Rheumatoid arthritis is characterized by a chronic inflammatory synovitis, eventually leading to destruction of bone and cartilage. Significant hyperplasia and infiltration of activated inflammatory cells play a major role in the destruction of joint. The proliferation of synovial cells could be derived from imbalance between apoptotic cell death and excessive proliferation of synovial cells. However, many reports regarding on the apoptosis or proliferation of synovial cells showed a little bit contradictory up to date. Induction of synovial cell apoptosis could be an interesting and attractive way of treatment by way of many signal transduction pathway, such as NFkB, P53, sentrin, FADD, etc. We discussed on the apoptosis and proliferation of synovial cells, and focused on the proposed mechanisms of resistance for apoptosis. Here, we reviewed literatures on the apoptosis and abnormal proliferation of synovial cells, and focused on the proposed mechanisms of resistance against apoptosis. In addition, we mentioned about the possibility of apoptosis induction as a modality of treatment against rheumatoid arthritis in future.
Apoptosis* ; Arthritis, Rheumatoid* ; Cartilage ; Cell Death ; Hyperplasia ; Joints ; Signal Transduction ; SUMO-1 Protein ; Synovitis

No abstract available.
Arthritis, Rheumatoid* ; Blood Sedimentation* ; Humans

MicroRNAs (miRNAs) are small, single-stranded, non-coding RNA molecules of 20~22 nucleotides, which are involved in many biologic functions such as development, cell proliferation, differentiation, and apoptosis. In addition to these biologic functions, recent reports have demonstrated that miRNAs play important roles in the development of the immune system and the regulation of immune responses. Dysregulation of miRNAs might be involved in the pathogenesis of autoimmune diseases such as rheumatoid arthritis (RA). Recent studies have shown that miR-146a, miR-155, and miR-203 are overexpressed in RA and that miR-124a is under expressed in RA. miR-146 downregulates the expression of IL-1 receptor associated kinase 1 and TNF receptor-associated factor 6 involved in IL-1beta signaling, and miR-155 suppresses the expression of matrix metalloproteinases 1 and 3, suggesting that these miRNAs act as negative feedback regulators of inflammation and tissue damage in RA. In this report, we review the current knowledge about miRNAs and summarize the involvement of miRNAs in RA.
Apoptosis ; Arthritis, Rheumatoid ; Autoimmune Diseases ; Cell Proliferation ; Immune System ; Inflammation ; Interleukin-1 ; Matrix Metalloproteinases ; MicroRNAs ; Nucleotides ; Phosphotransferases ; RNA, Untranslated ; TNF Receptor-Associated Factor 6

MicroRNAs (miRNAs) are small, single-stranded, non-coding RNA molecules of 20~22 nucleotides, which are involved in many biologic functions such as development, cell proliferation, differentiation, and apoptosis. In addition to these biologic functions, recent reports have demonstrated that miRNAs play important roles in the development of the immune system and the regulation of immune responses. Dysregulation of miRNAs might be involved in the pathogenesis of autoimmune diseases such as rheumatoid arthritis (RA). Recent studies have shown that miR-146a, miR-155, and miR-203 are overexpressed in RA and that miR-124a is under expressed in RA. miR-146 downregulates the expression of IL-1 receptor associated kinase 1 and TNF receptor-associated factor 6 involved in IL-1beta signaling, and miR-155 suppresses the expression of matrix metalloproteinases 1 and 3, suggesting that these miRNAs act as negative feedback regulators of inflammation and tissue damage in RA. In this report, we review the current knowledge about miRNAs and summarize the involvement of miRNAs in RA.
Apoptosis ; Arthritis, Rheumatoid ; Autoimmune Diseases ; Cell Proliferation ; Immune System ; Inflammation ; Interleukin-1 ; Matrix Metalloproteinases ; MicroRNAs ; Nucleotides ; Phosphotransferases ; RNA, Untranslated ; TNF Receptor-Associated Factor 6

