Search PubMed⌕ Search

Biomedical subjects

R C Burton

Publications and source records attributed to R C Burton.

At least 91 records · Page 5Linked to original sources
PubMed1981

T cell responses to alloantigens. II. In vitro induction of specific Ts by heat-inactivated allogeneic lymphoid cells.

When viable B6AF1 murine spleen cells were cultured in combination with heat-inactivated B10.D2 spleen cells under appropriate conditions, alloantigen-specific suppressor T cells (Ts) were generated. The optimal conditions for generation of specific Ts included a responder cell number of 2 to 4 X 10(6)/ml, a high stimulator to responder ratio, the use of at least 30 min of heat treatment (45 C) of stimulator cells, and 6 or more days of culture.

Animals↗
PubMed1981

T cell responses to alloantigens. III. Prolonged circulation of specific cytotoxic T memory cells following skin allograft rejection in mice.

A limit dilution technique was used to study specific circulating cellular memory to alloantigens in the blood of B6AF1 mice that had rejected B10.D2 or B10.BR skin grafts. A specific increase in cytotoxic T cell (Tc) precursor (CTL-P) frequency was detected as the skin grafts were rejected, and this persisted for the duration of the experiment (8 months) in the B6AF1 mice that had rejected B10.D2 skin grafts. By contrast, the CTL-P frequency for H-2Dk in the blood of B6AF1 mice that had rejected B10.BR skin grafts had returned to normal by 4 months after graft rejection. In addition, it was shown that peripheral blood lymphocytes from these immune mice could respond to heat-inactivated spleen cells of donor origin, whereas those of naive mice could not.

Animals↗
PubMed1981

Treatment of acute renal allograft rejection with OKT3 monoclonal antibody.

Eight cadaver donor renal allograft recipients, who had received azathioprine and prednisone from the day of transplantation, were treated with OKT3 monoclonal antibody (reactive with all mature peripheral blood T cells) at the time of diagnosis of acute rejection. In all cases, loss of essentially all detectable peripheral blood OKT3-reactive cells was noted within minutes after the initial 1- to 5-mg i.v. infusion. Chills and fever invariably occurred following the first or second infusion of monoclonal antibody, but were not noted during the subsequent, 10- to 20-day course of therapy, suggesting rapid cell lysis as the etiology of this toxicity. The established rejection episode was reversed in all cases within 2 to 7 days without addition of any therapy other than OKT3 antibody and despite continued lowering of the steroid dosages. During the subsequent 3- to 12-month follow-up period, further rejection episodes occurred in five of these patients, two of these were irreversible with conventional therapy so that six of the eight allografts continue with excellent renal function. These preliminary observations suggest that homogeneity, limited dosage requirements, and ease of in vitro monitoring of dosage effects should markedly simplify the use of monoclonal antibody to T cell populations in human allograft recipients. This second generation of antilymphocyte preparations offers the potential for not only increased effectiveness but also the possibility of manipulating specific T cell subsets.

Antibodies, Monoclonal↗
PubMed1981

Increased natural killer cell activity in experimental American trypanosomiasis.

These studies showed that increased natural killer (NK) cell activity develops during experimental American Trypanosomiasis in mice. Increased cytotoxicity against YAC target cells by peritoneal cavity cells (PEC) was detected as early as 1 day into infection in both C3H/He and C57BL/6 mice. Peak activity occurred 2 days into infection, with significant but variable increases detected in the spleen cells (SC) from these mice. The response subsided in PEC and to a lesser extent in SC by 4 days post-infection. Similar responses were not detected in infected C57BL/6 bgJ/bgJ (beige mutant) mice until the fourth day of infection and peaked at significantly lower levels than the peak on day 2 in beige hybrid mice ([C57BL/6 +/+ X C57BL/6 bgJ/bgJ]F1). The effector cell from infected mice was sensitive to pretreatment with anti-NK 1.2 serum plus complement (C), partially sensitive to anti-Thy 1.2 + C, and insensitive to polyvalent anti-mouse immunoglobulin + C. The cytotoxic activity induced in cells from mice infected for 2 days was recovered in subpopulations nonadherent to plastic or Sephadex G-10. Thus, the anti-YAC effector cell found very early in mice infected with T. cruzi possessed many of the characteristics of natural killer (NK) cells found in normal mice. Other experiments demonstrated that injection of heat-killed preparations of blood-form trypomastigotes (BFT) induced increases in NK activity. The presence of augmented NK activity against YAC tumor cells in both resistant and susceptible strains of mice, together with the presentation of the resistance phenotype in beige mutant mice, which had a lower NK response to infection, is not indicative of a direct role for host protection during infection with T. cruzi by NK cells.

Animals↗
PubMed1981

Studies on natural killer (NK) cells. II. Serologic evidence for heterogeneity of murine NK cells.

