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D Male

Publications and source records attributed to D Male.

30 records · Page 2Linked to original sources
PubMed1989

Antigen presentation in brain: brain endothelial cells are poor stimulators of T-cell proliferation.

The capacity of rat brain capillary endothelium to present antigen to primed peripheral lymph node cells or to ovalbumin-specific T-cell lines was examined in vitro. Brain endothelium can present antigen, but it is generally ineffective at stimulating T-cell division. Division is only seen when indomethacin is included in the cultures to suppress eicosanoid production. Even under these conditions an endothelial monolayer is only 1/40 as effective as a thymocyte monolayer in stimulating division. The failure to act as an effective antigen presenting tissue is not due to lack of IL-1 production, nor is it related to the extended time required to induce MHC class II molecules on these cells. In the presence of high levels of antigen-specific T cells, the endothelium appears to be subject to cytotoxic damage, so that T-cell stimulation is lowest with higher numbers of T cells--the opposite of that seen with conventional antigen-presenting cells. These findings support the view that brain endothelial cells are not important in stimulating T-cell division during the development of immune reactions in brain, although these cells may be recognizable by class II-restricted cytotoxic cells.

Animals↗
PubMed1988

Synergy between interferons and monokines in MHC induction on brain endothelium.

Rat brain endothelial cells were cultured as confluent monolayers and stimulated with combinations of interferon-beta (IFN beta), interferon-gamma (IFN gamma), tumour necrosis factor (TNF) and interleukin 1 (IL-1). After 4 days of stimulation the cell surface expression of class I and class II MHC molecules was quantitated by enzyme immunoassay. TNF by itself enhances class I expression and it synergises with IFN gamma in enhancing class I expression and inducing class II. IL-1 does not affect class I expression, nor does it synergise with IFN gamma in this respect. High doses of IL-1 slightly reduce IFN gamma mediated class II induction, but have no synergistic effect at lower doses. IFN beta stimulates class I weakly and induced class II in one experiment but the effects seen when IFN gamma and IFN beta were used together were additive, not synergistic. IFN gamma is the most potent modulator of MHC expression on these cells, although TNF acts as a strong co-stimulator, while IL-1 and IFN beta have only minor effects.

Animals↗
PubMed1988

Kinetics of MHC gene expression and mRNA synthesis in brain endothelium.

Rat brain endothelium was examined in vitro to determine the sequence of events in MHC gene activation following IFN-gamma stimulation. The cell-triggering time, kinetics of mRNA synthesis, rate of MHC induction and rate of decay were measured by quantifying cell-surface MHC expression in the presence or absence of alpha-amanitin. Enhanced class I expression is triggered immediately after IFN-gamma stimulation, and is maximally induced by 4 hr of stimulation. New class I mRNA synthesis starts immediately and proceeds over the next 24 hr. This is followed by increased expression of class I molecules, which reaches plateau levels by 24 hr. While IFN-gamma is present, enhanced class I expression is maintained at 140-200% of that seen on resting cells. On removal of IFN-gamma, class I expression decays towards the levels seen on resting cells, with a half-life of approximately 40 hr. Class II molecules can be induced on these cells as well, but it requires the continuous presence of higher levels of IFN-gamma for more than 48 hr to trigger the cells. Induced class II molecules start to appear 2 days after pulsing and continue to increase until Day 4. If the IFN-gamma is removed from the cultures, class II expression declines rapidly towards zero, with a half-life of approximately 30 hr.

Animals↗
PubMed1985

Molecular analysis of induced idiotypes associated with autoanti-thyroglobulin.

Idiotype (Id) and autoanti-thyroglobulin were induced in different strains of mice by priming with anti-Id to monoclonal anti-thyroglobulins (D8 and G4) and challenged with a subimmunogenic dose of thyroglobulin (Tg). Both D8.Id and G4.Id were induced in CBA mice by priming with the appropriate anti-Id, but only priming with anti-D8.Id also induced an increase in anti-Tg. D8.Id was induced in other strains by the same schedule but it only appeared to be associated with anti-Tg in 129 and, to a lesser extent, BALB/c mice, both of which have the allotype Iga. The extent of the overlap between the D8 Id and the anti-Tg was estimated and shown to be greatest in the CBA strain from which the D8 clone was originally derived. Spectrotypic analysis of the induced Ids in CBA mice showed that some of the D8.Id, but none of the G4.Id, was identical to the original clonotype, implying that CBA mice normally have cells which can be induced to produce D8.Id-positive autoanti-Tg, which are normally weakly expressed or regulated. The observation that anti-D8.Id priming in some strains increased D8.Id-negative anti-Tg responses suggests that the D8.Id may also be associated with anti-Tg T-cells.

Animals↗
PubMed1985

Serum IL-2 inhibitor in mice. II. Molecular characteristics.

The molecular characteristics of a serum IL-2 inhibitor were determined by fractionating active sera from normal and malaria-infected mice, and assaying inhibitory activity in blocking production and expression of IL-2 activity. Using isoelectric focusing and ion exchange chromatography, the activity resolved in a single peak (pI = 6.2). HPLC gel filtration resolved two peaks of activity (50,000 and 25,000 MW) which are probably related. The molecule is precipitated by 50% saturated ammonium sulphate, and is destroyed by heating above 56 degrees or by acidification below pH 4.

Animals↗
PubMed1983

The occurrence of defined idiotypes on autoantibodies to mouse thyroglobulin.

Anti-idiotypic antibodies were raised in rabbits to three monoclonal mouse autoanti-thyroglobulins. Of the idiotypes recognized, one was unique to that monoclonal, while the other two showed evidence of sharing idiotopes with other monoclonal anti-thyroglobulin (TG) idiotypes, the IgM idiotype in particular being found on nearly half of the hybridomas studied. Two of the idiotypes could be detected in the sera of mice with experimental allergic thyroiditis (EAT), but they constituted only a very small percentage of the total anti-TG present. In spite of its low levels in EAT mice the D8 idiotype could be induced by injection of anti-idiotype and TG and in this case it constituted up to 20% of the anti-TG activity in individual mice, showing a strain-related association between the idiotype and autoanti-TG.

Animals↗
PubMed1983

A rapid assay for immunoglobulin in hybridoma supernatants.

A single step assay is described which allows detection of IgM and IgG in tissue culture supernatants at concentrations below 100 ng/ml. The assay is based on the agglutination of staphylococcal protein A coated sheep red blood cells (E-spA) in the presence of an enhancing antibody. The assay was designed for the rapid screening of antibody production by hybridoma cultures.

Animals↗
PubMed1980

Analysis of immune complexes in synovial effusions of patients with rheumatoid arthritis.

Immune complexes were isolated from the synovial effusions of patients with seropositive definite or classical rheumatoid arthritis by centrifugation over a sucrose-polyethylene glycol gradient. Physiochemical and immunochemical analysis showed IgG and IgM to be the predominant molecular species with lesser amounts of Clq and moderate amounts of IgA and activated C4 and C3. Very low concentrations of Clr, Cls, factor B and beta 2-microglobulin were detected. Trace amounts of four other components totalling less than 4% of the total protein, were seen and their molecular weights established. Reasons were advanced for thinking that fibrinogen, human serum albumin and alpha 2-macroglobulin were only secondarily associated with the complexes. The data are consistent with the hypothesis that IgG is the main, if not the only antigen, responsible for provoking and maintaining the pathological changes in rheumatoid arthritis.

Antigen-Antibody Complex↗