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K H Stenzel

Publications and source records attributed to K H Stenzel.

At least 109 records · Page 6Linked to original sources
PubMed1981

Mitogenic and co-mitogenic properties of hemin.

We report here that hemin, an agent known to induce cellular differentiation in Friend erythroleukemia cells, induces mitogenesis in human T cells and enhances mitogenic responses to supraoptimal concentrations of Con A. Mitogenesis induced by suboptimal or optimal concentrations of Con A is not affected by concentrations of hemin that markedly potentiate responses to supraoptimal amounts of Con A. Maximum mitogenic responses are reached 4 to 5 days after initiation of the cultures. The mitogenic response is macrophage dependent, whereas enhancement of responses to supraoptimal concentrations of Con A is not. Indeed, a greater degree of enhancement is observed after removal of adherent cells. Responses to other mitogens (phytohemagglutinin, wheat germ agglutinin, and sodium periodate) are also enhanced by hemin. Compounds that are metabolically or structurally related to hemin are neither mitogenic nor co-mitogenic. Protoporphyrin IX, which is nonmitogenic, is rendered mitogenic by the chemical insertion of iron to form hemin. Hemin does not affect Con A binding to lymphocytes. These findings indicate that hemin is a macrophage-dependent T cell mitogen with the unusual and remarkable property of overcoming the inhibition of mitogenesis induced by high concentrations of Con A. Since hemin has a limited number of metabolic effects, it provides a useful probe for determination of molecular events associated with lymphocyte activation.

Adult↗
PubMed1980

Chemical inducers of differentiation in Friend leukaemia cells inhibit lymphocyte mitogenesis.

Several phorbol esters, the potent tumour-promoting agents isolated from croton oil, induce proliferation of human lymphocytes and enhance the mitogenic effect of lectins on bovine lymphocytes. While studying the mitogenic properties of one of these agents, phorbol myristate acetate (PMA), we found that dimethyl sulphoxide (DMSO), frequently used as a solvent for PMA, markedly inhibits PMA-induced mitogenesis at DMSO concentrations that have little effect on phytohaemagglutinin (PHA)-induced responses. DMSO, as well as a variety of other organic compounds, induce erythroid differentiation in Friend leukaemia (FL) cells. Phorbol esters, on the other hand, are potent inhibitors of both spontaneous and induced cellular differentiation. We therefore investigated the relationship between the potency of compounds to induce erythroid differentiation in FL cells and their potency to inhibit lymphocyte proliferation induced by PMA and other mitogens. We report here that many of the compounds that induce erythroid differentiation in FL cells are similar to DMSO in selectively suppressing PMA-induced lymphocyte mitogenesis.

Animals↗
PubMed1980

Generation of a lymphocyte growth factor by treatment of human cells with neuraminidase and galactose oxidase.

Supernates of neuraminidase and galactose oxidase (NAGO)-treated lymphocytes induce blastogenesis in nonproliferating cells harvested 7--14 d after treatment with mitogen or alloantigen and in cells incubated with mitogen for 7--14 d but not in freshly isolated peripheral blood lymphocytes9 Virtually all the growth factor is produced by NAGO-treated cells during the first 24 h of incubation, and no increase in factor activity is detected upon further cell culture. Serum is not required for growth factor production. NAGO-primed medium induces generation of specific cytotoxic T cells from mixed lymphocyte culture (MLC) memory cells to approximately the same extent as that induced by allogeneic cells (stimulating cells in the primary MLC). NAGO-primed medium provides a useful reagent for isolation and characterization of lymphocyte growth factors and other lymphokines.

Adult↗
PubMed1980

HLA-A28 and steroid-induced diabetes in renal transplant patients.

Between July 1971 and March 1977, steroid-induced diabetes (SD) developed postoperatively in 31 (10.8%) of 286 nondiabetic adult kidney transplant recipients who were observed for a total of 410 patient transplant years. There was a highly significant association between HLA-A28 and SD. There was no significant association between SD and BB or Bw 15. Age was also associated with SD. However, A28 was associated with SD even when corrected for age. A28 occurred more frequently in blacks than whites, 25.4% and 6.3%, respectively, and accounted for the higher incidence of SD in black adults. There were no significant associations between SD and patients' sex, donor source, number of short-term rejection treatments, or maintenance dose of corticosteroids. Steroid-induced diabetes had no adverse effects on graft or patient survival.

Adult↗
PubMed1980

Kidney transplant nephrotic syndrome: relationship between allograft histopathology and natural course.

We analyzed clinical and pathologic data from 36 recipients of 38 renal allografts who developed nephrotic syndrome following transplantation. Three groups were identified on the basis of histologic changes in the graft, and each group had a distinct clinical course. Nine grafts (23.7%) had recurrent glomerulonephritis (GN) (5 membrano-proliferative, 4 focal glomerulosclerosis) and developed nephrotic syndrome at 5.1 months (mean) posttransplant. Renal function deteriorated rapidly, with a 2-year graft survival of 29.7%. Four grafts (10.5%) with de novo GN (3 epimembranous, 1 minimal change) developed nephrotic syndrome at 32 months posttransplant, and all functioned for more than 3 years. Twenty-five grafts (65.8%) had allograft glomerulopathy with the onset of nephrotic syndrome at 9.1 months posttransplant and a 2-year graft survival of 66.6%. The differences in duratin of graft function between grafts with allograft glomerulopathy and recurrent GN (P < 0.01) and in graft survival rates at 2 years among the three groups (P < 0.05) are statistically significant. This analysis indicates that allograft glomerulopathy is the most common cause of kidney transplant nephrotic syndrome. Membranoproliferative GN and focal glomerulosclerosis may recur soon after transplantation and rapidly progress to renal failure in marked contrast to grafts with either de novo epimembranous nephropathy or minimal glomerular change, lesions that are compatible with prolonged graft function.

