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O Lantz

Publications and source records attributed to O Lantz.

At least 73 records · Page 4Linked to original sources
PubMed1988

Multiple drug combinations with "low-dose" cyclosporin for renal transplantation. Multivariate analysis of risk factors determining short-term graft survival within one renal transplant center.

The factors affecting graft survival in transplant recipients receiving cyclosporin (CsA) are still being debated. Our report is based on an analysis of 202 successive transplantations performed in our institution from May 1984 to December 1986, using low-dose CsA as the basic means of immunosuppression. A total of 142 patients received the triple combination CsA, azathioprine (AZA), and corticosteroids. Sixty patients received a prophylactic combination of CsA, corticosteroids, and antilymphocyte globulins (ALG). From January to December 1986, both regimens were compared in a prospective randomized trial. The factors that affect graft survival were analyzed using the Cox multivariate hazard analysis. The relative risks were calculated for pretransplant baseline risk factors and for outcome-dependent post-transplant risk factors for surviving grafts at 1 month. Transplants performed with a prolonged ischemia time and patients whose graft did not function immediately were statistically at higher risk of graft loss. Adding prophylactic ALG to CsA was associated with better graft survival. Patients who experienced more than 1 rejection crisis and patients whose 1-month CsA dose was lower than or equal to 5 mg/kg per day were also at significantly higher risk of further graft loss. Neither HLA matching, peak panel reactivity, age of the recipient, occurrence of post-transplant renal dysfunction nor 1-month renal function affected the short-term graft outcome.

Adrenal Cortex Hormones↗
PubMed1988

Interleukin-2 production in Brown-Norway rats with HgCl2-induced autoimmune disease: paradoxical in vivo versus in vitro findings.

In autoimmune diseases, mitogen-induced IL-2 production in vitro is generally considered to be diminished despite evidence of lymphoid hyperactivity in vivo. HgCl2 is known to cause T-dependent polyclonal B cell activation in Brown-Norway (BN) rats, resulting in autoimmune disease. We show here that the IL-2 producing capacity of cells from HgCl2-treated BN rats is low, but that HgCl2 treatment in vitro (10(-7) M) enhances IL-2 production of normal BN splenocytes. Lewis (LEW) rats are resistant to HgCl2-induced autoimmune disease. HgCl2 treatment of these rats in vivo does not significantly decrease the IL-2 production of their splenocytes. However, HgCl2 treatment of normal LEW splenocytes in vitro enhances their IL-2 production but this requires an HgCl2 concentration ten times greater (10(-6) M) in LEW than in BN rats. These findings are discussed in an attempt to resolve the paradox between the in vivo immune hyperactivity seen in HgCl2-treated BN rats, and the apparently low IL-2 production of their splenocytes in vitro.

Animals↗
PubMed1987

rIL 2-induced proliferation of human circulating NK cells and T lymphocytes: synergistic effects of IL 1 and IL 2.

Cells participating in the rIL 2-induced proliferation of resting PBMC were identified by using different methods of cell purification. NK cells recovered in the light density fraction of Percoll gradients responded, as already known, directly to rIL 2 by strong proliferation. In contrast, large T lymphocytes co-purifying with NK cells, and small T cells sedimenting in the high density area of the Percoll gradients, were virtually unresponsive when cultivated in the sole presence of rIL 2. However, the addition of either irradiated autologous monocytes or highly purified IL 1 allowed both kinds of T cells to undergo cell division. Stringent elimination of possibly contaminating NK cells (NKH-1+) and/or activated T cells (TNKTAR, Tac+, HLA-DR+) from the high density T cells by complement lysis did not impair rIL 2-induced cell proliferation, indicating entire responsiveness of these cells to the synergistic action of IL 1 plus IL 2. Both high density CD4+ and CD8+ participated in this phenomenon, with an apparent advantage for CD4+ cells. All Tac+ cells emerging in a 6-day culture of these cells expressed the WT31 antigen, which indicates that T cells involved in rIL 2-induced proliferation are conventional mature T cells. The relative precursor frequencies of NK cells, large T lymphocytes, and small T lymphocytes that proliferated in response to rIL 2 were analyzed by limiting dilution analysis. The frequencies of clonal growth of NK cells and low density T lymphocytes were approximately the same (1/103 vs 1/185), whereas that of high density T cells was four times lower (1/458). Thus, we clearly demonstrate that resting T cells, defined as such by morphological, density, and phenotypic criteria, are able to proliferate in response to IL 2 in the presence of IL 1 without antigenic or mitogenic triggering.

