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Query: UMLS:C0003864 (arthritis)
 69,039 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Lentiviruses are unique retroviruses which cause diseases with long incubation periods and prolonged clinical courses. The prototype lentiviruses, visna/maedi of sheep and arthritis-encephalitis virus of goats (CAEV), infect cells of the monocyte-macrophage system and replicate at a restricted level in these cells. The virus life cycle is closely associated with maturational factors in the cells; monocytes support the early stages of the replication cycle which goes to completion only when the cells mature to macrophages. Virus replication in the monocyte-macrophage results in lesions characterized by mononuclear cell infiltration of the central nervous system (CNS), lungs, synovium and mammary gland and their draining lymph nodes. Co-cultivation of sheep or goat lymphocytes with macrophages infected with visna or CAE viruses results in production of a unique interferon (LV-IFN). LV-IFN is a non-glycosylated protein of 54,000 to 64,000 daltons and has biological properties which have several implications for pathogenesis. Firstly, it retards the rate of maturation of monocytes and thus indirectly slows the rate of virus replication. Second, it restricts the rate of virus replication in mature macrophages by preventing virus maturation. Third, it induces expression of class II (Ia) antigens of the major histocompatibility complex on cells of macrophage lineage. Thus, by curtailing virus replication and enhancing expression of MHC class II antigens, LV-IFN may contribute to the induction and augmentation of the host's lymphoproliferative response to the virus.
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PMID:Pathogenesis of visna/maedi and caprine arthritis-encephalitis: new leads on the mechanism of restricted virus replication and persistent inflammation. 303 19

The effects of recombinant gamma-interferon (rec gamma-IFN) on collagen production by confluent monolayer cultures of progressive systemic sclerosis (PSS) dermal fibroblasts were studied. Five cell lines obtained from patients with rapidly progressive disease of recent onset were examined. All PSS fibroblast cell lines exhibited increased collagen production when compared with normal skin cell lines. It was found that rec gamma-IFN caused potent inhibition of PSS fibroblast collagen production in a concentration-dependent manner. Greater than 50% inhibition was observed with as little as 50 antiviral units/ml, and maximal effects were attained at a concentration of 500 units/ml. The rec gamma-IFN caused reproducible inhibition of collagen production by the 5 PSS fibroblast cell lines, ranging from 58.9% to 85.6% of control values. Measurement of type I and type III procollagen messenger RNA (mRNA) levels with specific complementary DNA probes demonstrated a coordinate reduction of greater than 60% in mRNA for both transcripts in rec gamma-IFN-treated cells, compared with control cells. These findings indicate that rec gamma-IFN can modulate the excessive collagen biosynthesis characteristic of PSS fibroblasts and that this effect can be explained largely by the gamma-IFN-mediated decrease in specific collagen mRNAs.
Arthritis Rheum 1986 Jul
PMID:Inhibition of excessive scleroderma fibroblast collagen production by recombinant gamma-interferon. Association with a coordinate decrease in types I and III procollagen messenger RNA levels. 309 Oct 39

Ia antigens (class II HLA molecules) have been detected on cells eluted from affected human cartilage in certain disease states, but not on normal cartilage cells. Because the presence of Ia antigens on chondrocytes may play an important role in rheumatic diseases, we investigated the induction of these molecules by gamma-interferon (gamma-IFN), a potent Ia-inducing lymphokine. Human articular chondrocytes were incubated with recombinant gamma-IFN, and the expression of Ia antigens was studied by cell sorter analysis, using a panel of reagents that detect monomorphic and polymorphic specificities of the DR and DQ Ia antigen families. While the induction of DR antigens, including polymorphic DR specificities, was readily obtained with gamma-IFN (50-95% positive cells), DQ antigens were negative or were displayed only on a lower percentage of chondrocytes (5-60%). In addition, incubation with gamma-IFN led to an increased expression of HLA class I antigens. The expression of various other surface markers either remained unchanged (as in 4F2 and BA-2) or showed tendencies toward decreased percentages (as in 83c2) or increased percentages (as in M phi R-17). No apparent change in cell morphology or growth pattern was observed.
Arthritis Rheum 1987 Jan
PMID:Changes in cell surface antigen expression on human articular chondrocytes induced by gamma-interferon. Induction of Ia antigens. 310 6

