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At least 397 records · Page 22Linked to original sources
PubMed1986

Regulation of complement gene expression.

The availability of molecular probes for approximately half of the 20 known complement genes now permits a detailed examination of the regulation of complement expression in liver and at extrahepatic sites in tissue macrophages. Primary cell culture, cell lines and cells transfected with DNA bearing complement genes have been used in this analysis. Pretranslational regulation of complement production has been induced by well defined cytokines such as interleukin-1 and gamma-interferon, as well as directly by endotoxin. The effect of those agents on complement genes is tissue and species specific and is developmentally regulated. These data form the basis for the elucidation of the genomic structural requirements for regulation of inflammation and, by extension, specific immune responsiveness.

Animals↗
PubMed1987

Effects of interferon-gamma on proto-oncogene expression during induction of human monocytic differentiation.

Activation of the proto-oncogenes c-fos, c-fms, and c-sis has been associated with monocytic differentiation. In the present study, we monitored the relationship of c-myc, c-fos, c-fms, and c-sis expression to interferon-gamma (IFN-gamma)-induced monocytic differentiation of human HL-60 promyelocytic leukemia cells. Treatment of HL-60 cells with 500 U/ml IFN-gamma arrested cell proliferation after 3 days. Appearance of the monocytic phenotype was manifested within 24 hr of IFN-gamma exposure by: increased nitroblue tetrazolium reduction; increased cell surface expression of the HLA-DR, Mo1, and MY4 antigens; and induction of transcripts for the second component of complement (C2) and tumor necrosis factor. In contrast, c-myc expression decreased as a later event after 72 hr of IFN-gamma exposure, and c-fos transcripts remained undetectable until 5 days of treatment. Furthermore, c-fms RNA and transcripts for the macrophage marker apolipoprotein E were induced only after 7 days. Finally, expression of the c-sis proto-oncogene at the RNA and protein levels remained undetectable after induction with IFN-gamma. These findings would thus suggest that declines in c-myc RNA, as well as induction of c-fos, c-fms, and c-sis expression, are not requisite events in the commitment of HL-60 cells to IFN-gamma-induced monocytic differentiation. Expression of c-fos and c-fms, however, is associated with acquisition of markers associated with maturation to macrophages.

Antigens, Surface↗
PubMedDate not supplied

[Complement system].

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Age Factors↗
PubMed1986

[Investigation of HLA in patients with glioma].

HLA was studied in 35 patients with gliomas (20 anaplastic gliomas, 11 astrocytomas, 2 ependymomas, 2 oligodendrogliomas) and 38 volunteers who served as controls, by using the microdroplet lymphocyte cytotoxicity test. Phenotype frequency (PF), gene frequency (GF) and relative risk (RR) of each HLA antigen were studied statistically with the chi 2-test, where corrected P (CP) less than 0.05 was considered significant. Concerning HLA-B antigens, either Bw 61 or Bw 62 was found in 45.7% of the patients and the both in 14.3%. HLA-Bw 61 had a tendency to increase in the patients (PF = 0.46, GF = 0.27, RR = 7.16, chi 2 = 9.64, P less than 0.002, CP less than 0.064). Contrary to HLA-B antigens, HLA-DRw 6 was absent in the patient (chi 2 = 8.3379, P less than 0.004, CP less than 0.04). No relation between HLA and histological types was found. HLA has its genetic locus on the short brachium of the 6th chromosome and complement C2, C4, properdin, etc are considered to link HLA. Immunoregulatory genes (Ir genes), immunosuppressive genes (Is genes), disease susceptibility genes and disease resistant genes are also considered to link HLA, especially HLA-B, D loci. Although diseases are multifactorial, according to our report, the incidence of HLA-Bw 61 is higher, while that of HLA-DRw 6 is lower in patients with glioma. These phenomena seem very interesting considering the previous evidence that HLA has a close relation between disease susceptibility and immunological competence.(ABSTRACT TRUNCATED AT 250 WORDS)

Brain Neoplasms↗
PubMed1987

Anticardiolipin and complement activation: relation to clinical symptoms.

Anticardiolipin antibodies which seldom occur in healthy persons are frequently found in systemic lupus erythematosus (SLE). Their presence, especially at high levels (greater than 10 units) are often accompanied by thromboembolic manifestations as well as thrombocytopenia and recurrent abortions. The incidence of cardiolipin antibodies was as great in SLE as in women with clinically unexplained recurrent abortions. The anticardiolipin levels remained unchanged in most patients for long periods and were remarkably unaffected by disease activity and therapy. On the other hand, in several cases the activated partial thromboplastin time which was prolonged in most patients with persistently high cardiolipin antibody levels, approached normal during treatment with prednisolone and salicylic acid. This seemed to facilitate a successful outcome of pregnancy. Absorption of sera with cardiolipin and other negatively charged phospholipids but not with uncharged phospholipids abolished the anticardiolipin activity in enzyme linked immunosorbent assay. In most sera with cardiolipin antibody levels greater than 10 units complement activation by the classical pathway could be demonstrated. Whether the anticardiolipin antibodies contributed to complement activation could not be determined.

Abortion, Habitual↗
PubMed1979

Immunofluorescence studies of dense deposit disease. The presence of railroad tracks and mesangial rings.

Immunopathologic analysis was carried out on renal tissue from patients with membranoproliferative glomerulonephritis, nine with type I and nine with type II (dense deposit disease). A specific finding in all patients with type II, but not type I, was the presence of C3 along the margin but not within the central portion of dense deposit material in the glomerular basement membrane giving a double linear appearance (railroad tracks); C3 was also present within the mesangium, outlining numerous circular structures (mesangial rings). By phase contrast, electron microscopy, and dual label fluorescence studies, the railroad tracks and mesangial rings were shown to outline dense deposit material. Mesangial rings contained properdin (four of nine patients); railroad tracks contained properdin (five of nine patients) and C4 (four of nine patients); no other complement components or immunoglobulins were present. Studies using rhodamine-conjugated rabbit antibody to human glomerular basement membrane demonstrated no reactivity with the dense deposit material itself. In type I and to a lesser extent in type II, granular deposits of C3, C4, properdin, IgM, and IgG were present along the glomerular basement membrane, suggesting that immune complexes play a role in both diseases. Dense deposit transformation of the glomerular basement membrane may be a consequence of a highly specific injury.

Autoantibodies↗