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At least 1,009 records · Page 56Linked to original sources
PubMed1976

Factor B of the alternative complement pathway on human lymphocytes.

A factor on human lymphocytes has been identified as factor B of the alternative pathway. Lymphocytes can replace factor B in the fluid phase formation of C3 convertase with cobra venom factor (CVF). This lymphocyte activity is inhibited by specific anti-human factor B, and it is shown by Burkitt lymphoma cell lines cultured in the absence of any factor B source. After the reaction with CVF all the C3-converting activity is found in the cell supernatant, and the same cells can undergo several successive cycles of 'activation' by CVF. Factor B is distinct from the C3b receptor, and its presence could not be detected antigenically on the lymphocyte membrane. It may be secreted by the cells, but the reaction was not affected by sodium azide or cytochalasin B. No detectable factor B activity was found in the culture medium of cells grown in the absence of CVF.

Animals↗
PubMed1994

Long-term follow-up of patients with myocarditis and idiopathic dilated cardiomyopathy after immunomodulatory therapy.

The randomized clinical trial with interferon-alpha (IFN) or thymic hormones versus conventional therapy was conducted in patients with myocarditis and idiopathic dilated cardiomyopathy (IDC). We enrolled 180 patients to receive IFN (3-5 million units per day) for 3 months, thymomodulin (10 mg three times per week) for 2 months, or conventional therapy alone. Patients were followed-up for 7 years after the end of treatment. Left ventricular function, exercise tolerance and survival rate were significantly better at long-term follow-up in patients treated with IFN or thymomodulin, than in conventionally treated patients. These results implicate that immune modulating therapy might represent important contribution in the treatment of myocarditis and IDC.

Adolescent↗
PubMed1975

Regulation of theta-antigen expression by agents altering cyclic AMP level and by thymic factor.

Thymic factor, cyclic AMP, and products increasing its cellular level, such as Prostaglandin E1, induce the appearance of the theta-antigen on T-cell precursors whether assessed by a rossette-inhibition assay or a cytotoxic assay after cell fractionation on BSA discontinuous gradiet. Synergism has been demonstrated between cyclic AMPT and TF for that effect. Conversely, decrease of theta expression has been obtained by altering cyclic AMP level in theta-positive cells either increasing it by dibutyryl cAMP treatment or decreasing it by indomethacin treatment. Finally, these data suggest the involvement of cyclic AMP in the regulation of theta expression under thymic hormone control.

Acetylcholine↗
PubMed1995

Immunomodulatory effects of alpha interferon and thymostimulin in patients with neoplasias.

In this report, we have evaluated the immunological effects following administration of alpha interferon (IFN-alpha) in combination with thymostimulin (TP-1), as well as of IFN-alpha and TP-1 alone in patients with neoplasias who underwent surgery and were subsequently treated with conventional chemotherapy. Data suggest that the combination of IFN-alpha and TP-1 is the most effective in the up-regulation of some immune parameters such as the CD4(+)-CD8+ cell-dependent antibacterial activity. Since this immune function plays an important role in the host protection against different targets such as invading microorganisms and/or neoplastic cells, the administration of TP-1-IFN-alpha is advisable for patients with neoplasias under chemotherapy.

Adjuvants, Immunologic↗
PubMed1976

Restoration of T-cell responsiveness by thymosin: development of antituberculous resistance in BCG-infected animals.

T-cell-depleted (adult thymectomized, lethally irradiated, bone marrow-reconstituted [THXB]), sham-thymectomized (XB) and normal control mice were injected daily with 3 mg of calf thymosin for 16 days. On day 8 of the treatment, the mice, together with untreated controls, were infected intravenously with 4 X 10(6) viable Mycobacterium bovis (BCG Montreal). Growth of the BCG in the lungs and spleens was compared quantitatively for up to 100 days. Thymosin treatment reversed the progressive weight loss seen in BCG-infected THXB mice and prevented their death due to the ongoing mycobacteriosis that developed in the T-cell-depleted animal. There was a late-developing anti-mycobacterial response in the thymosin-treated THXB mice, which resulted in a progressive decline in viability for the lung and spleen populations over the 40- to 80-day period, when the corresponding counts for the untreated THXB mice remained relatively constant. The histopathology of the lung and the increased antibacterial activity seen in the thymosin-treated THXB mice correlated with decreased [3H]deoxyribonucleic acid levels seen in the lungs and spleen compared with that present in the T-cell-depleted controls.

Animals↗
PubMed1976

Restoration of delayed hypersensitivity to sheep erythrocytes by thymosin treatment of T-cell-depleted mice.

Calf thymosin was injected subcutaneously in daily doses of 0.1 to 3 mg for 12 to 15 days into adult thymectomized, irradiated, bone marrow-reconstituted (THXB) mice. Thymosin partially restored the ability of the T-cell-depleted host to develop delayed-type hypersensitivity to sheep erythrocytes. The degree of restoration varied from 50 to 75% of control values. Thymosin treatment of normal mice potentiated the footpad responsiveness to sheep erythrocytes by as much as 50% over that of untreated controls. The optimum dosage of thymosin seemed to be in the 200- to 500-mug range, and multiple injections were essential for a significant response. Tweleve daily injections of 100 to 500 mug of thymosin restored T-cell reactivity to the THXB mouse, but the responsiveness decayed relatively rapidly once the treatment was stopped. The restoration of immune responsiveness to sheep erythrocytes in T-cell-depleted mice provides a convenient means of demonstrating activity in thymosin preparations in vivo.

Animals↗
PubMed1992

Purification of core-binding factor, a protein that binds the conserved core site in murine leukemia virus enhancers.

The Moloney murine leukemia virus causes thymic leukemias when injected into newborn mice. A major genetic determinant of the thymic disease specificity of the Moloney virus genetically maps to two protein binding sites in the Moloney virus enhancer, the leukemia virus factor b site and the adjacent core site. Point mutations introduced into either of these sites significantly shifts the disease specificity of the Moloney virus from thymic leukemia to erythroleukemia (N. A. Speck, B. Renjifo, E. Golemis, T. Frederickson, J. Hartley, and N. Hopkins, Genes Dev. 4:233-242, 1990). We have purified several polypeptides that bind to the core site in the Moloney virus enhancer. These proteins were purified from calf thymus nuclear extracts by selective pH denaturation, followed by chromatography on heparin-Sepharose, nonspecific double-stranded DNA-cellulose, and core oligonucleotide-coupled affinity columns. We have achieved greater than 13,000-fold purification of the core-binding factors (CBFs), with an overall yield of approximately 19%. Analysis of purified protein fractions by sodium dodecyl sulfate (SDS)-polyacrylamide gel electrophoresis reveals more than 10 polypeptides. Each of the polypeptides was recovered from an SDS-polyacrylamide gel, and those in the molecular size range of 19 to 35 kDa were demonstrated to have core-binding activity. The purified CBFs were shown by DNase I footprint analyses to bind the core site in the Moloney virus enhancer specifically, and also to core motifs in the enhancers from a simian immunodeficiency virus, the immunoglobulin mu chain, and T-cell receptor gamma-chain genes.

Base Sequence↗