Rheumatoid arthritis is a common, chronic inflammatory arthritis that affects mainly the small diarthrodial joints of hands and feet. Although the cause of this disease remains unknown, the extensive researches to the pathophysiology of rheumatoid arthritis have resulted dramatic evolution in understanding its pathogenesis over the past a few years. Especially, the increasing knowledge about the role of cytokines in the pathogenesis of rheumatoid arthritis has led to a new strategy to treat this disease. In this review, we discuss the current knowledge about the expression of proand anti-inflammatory cytokines and their roles in rheumatoid arthritis.
Arthritis ; Arthritis, Rheumatoid* ; Cytokines* ; Foot ; Hand ; Joints

Alveolar soft-part sarcoma of the female genital tract are extremely rare. Fewer than 30 cases have been described in the literature. We experienced a case of alveolar soft-part sarcoma of the female genital tract which was diagnosed by routine light microscopic study using ultrastructural and immunohistochemical stain. We report this case with a brief review of the literature.
Female* ; Humans ; Sarcoma, Alveolar Soft Part*

Prostaglandins have numerous biologic effects on a variety of physiological and pathological activities such as inflammation, platelet aggregation, neurotransmitter release, smooth muscle contraction, and so forth. PGE2 is one of the well-studied inflammatory prostaglandins and causes vasodilatation, edema, fever and pain. Also PGE2 induces the production of matrix metalloproteinases (MMPs) which involve in destruction of tissue. In rheumatoid arthritis, macrophages isolated from patients secrete large amounts of PGE2 and PGE2 promote inflammation and participate in destructive mechanisms of the rheumatoid joint. In addition to its proinflammatory effects, PGE2 acts also as an immunomodulator, promote humoral and Th2-type immune responses and inhibit Th1-type immune responses. Also PGE2 inhibits the production of tumor necrosis factor (TNF-alpha), IL-1beta, IL-8 and IL-12 and stimulates the production of IL-10 by macrophages. Thus PGE2 should be regarded not as proinflammatory molecule but as modulator of immune responses. In this review, we will focus on the current knowledge about PGE2 as the modulator of immune responses and summarize the effects of PGE2 on the immune systems and inflammation.
Arthritis, Rheumatoid ; Dinoprostone* ; Edema ; Fever ; Humans ; Immune System ; Inflammation* ; Interleukin-10 ; Interleukin-12 ; Interleukin-8 ; Joints ; Macrophages ; Matrix Metalloproteinases ; Muscle, Smooth ; Neurotransmitter Agents ; Platelet Aggregation ; Prostaglandins ; Tumor Necrosis Factor-alpha ; Vasodilation

IgA nephropathy can occur rarely as a complication of D-penicillamine treatment, but it is exact pathogenesis remains unclear. If a patients has gross or microscopic hematuria during D-penicillamine treatment, D-penicillamine induced IgA nephropathy should be suspected as a cause of hematuria. In those cases, renal biopsy should be taken for diagnosis and proper management. We experienced a case of IgA nephropathy confirmed by renal biopsy in a 39-years-old female patient with scleroderma during D-penicillamine therapy and report this case with a review of literature.
Biopsy ; Diagnosis ; Female ; Glomerulonephritis, IGA* ; Hematuria ; Humans ; Immunoglobulin A* ; Penicillamine*

Cytokines are secreted proteins and interact with their specific cell surface receptors, triggering intracellular signal transduction pathways that activate a number of genes crucial for the biological functions of cytokines. These cytokine signal transduction pathways are tightly regulated processes. The negative regulations of cytokine signaling are achieved by receptor internalization and degradation, dephosphorylation of signaling intermediates, expression of protein inhibitors such as suppressor of cytokine signaling (SOCS) and protein inhibitors of activated STAT (PIAS). The observation that cytokines are central to the inflammatory and destructive process in several autoimmune diseases suggests that interventions targeting the cytokine intracellular signaling will be a new therapeutic strategy in autoimmune diseases. We review the current knowledge about negative regulation of cytokine signal transduction.
Autoimmune Diseases ; Cytokines ; Protein Inhibitors of Activated STAT ; Receptors, Cell Surface ; Signal Transduction* ; Social Control, Formal

No abstract available.
Candidiasis* ; Fluconazole*