NK cells are divided into 2 subclasses on the basis of cell surface antigens: NKA cells, which preferentially lyse lymphoma cells and which are readily destroyed by treatment with anti-H-2, rabbit anti-mouse, or anti-NK specific antibodies in the presence of C; and NKB cells, which preferentially lyse nonlymphoma tumor cells and which are resistant to anti-NK specific antibodies, partially sensitive to anti-H-2 specific antibodies, and only fully sensitive to rabbit anti-mouse serum and C. Thus, suspensions of spleen cells that were treated with anti-NK-1.2 antibodies and C lost virtually all lytic activity for 6 lymphoma cell lines, whereas lytic activity for 2 nonlymphoma cell lines remained largely intact. It must be noted, however, that unlike NK-1.2 expression, target cell preference is not an absolute indicator of NK cell subclass. Cytotoxic T cells were readily distinguished from NKA and NKB cells on the basis of their sensitivity to monoclonal anti-Thy-1.2 antibodies and resistance to anti-NK-1.2 antiserum and C.

Animals↗
PubMed1981

Studies on natural killer (NK) cells. I. NK cell specific antibodies in CE anti-CBA serum.

An antiserum prepared by injecting CE mice with CBA spleen cells has been shown to contain antibodies specifically reactive with NK cells. The serum also contains antibodies detectable in C-dependent dye exclusion tests, but in a study of (CE X CBA)F1 X CE mice reactivity in this test was found to segregate independently of sensitivity of NK cells to inactivation. Moreover, abrogation of NK activity was observed with concentrations of antiserum and C that were considerably lower than those required for detectable cytotoxicity as measured by dye uptake. Thus, it is possible to use this antiserum for the selective removal of NK activity. Analysis of the strain distribution of NK cell sensitivity to CE anti-CBA serum suggests that this reagent may detect an allele of the NK-1 system, and we have tentatively designated the allelic product as NK-1.2, and the corresponding antibodies as anti-NK-1.2. However, the possibility that CE anti-CBA serum detects a new system of NK-specific antigen has not been excluded.

Absorption↗
PubMed1981

Definitive evidence that natural killer (NK) cells inhibit experimental tumor metastases in vivo.

Effector lymphoid cells that inhibit hematogenous tumor metastasis in normal unimmunized mice were studied. Mice pretreated with cyclophosphamide (Cy) exhibited a diminished ability to destroy circulating tumor cells, which, in turn, caused an increased incidence of experimental pulmonary metastasis. Adoptive transfer of spleen cells from unimmunized syngeneic donors abrogated the Cy-induced enhancement of metastasis formation. The effector cell active in these adoptive transfer experiments was sensitive to treatment with specific anti-NK-1.2 antibodies and complement. This treatment was shown by in vitro tests to deplete or inactivate NK cells selectively. These findings provide direct evidence that NK cells play a significant role in the inhibition of hematogenous tumor metastases in vivo.

Animals↗
PubMed1980

T cell responses to alloantigens. I. Studies of in vivo and in vitro immunologic memory and suppression by limit dilution analysis.

A limit dilution technique was used to study the frequency of cytotoxic T cell precursors (f pre Tc) in the peripheral blood lymphocytes (pbl) of naive and alloimunized mice. It was found that alloimmune mice showed a 2- to 5-fold specific increase in the f pre Tc reactive to the immunizing alloantigens. This technique was further adapted for use as a sensitive in vitro assay for alloantigen-specific suppressor T cells. It was found that nonimmunosuppressed B6AF1 mice bearing surviving B10.BR cardiac allografts had circulating alloantigen-specific suppressor cells. In vitro it was shown that the culture of heat-inactivated B10.D2 spleen cells with B6AF1 spleen cells gave rise to alloantigen-specific B6AF1 suppressor cells.

Animals↗
PubMed1980

Differential natural killer cell reactivity against T cell lymphomas by cells from normal or stimulated mice.

One of the major problems confronting the study of NK cell populations concerns their potential recognition patterns and specificity. In this study three T cell lymphomas that differ markedly in their susceptibility to NK-mediated lysis from normal mice are shown to bear quantitatively but not qualitatively different degrees of NK target structures. The ability of these tumors to be lysed by NK cells can be drastically changed by augmentation of NK activity by LCM virus, but in a manner that differs relatively for the different targets. Comparison of the growth of these tumors in vivo strongly suggests an in vivo action for NK cells.

Animals↗
PubMed1980

Tumor immunity to murine plasma cell tumors. V. Genetic control of the in vitro cytotoxic T-cell response to plasma cell tumor-associated antigens of NZB mice.

Cytotoxic T-lymphocytes (Tc) were induced in vitro to plasmacytoma tumor-associated antigens (TAA) by coculture of irradiated cells of plasma cell tumors (PCT) from NZB mice and viable nonimmune or PCT-immune spleen cells from NZB. (NZB X C57BL)F1, (NZB X B10.D2)F1, and (NZB X B10,BR)F1 mice. When nonimmune spleen cells were used, major histocompatibility complex (MHC)-linked genetic control of te primary in vitro induction of Tc to NZB PCT was demostrated for a shared TAA expressed on NZB and BALB/c PCT. Evidence was also obtained for a non-MHC-linked genetic control of the primary in vitro induction of Tc to a second TAA that ws expressed on both PCT and T-lymphomas. When the spleen cells were obtained from mice preimmunized to an NZB PCT, a secondary in vitro Tc response was observed, and a PCT-specific and strain-specific TAA or NZB mice was identified. In addition, results with the F1 hybrids also indicated an MHC-linked genetic control of the in vitro Tc response to this strain-specific TAA.

Animals↗