Recent study of the expression of monocyte differentiation antigens (MAg) and HLA-DR on peripheral blood monocytes (PBM) has led to the recognition of resting and activated monocyte phenotypes. The former is identified by the expression of large amounts of MAg (i.e., Mo2 and 63D3) and small amounts of HLA-DR, while the latter is identified by the reverse. We studied the phenotypes of PBM and synovial fluid monocytes (SFM) of patients with chronic inflammatory arthritis and found that PBM were primarily resting and SFM were usually activated. In addition, we measured the degree of modulation of MAg and HLA-DR by gamma-interferon (gamma-IFN). Patient PBM reacted the same as PBM from normal individuals (i.e., MAg decreased and HLA-DR increased after exposure to gamma-IFN). However, in patient SFM, HLA-DR did not increase with exposure to gamma-IFN because expression was already maximal. Interestingly, MAg could still be down-regulated on gamma-IFN-treated SFM, even when expression began at a very low level (i.e., activated phenotype). This independent regulation of MAg and HLA-DR suggests that macrophage activating factors other than gamma-IFN may be responsible, in part, for the activated phenotypes observed.
Arthritis Rheum 1987 Aug
PMID:Peripheral blood and synovial fluid monocyte activation in inflammatory arthritis. I. A cytofluorographic study of monocyte differentiation antigens and class II antigens and their regulation by gamma-interferon. 311 73

Because synovial fluid monocytes (SFM) in patients with inflammatory arthritis bear an activated phenotype (i.e., high expression of HLA-DR and low expression of the monocyte differentiation antigen Mo2), we assessed the role of gamma-interferon (gamma-IFN) in the activation of these cells. Sensitive and specific radioimmunoassays detected only 0.40 +/- 0.20 units/ml of gamma-IFN in the SF of patients with rheumatoid arthritis (RA) and 0.61 +/- 0.67 units/ml of gamma-IFN in the SF of patients with other forms of chronic inflammatory arthritis. There was no detectable alpha-IFN in any SF studied by radioimmunoassay. Bioassays failed to detect nonimmunoreactive IFN. Synovial tissue (ST) explants produced very little gamma-IFN (0.14 +/- 0.091 units/ml), and production was not increased by the presence of indomethacin in the cultures or by removal of adherent cells. However, gamma-IFN was produced if ST was cultivated in the presence of phytohemagglutinin. In SF and ST supernatants, gamma-IFN-mediated induction of HLA-DR on monocytes was inhibited, even though the amount of immunoreactive IFN was not affected. Prostaglandin E2 was shown to be one possible inhibitor. We demonstrated that a factor that induces HLA-DR on some individuals' peripheral blood monocytes, and cannot be neutralized by monoclonal anti-gamma-IFN antibody, is present in SF and ST supernatants. These data suggest that activation of SFM may occur by mechanisms other than gamma-IFN.
Arthritis Rheum 1987 Aug
PMID:Peripheral blood and synovial fluid monocyte activation in inflammatory arthritis. II. Low levels of synovial fluid and synovial tissue interferon suggest that gamma-interferon is not the primary macrophage activating factor. 311 74

Gamma-interferon (gamma-IFN) is a T cell-derived lymphokine that has potent macrophage-activating properties. It increases Fc receptor density, increases the formation and release of reactive oxygen intermediates, increases the synthesis and release of complement cascade proteins, especially C2 and factor B, and increases class II (HLA-DR) antigen expression. These effects may play a role in the potentiation of inflammation in rheumatoid arthritis. We examined the possibility that gold sodium thiomalate (GST), an effective treatment for rheumatoid arthritis, would inhibit gamma-IFN-mediated stimulation of monocyte/macrophages. GST in concentrations attainable in vivo was shown to inhibit both spontaneous and gamma-IFN-stimulated C2 production up to 50%. GST inhibition could be only partially overcome with increasing concentrations of gamma-IFN. In addition, GST inhibited gamma-IFN-stimulated HLA-DR expression at the highest concentrations tested (20-50 micrograms/ml). GST alone in low concentrations (0.1-5 micrograms/ml) was found to increase HLA-DR antigen expression as quantitated by several methods, including flow cytometry, cell surface enzyme-linked immunosorbent assay, and Western blotting. This GST-stimulated increase in HLA-DR antigen expression paralleled an increased ability of monocytes to present antigen. The mechanism by which low concentrations of GST stimulate HLA-DR antigen expression is unclear, but was shown by 35S-methionine cell labeling not to involve increased HLA-DR protein synthesis.
Arthritis Rheum 1987 Sep
PMID:Effects of gold sodium thiomalate on interferon stimulation of C2 synthesis and HLA-DR expression by human monocytes. 311 66

