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S Macphail

Publications and source records attributed to S Macphail.

48 records · Page 3Linked to original sources
PubMed1982

Primary in vitro cytotoxic T cell response to non-major histocompatibility complex alloantigens in normal mice.

We have shown for the first time that it is possible to consistently generate a primary in vitro cytotoxic T cell (Tc) response to non-major histocompatibility complex alloantigens using responder cells from a normal mouse strain. This was achieved by carrying out, in the generating phase, a limiting dilution procedure in which it appears that suppressor cells that inhibit Tc activation or expansion are too dilute to manifest their effect. Moreover, the response was observed in mouse serum-(MS) as well as fetal calf serum- (FCS) supplemented media, an important finding in the light of the anomalous nonspecific effects induced by FCS. The cytotoxic response produced in MS-supplemented media was shown to be highly specific in both the generating and effector phases, whereas the responses in FCS had a strong nonspecific component.

Animals↗
PubMed1980

Generation of primary cytotoxic lymphocytes against non-major histocompatibility complex antigens by anti-Ia serum plus complement-treated lymphocytes.

The results presented in this paper demonstrate that responding cells that remain after anti-Ia serum plus complement (C) treatment generate a highly significant in vitro cytotoxic response against minor histocompatibility complex antigens. The cytotoxic response appears to be antigen specific in that target cells of strains other than the sensitizing strain are not lysed, or lysed to a lesser extent. The cytotoxic cells are susceptible to anti-Thy-1 plus C lysis. Anti-Ia serum may function by removing an unprimed suppressor cell, although other mechanisms cannot be ruled out.

Animals↗
PubMed1980

H-2 I alloantigens and recall of memory cytotoxic responses.

AQR mice were immunized with H-2K and H-2 I encoded alloantigens presented by (Ax6R)F1 splenocytes. Spleen cells from these alloimmune mice were subsequently restimulated in vitro with B10.A lymphocytes and/or B10.T(6R) lymphocytes, thus presenting them with the immunizing H-2K and H-2 I alloantigens independently. When stimulated with B10.A lymphocytes, alloimmune lymphocytes develop significant cytotoxicity against the immunizing H-2K target antigens. When stimulated with a similar number of B10.T(6R) spleen cells, alloimmune lymphocytes undergo a prominant proliferative response, but develop little, if any, cytotoxicity against the immunizing H-2 K target antigens. The most efficient restimulation of cytotoxicity occurs when the alloimmune spleen cells are simultaneously restimulated by B10.A and B10.T(6R) lymphocytes. Stimulation with the immunizing H-2 I alloantigens alone is not sufficient for regeneration of detectable cytotoxic responses from alloimmune spleen populations. Stimulation with the immunizing H-2K alloantigens alone appears to be both necessary and sufficient to stimulate alloimmune cytotoxic responses. Although the immunizing H-2 I alloantigens are apparently not required to generate alloimmune cytotoxic responses, they markedly potentiate the cytotoxic responses induced by the immunizing H-2K alloantigens.

Animals↗
PubMed1980

Non-H-2 T-lymphocyte-mediated cytotoxicity after primary in vivo sensitization.

A low level of T-lymphocyte-mediated cytotoxic activity was demonstrated after primary in vivo immunization in an H-2-compatible strain combination (B10.D2--DBA2). This phenomenon was demonstrated in a second responder strain (BALB/c) and was thus shown not to be restricted to the B10.D2 genetic background. Results on F1 hybrid mice indicate that the M-locus determinant might be involved in this reaction. It is possible that it is involved in the afferent, efferent, or both limbs of the reaction.

Animals↗
PubMed1980

Requirements for T cells in alloantigen-induced generation of non-T cell-mediated cytotoxicity against syngeneic mouse sarcoma cells.