Adolescent↗
PubMed1980

Detection of alloimmune memory cells by chemical modification of the cell surface with mitogenic oxidizing agents.

The mitogenic oxidizing agents, neuraminidase and galactose oxidase (NAGO), and sodium periodate (IO-4) were used to induce the differentiation of human alloimmune memory cells. NAGO or IO-4 treatment of peripheral blood mononuclear (PBM) cells obtained from 10 sensitized potential allograft recipients resulted in the induction and augmentation of cytolytic activity to a D locus-defined lymphoblastoid cell panel (B cell panel) and to a HLA-disparate peripheral blood lymphocyte cell panel (PBL cell panel). The acquisition of cytolytic activity was determined in a 4-hr 51Cr release assay. Treatment of in vitro-primed PBM cells (alloimmune memory cells generated in primary long-term mixed lymphocyte cultures) obtained from normal subjects with NAGO or IO-4 also resulted in the induction of specific secondary cytolytic activity. In contrast, NAGO or IO-4 treatment of unprimed PBM cells from normal subjects did not result in the induction of cytolytic activity despite the extensive proliferation induced by such treatment. The strikingly similar results observed with PBM cells from sensitized patients and with in vitro-primed PBM cells suggest that in vivo- and in vitro-generated alloimmune memory cells can be detected by chemical modification of the cell surface induced by NAGO or IO-4. Furthermore, our findings indicate that alloantigen-independent activation of memory cells can be accomplished by treating the memory cells with the mitogenic oxidizing agents.

B-Lymphocytes↗
PubMed1980

A new class of inhibitors of lymphocyte mitogenesis: agents that induce erythroid differentiation in Friend leukemia cells.

Addition of the polar organic compounds, dimethylsulfoxide, N,N-dimethylformamide, N,N-dimethylacetamide, and butyric acid, to human lymphocyte cultures stimulated with the tumor-promoting agent, phorbol myristate acetate, results in greater than 90% inhibition of lymphocyte proliferation. Inhibition is achieved at concentrations of the organic compounds reported to be optimal for induction of erythroid differentiation in Friend leukemia cells. Butyric acid is the most potent compound tested. Compounds that are structurally related to butyric acid, but that do not induce erythroid differentiation, do not inhibit lymphocyte mitogenesis. Lymphocyte responses to other mitogens are also suppressed by the polar organic compounds, although higher concentrations are required. These agents are much less inhibitory when added 24 hr after initiation of the cultures, indicating that they may affect an early phase of lymphocyte activation. Compounds that induce erythroid differentiation in Friend leukemia cells constitute a new class of inhibitors of lymphocyte mitogenesis.

Acetamides↗
PubMed1979

Parainfluenza type 3 in a transplant unit.

We observed an epidemic of parainfluenza type 3 viral infection in a renal transplantation service among 16 recent transplant recipients. To assess the effect of infection on transplant function, we retrospectively compared the infected patients with a matched, uninfected control group. In addition to symptoms of a mild upper respiratory tract infection associated with the epidemic, there was an increase in the frequency of acute rejection episodes during the period of infection in the infected group. Nevertheless, outcome in terms of patient and graft survival at six months was not affected when compared with the survival rates of the control group.

Acute Disease↗
PubMed1979

Delayed hyperacute rejection in recipients of kidney transplants from HLA identical sibling donors.

Delayed hyperacute rejection, with its characteristic clinical course and histopathologic findings, occurred within one month after transplantation in five recipients of kidney transplants from HLA-A, B and D identical sibling donors. In all cases, unidirectional mixed lymphocyte cultures and immunologic studies to detect cytotoxic antibodies in the recipients against their respective donors, before kidney transplantation and after transplant nephrectomy, were unresponsive or negative. Onset of delayed hyperacute rejection was preceded by bacteremia in two of these patients. Two of these received second kidney transplants, three to six months later, from HLA-A, B and D identical sibling donors again. Although both have had an episode of acute rejection in the early postoperative period, the grafts have maintained excellent function for 21 and 25 months, respectively. Irreversible forms of transplant rejection, such as delayed hyperacute rejection, do occur even in recipients of kidney transplants from HLA-A, B and D identical sibling pairs, indicating that genetic determinants other than HLA-A, B and D loci, and perhaps other nongenetic immune mechanisms, play an important role in the ultimate results of kidney transplantation.

Adult↗
PubMed1979

Detection of memory cells by chemical modification of the lymphocyte cell surface.

Stringent alloantigen requirements, necessary for the differentiation of human memory cells into specific secondary cytolytic T cells (2 degrees CTL), can be bypassed by chemical modification of memory cells with the mitogenic oxidising agent, galactose oxidase. Treatment of memory cells generated in a long-term primary mixed lymphocyte culture with neuraminidase and galactose oxidase (NAGO) results in the differentiation of memory cells into 2 degrees CTL. In contrast, treatment of unprimed cells with NAGO does not result in CTL production despite the proliferation resulting from such treatment.

Cell Membrane↗