We investigated the effect of gamma-interferon (gamma-IFN) on the development of type II collagen (CII)-induced arthritis. DBA/1 mice were immunized with rat CII and 16 days later, were treated with subcutaneous injections of recombinant rat gamma-IFN into the right paws twice a week. Compared with controls, the gamma-IFN-treated mice developed arthritis with a higher frequency and severity. Immunohistochemical analysis of gamma-IFN-treated paws from CII-immunized mice revealed an increase in the numbers of class II antigen-expressing cells and an infiltration of CD4+ lymphocyte-like cells. The auto-antibody response toward CII was suppressed by gamma-IFN treatment. The findings implicate gamma-IFN in a role that triggers arthritis by enhancing local inflammatory processes in the joints, or possibly, by permitting homing of T cells to the joints.
Arthritis Rheum 1988 Oct
PMID:Treatment with gamma-interferon triggers the onset of collagen arthritis in mice. 314 Aug 21

Using cultured human osteoblast-like cells, we studied the effects of tumor necrosis factor (TNF) and recombinant human gamma-interferon (gamma-IFN) on osteoblast growth and function, and demonstrated that TNF stimulated bone cell proliferation and prostaglandin production while inhibiting 1,25-(OH)2D3-stimulated alkaline phosphatase activity and osteocalcin release. In contrast, gamma-IFN inhibited proliferation and stimulated alkaline phosphatase activity of the cells, while inhibiting 1,25-(OH)2D3-stimulated osteocalcin production and having variable effects on the release of prostaglandins, depending on the presence of other factors. Our results suggest that TNF and gamma-IFN can act directly on bone-forming cells to affect both their proliferation and their differentiated function, and that changes in the ability of cells to produce these factors in disease states may contribute to alterations in the integrity of connective tissue matrices.
Arthritis Rheum 1988 Dec
PMID:Actions of recombinant human gamma-interferon and tumor necrosis factor alpha on the proliferation and osteoblastic characteristics of human trabecular bone cells in vitro. 314 69

From these data it appears that IFN is capable of stimulating prostaglandin E and hyaluronic acid production by human synovial fibroblasts in vitro and of initiating an inflammatory reaction in animal joints. In chronic arthritis its production may result from persisting viral or other antigenic stimulation. IFN may enhance the immune response and mediate the inflammatory process in the joint. Its role in the pathogenesis of rheumatic and various other autoimmune diseases is undergoing further study.
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PMID:Interferon triggers experimental synovitis and may potentiate auto-immune disease in humans. 620 74

Alpha-interferon (alpha-IFN) was added to pokeweed mitogen (PWM) or Epstein-Barr virus stimulated human peripheral blood mononuclear cell cultures from normal subjects or patients with rheumatoid arthritis (RA). Alpha-IFN enhanced in vitro production of PWM induced IgG and IgM, and significantly enhanced PWM induced IgM rheumatoid factor (IgM-RF) production by lymphocytes both from normal subjects and RA patients. Enhancement was recorded whether cells were preincubated with alpha-IFN for 16 hours or with alpha-IFN present throughout the culture period. Alpha-IFN did not enhance IgM-RF production in the absence of PWM or T cells. Enhancement of IgM-RF production was not seen in Epstein-Barr virus stimulated cultures.
Arthritis Rheum 1983 Sep
PMID:Human alpha-interferon enhances in vitro IgM rheumatoid factor synthesis by lymphocytes from normal subjects and rheumatoid arthritis patients. 631 Dec 24


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