In vitro stimulation of BALB/c spleen cells with allogeneic normal cells results in the generation of effector cells cytotoxic for syngeneic SV40 virus-induced MKSA fibrosarcoma cells. The conclusion that natural killer (NK) cells are activated that lyse the syngeneic tumor cells derives from findings that 1) treatment of the allostimulated BALB/c effector cells with anti-theta serum and complement does not ablate cytotoxicity against syngeneic MKSA tumor cells and 2) allostimulation of congenitally athymic (nu/nu) BALB/c mice results in significant cytotoxicity against MKSA tumor cells but not against allogeneic target cells. The requirement for the presence of theta-positive cells in alloantigen-induced activation of NK cells cytotoxic for syngeneic tumors was studied. Spleen cells from conventional BALB/c mice are cytotoxic for syngeneic MKSA tumor cells after stimulation with anti-theta serum-treated allogeneic cells or with allogeneic nude cells. In contrast, stimulation of BALB/c nude spleen cells with anti-theta serum-treated allogeneic cells or allogeneic nude cells fails to give rise to anti-tumor effector cells. Thus, theta-positive cells (presumably T cells) are required for alloantigen induced non-T cell-mediated lysis of syngeneic tumors.

Animals↗
PubMed1976

The class of antibody involved in the antibody-dependent cell-mediated lysis of chicken erythrocytes.

Affinity chromatographic experiments demonstrated that IgG was the class of antibody involved in the in vitro lysis of chicken erythrocytes by antibody and normal mouse effector cells. Further experiments designed to investigate the subclass of IgG involved, indicated that IgG2a was active and provided further evidence for the inactivity of IgM, either in the native 19S or chemically degraded 7S form. From the results obtained, the possibility of ADCC-inducing activity in the other IgG subclasses could not be excluded.

Animals↗
PubMedDate not supplied

Mls allo-determinants are recognized in an MHC class II antigen-dependent but unrestricted fashion by a discrete set of T cells.

Blocking studies carried out with anti-H-2 class II antigen antibodies show that H-2 class II molecules are intimately involved in the recognition of Mlsa determinants by unprimed, specifically responsive T cells. The blocking of the anti-Mlsa response by these antibodies were not due to inhibition of IL-1 production by H-2 class II antigen positive macrophages. A strain analysis indicates that the response to Mlsa is regulated by H-2-linked genes and that this effect is exerted at the level of the stimulator cells; however, the response to Mls epitopes does not appear to be H-2 restricted. Finally, the ability of spleen cells from Mls-incompatible mice to induce a state of Mls-specific, clonal deletion type tolerance by neonatal injection, shows that Mls determinants exist in qualitatively allelic forms and suggests that these determinants are recognized by specific clones of T cells.

Animals↗
PubMedDate not supplied

Midtrimester thoracoamniotic shunting for the treatment of fetal hydrops.

The management of fetal hydrops in the second trimester is changing as the underlying etiologies are better understood. We report a case which was diagnosed at 18 weeks gestation. There was no underlying anatomical abnormality. Fetal blood sampling confirmed a normal karyotype and there was no evidence of fetal infection. Bilateral thoracocentesis and paracentesis caused temporary improvement of the fetal condition but subsequent fluid reaccumulation was noted within the left pleural cavity. A pleuroamniotic shunt inserted at 22 weeks caused permanent resolution of the hydrops. The infant was normal at 1-year follow-up.

Adult↗
PubMedDate not supplied

Fetal urine production rates following intrauterine transfusion.

This study investigates the hypothesis that following an intrauterine, intravascular transfusion (IVT), one of the physiologic adaptations might be an increase in the fetal urine production. The hourly fetal urine production rate (HFUPR) was measured for the first hour following 12 transfusions and for 24 h following 5 transfusions in anemic isoimmunized fetuses. The HFUPR was also measured in 5 control fetuses who underwent fetal blood sampling without transfusion. Fetal hemoglobin, hematocrit and blood viscosity were measured before and after each transfusion. The HFUPR fell significantly from a mean (SEM) of 19.2 (2.85) to 7.4 (2.2) ml/h, and remained low for at least 4 h posttransfusion returning to pretransfusion rates by 24 h. There was no change in the HFUPR in the control fetuses. The study suggests that in human fetuses the rapid excretion of excess fluid via the renal tract is not an acute adaptive response to an IVT.

Adaptation, Physiological↗