells, B cells and macrophages from WSC-treated or normal mice were combined and then tested for responsiveness to SRBC in vitro. Results of these experiments also indicated that T cells were particularly susceptible to WSC exposure. T cells from WSC-treated mice were unable to co-operate with normal B cells and macrophages in the response to SRBC. A less marked suppression of B-cell function was noted in condensate-treated mice. While B cells from such animals were able to co-operate with normal T cells and macrophages to give a detectable primary response to SRBC, the response was depressed. In contrast, macrophages from WSC-treated animals enhanced the response of normal T and B cells to SRBC.

Animals↗
PubMed1976

Lymphocyte function in experimental african trypanosomiasis: mitogenic effects of trypanosome extracts in vitro.

Extracts of Trypanosoma brucei and Trypanosoma congolense were incubated in vitro with nonimmune lymphocytes of mice, rats, guinea pigs, and rabbits in order to test for mitogenic effects or for other characteristics of polyclonal B lymphocyte activators. Trypanosome extracts (TE) were not mitogenic for spleen cells of mice, rats, and guinea pigs in vitro, nor did the parasite extracts alter the mitogenic responses of lymphocytes from these animals to known B- and T-cell mitogens. TE also failed to induce polyclonal antibody synthesis in mouse spleen cell cultures in an in vitro antibody response system, in contrast to the effects of bacterial lipopolysaccharide, a known polyclonal B cell activator. Rabbit spleen cell and peripheral blood lymphocyte cultures, however, were stimulated by TE to undergo blastogenesis in vitro. Incubation of rabbit lymphocytes with phytohemagglutinin (PHA) and TE or anti-rabbit immunoglobulin serum and TE revealed an additive effect only in terms of the TE-plus-PHA culture responses; these findings suggest that a non-PHA responsive lymphocyte population, possibly B lymphocytes, is stimulated by TE in rabbits. The relationship of trypanosome-induced lymphocyte mitogenic stimulation to other immunological dysfunctions occurring in chronic African trypanosomiasis is discussed.

Animals↗