Cytotoxicity, Immunologic↗
PubMed1987

Fluoride-induced chronic renal failure.

Renal fluoride toxicity in human beings is difficult to assess in the literature. Although experimental studies and research on methoxyflurane toxicity have shown frank renal damage, observations of renal insufficiency related to chronic fluoride exposure are scarce. We report a case of fluoride intoxication related to potomania of Vichy water, a highly mineralized water containing 8.5 mg/L of fluoride. Features of fluoride osteosclerosis were prominent and end-stage renal failure was present. The young age of the patient, the long duration of high fluoride intake, and the absence of other cause of renal insufficiency suggest a causal relationship between fluoride intoxication and renal failure.

Adult↗
PubMed1987

[Anti-cytomegalovirus T-cell immunity and HLA restriction in the transplanted kidney patient].

Cytomegalovirus (CMV)-specific immune T-cells, present in the circulation of previously infected kidney transplant recipients (anti-CMV serum antibody titer greater than 1/40) can be reactivated to give rise to specific helper and cytotoxic effector cells by co-culturation with fresh autologous blasts coated with CMV antigen in vitro. The reactivated cells are able: 1) to proliferate when stimulated with CMV antigen, 2) to kill the autologous target coated with CMV antigen and not autologous blasts alone when assayed in 51Cr release test. These specific effector cells lie in the E+ T cell subset by removing NK cells with sheep-erythrocytes rosetting. When the reactivated cells are tested against allogeneic CMV coated blasts the level of cytotoxicity is in general related to the extent of HLA-A and B antigen sharing between effector and target cells. The results provide strong evidence that: 1) only previously infected individuals can generate immune T cells against CMV in vitro, 2) there is a correlation between the index of proliferation and cytolysis, 3) there is an HLA restriction of immune T cell cytotoxicity of CMV, 4) monoclonal antibodies directed at several antigenic sites of CMV are able to block cytolysis.

Adolescent↗
PubMed1987

[Demonstration of complex dysregulation of anti-cytomegalovirus T-cellular immunity in Kaposi's sarcoma following renal transplantation].

An increased incidence of Kaposi's sarcoma is well known in renal transplant recipients in whom it may represent up to 3 p. 100 of all de novo tumours. This sarcoma has a close relationship with the potential oncogenicity of the cytomegalovirus (CMV) and with chronic immunological deficiency. Anti-CMV immunity is based on the integrity of cytotoxic cellular functions such as those of cytotoxic T lymphocytes (CTL), "natural killers" cells, and K cells which function in the antibody-dependent cell cytotoxicity (ADCC) system. Two cases of Kaposi's sarcoma were observed out of a total of 700 renal transplant recipients; they underwent the following investigations: lymphocyte sub-group counts by murine monoclonal antibodies, lymphocyte proliferation to lectins and allogenic cells, NK activity and generation of specific auxiliary and cytotoxic anti-CMV cells. Both cases of Kaposi's sarcoma were seropositive for CMV and seronegative for LAV. In one case, an abnormal number of peripheral OKT9 + lymphocytes (normally a thymocytic marker) was observed with small numbers of OKT4/OKT8, a reduced proliferative response to mitogens and allogenic cells. All these in vitro changes persisted despite reduction of immunosuppressive therapy and clinical improvement. A clinical and biological cure was only obtained after withdrawal of immunosuppressive therapy and return to haemodialysis. In the second case of Kaposi's sarcoma, the initial biochemical changes were minimal and a clinical cure was obtained by decreasing the immunosuppressive therapy. These two cases illustrate the complex dysregulation of the immune system in Kaposi's sarcoma.

Adult↗