1,720,979 research outputs found
Infliximab. Role in the treatment of psoriasis
No full textPsoriasis is one of the immune-mediated inflammatory diseases (IMIDs), in whose pathogenesis Th1-mediated immune responses are considered crucial. Infliximab is a chimeric monoclonal antibody directed against the Th1-cytokine TNF-alpha that has already been approved for the therapy of psoriatic arthritis (in combination with methotrexate). In clinical studies, infliximab has proved safe and effective in treating plaque-type psoriasis. In 80% of treated patients, the Psoriasis Area and Severity Index (PASI) decreased after 10 weeks by >= 75%. Infliximab is expected to be approved as second-line therapy in Germany this year for the treatment of psoriasis vulgaris
Evidence for a PPARgamma agonist-induced proteasomal degradation of cyclin D1 in melanoma cell lines
No full textGranulocyte colony-stimulating-factor-induced psoriasiform dermatitis resembles psoriasis with regard to abnormal cytokine expression and epidermal activation
No full textPsoriasis is a chronic inflammatory skin disorder characterized by accumulation of Th1-type T cells and neutrophils, regenerative keratinocyte proliferation and differentiation, and enhanced epidermal production of antimicrobial peptides. The underlying cause is unknown, but there are some similarities with the immunologic defense program against bacteria. Development of psoriasiform skin lesions has been reported after administration of granulocyte colony-stimulating factor (G-CSF), a cytokine induced in monocytes by bacterial antigens. To further investigate the relation between this type of cytokine-induced dermatitis and psoriasis, we analyzed the cutaneous cytokine profile [tumor necrosis factor-alpha (TNF-alpha), interferon-gamma, transforming growth factor-beta1 (TGF-beta1), interleukin-10 (IL-10), IL-12p35 and p40, and IL-8] and expression of markers of epidermal activation [Ki-67, cytokeratin-16, major histocompatibility complex (MHC) class II, intercellular adhesion molecule-1 (ICAM-1)] in a patient who developed G-CSF-induced psoriasiform dermatitis by using quantitative real-time reverse transcriptase-polymerase chain reaction and immunohistology. The histologic picture resembled psoriasis with regard to epidermal hyperparakeratosis and the accumulation of lymphocytes in the upper corium. CD8(+) T cells were found to infiltrate the epidermis which was associated with an aberrant expression of Ki-67, cytokeratin-16, MHC class II, and ICAM-1 on adjacent keratinocytes. As compared to normal skin (n = 7), there was an increased expression of TNF-alpha, IL-12p40, and IL-8, a decreased expression of TGF-beta1, and a lack of IL-10, similar to the findings in active psoriasis (n = 8). Therefore, G-CSF may cause a lymphocytic dermatitis that, similar to psoriasis, is characterized by a pro-inflammatory Th1-type cytokine milieu and an epidermal phenotype indicative of aberrant maturation and acquisition of non-professional immune functions
Evidence for a PPARgamma agonist-induced proteasomal degradation of cyclin D1 in melanoma cell lines
No full textThe expression of leukocyte-chemoattractive factors suggest a pathophysiological link between psoriatic skin and bone disease
No full textA close look at autoimmune muscle disorders: association of Lambert-Eaton myasthenic syndrome with dermatomyositis
No full textDermatomyositis/ polymyositis (DM/PM) and Lambert- Eaton myasthenic syndrome (LEMS) are two autoimmune disorders that have very rarely been reported to occur together in the same patient. We report on two patients with DM who were later diagnosed with concomitant LEMS, and point out diagnostic challenges in identifying LEMS in patients with DM/PM. As specific treatment for LEMS is available, it is important to identify those DM/PM patients who suffer from concomitant LEMS
Association analysis of IL19, IL20 and IL24 genes in palmoplantar pustulosis
No full textBackground Interleukin (IL) 19, IL-20 and IL-24 belong to the IL-10 cytokine family and have been identified to play a role in the regulation of epidermal functions and in inflammation. The genes encoding IL-19, IL-20 and IL-24 are located within a gene cluster on chromosome 1q31-32 and carry frequent genetic variations. Objectives This study investigated whether variations in the IL19, IL20 and IL24 genes that have previously been associated with plaque-type psoriasis may also play a role in palmoplantar pustulosis (PPP). Patients Fifteen polymorphisms were analysed in 43 patients with PPP and in 149 healthy control subjects. Results The rare allele of IL20 1380 A -> G (rs2981573) was less frequent in patients with PPP compared with healthy controls (OR 1.95, 95% CI 1.00-3.79). Haplotype analyses of IL19 and IL20 suggested an increased risk for PPP associated with IL20 haplotype GAA (OR 2.39, 95% CI 1.17-4.86) and a reduced risk for PPP associated both with IL19 haplotype GATGATA (OR 0.41, 95% CI 0.16-1.05) and IL20 haplotype GGG (OR 0.48, 95% CI 0.23-0.98). Extended haplotype analysis revealed an association of IL19/IL20 haplotype GACACCGGAA with a higher risk for PPP (OR 2.31, 95% CI 1.05-5.10) and of IL20/IL24 haplotype CAAAC with a reduced risk for PPP (OR 0.12, 95% CI 0.02-0.82). Conclusion This exploratory study supports the hypothesis that variations of genes of the IL-19 subfamily of cytokines influence susceptibility to PPP. However, due to the limited size of the study samples, this current concept should be considered as preliminary and the results need to be confirmed in future independent studies
Absence of reuptake of serotonin influences susceptibility to clinical autoimmune disease and neuroantigen-specific interferon-gamma production in mouse EAE
No full textSerotonin (5-hydroxytryptamine, 5-HT) is one of the most extensively studied neurotransmitters of the central nervous system. It also has been identified in constituents of the immune system. Therefore serotonin has been suggested to serve as a mediator of bidirectional interactions between the nervous system and the immune system. We investigated this interaction in experimental autoimmune encephalomyelitis (EAE), a well-defined animal model of autoimmune disease of the central nervous system (CNS) mimicking features of the human disease multiple sclerosis. EAE was induced by immunization with the autoantigens myelin basic protein (MBP) or the immunodominant peptide of myelin oligodendrocyte glycoprotein (MOG) spanning amino acids 35-55 (MOGp 35-55). We studied EAE in knockout (KO) mice lacking the 5-HT transporter (5-HTT) on a C57.BL/6 background, in comparison with wild-type C57.BL/6 animals. After immunization with MOGp 35-55, or with rat MBP, the disease courses of the 5-HTT knockout mice were attenuated as compared to wildtype control mice. This difference was more pronounced in female animals. To dissect potential immune mechanisms underlying this phenomenon, histological studies of the CNS and cytokine measurements in mononuclear cells from the spleens of 5-HTT KO mice and wild-type controls were performed. We found a reduction of the inflammatory infiltrate in the CNS and of the neuroantigen-specific production of IFN-gamma in splenocytes, again accompanied by a gender difference. These findings suggest a potential role of extracellular 5-HT homeostasis in the fine-tuning of neuroantigen-specific immune responses
Agonists of peroxisome proliferator-activated receptor (PPAR) g inhibit cell growth in malignant melanoma
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