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Immunopathogenic Mechanisms (immunopathogenic + mechanism)

Distribution by Scientific Domains

Medical Sciences	100%

Selected Abstracts

Immunopathogenic mechanisms in tourette syndrome: A critical review,,

MOVEMENT DISORDERS, Issue 9 2009
Davide Martino MD
Abstract Tourette syndrome (TS) has a multifactorial etiology, in which genetic, environmental, immunological and hormonal factors interact to establish vulnerability. This review: (i) summarizes research exploring the exposure of TS patients to immune-activating environmental factors, and (ii) focuses on recent findings supporting a role of the innate and adaptive immune systems in the pathogenesis of TS and related disorders. A higher exposure prior to disease onset to group A ,-haemolytic streptococcal (GABHS) infections in children with tics and obsessive-compulsive (OC) symptoms has been documented, although their influence upon the course of disease remains uncertain. Increased activation of immune responses in TS is suggested by changes in gene expression profiles of peripheral immune cells, relative frequency of lymphocyte subpopulations, and synthesis of immune effector molecules. Increased activity of cell-mediated mechanisms is suggested by the increased expression of genes controlling natural killer and cytotoxic T cells, increased plasma levels of some pro-inflammatory cytokines which correlate with disease severity, and increased synthesis of antineuronal antibodies. Important methodological differences might account for some inconsistency among results of studies addressing autoantibodies in TS. Finally, a general predisposition to autoimmune responses in TS patients is indicated by the reduced frequency of regulatory T cells, which induce tolerance towards self-antigens. Although the pathogenic role of immune activation in TS has not been definitively proven, a pathophysiological model is proposed to explain the possible effect of immunity upon dopamine transmission regulation and the generation of tics. © 2009 Movement Disorder Society [source]

Lymphocytapheresis in the treatment of psoriasis vulgaris ,,

JOURNAL OF CLINICAL APHERESIS, Issue 3 2006
Giancarlo Maria Liumbruno
Abstract Psoriasis is a common autoimmune chronic inflammatory skin disease that affects approximately 2% of the world's population; fundamental for its immunopathogenic mechanism is secretion of type 1 (Th1) cytokines by T cells and their activation. Since cytapheresis has been widely applied to autoimmune disorders, emphasizing the recently reported results of granulocyte and monocyte adsorption apheresis in psoriasis, a small series of psoriasis vulgaris (PV) patients underwent lymphocytapheresis (LCA) with the aim to remove lymphocytes. Five patients were submitted to weekly LCA. The severity of the disease had been evaluated through psoriasis area and severity index (PASI) score before LCA and one week after the last apheresis. PASI score before: patient A: 66; patient B: 33; patient C: 50; patient D: 56; patient E: 29. All the patients showed improvement of skin lesions. PASI score after LCA: patient A: 24; patient B: 8; patient C: 5; patient D: 36; patient E: 2.1. No side effects linked to apheresis were reported. LCA seems to produce interesting results in PV, and PASI improvement related to apheresis is clinically significant. Further studies to address its mechanism of action and potential long-term side effects are needed. It could become a valuable therapeutic alternative or a complementary tool, which might even be used to reduce the dosages of conventional pharmacological therapies adopted for this chronic disease. J. Clin. Apheresis 2006. © 2006 Wiley-Liss, Inc. [source]

Immunopathogenesis of cholestatic autoimmune liver diseases

EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 1 2001
J. Medina
Primary biliary cirrhosis and primary sclerosing cholangitis are well recognized chronic cholestatic liver diseases that are considered to have an autoimmune basis. Recent progress in the study of autoimmune liver diseases has improved the recognition and characterization of these conditions. An important component of this progress has been the identification of liver disease-associated autoantibodies and their respective target antigens, and the development of specific assays for these autoantibodies. In addition, some nonhumoral immunological findings imply an involvement of specific immunopathogenic mechanisms in the development of these conditions. Furthermore, immunogenetic factors associated with increased susceptibility to some of these diseases have been identified. This article reviews the most relevant information relating to the postulated autoimmune pathogenesis of these diseases, with special emphasis on their associated humoral and cellular immunological abnormalities and immunopathogenetic factors. Some of the remaining important unresolved issues relating to the pathogenesis of these diseases, that need to be addressed in further research, are highlighted. [source]

Management of systemic lupus erythematosus in the coming decade: potentials and challenges

INTERNATIONAL JOURNAL OF RHEUMATIC DISEASES, Issue 4 2006
Hiok Hee CHNG
Abstract The management of systemic lupus erythematosus (SLE) has improved in the past 50 years, but there is still a 3,5-fold increased mortality compared to the general population, with major organ failure due to active disease, infection and cardiovascular disease as the major challenges for the coming decade. Research advances at cellular, molecular and genetic levels enhance our understanding of the immunopathogenic mechanisms of SLE, leading to the development of drugs targeting specific sites of immune dysregulation , with therapies directed at cytokines, B- and T-cells, and their interactions showing promise. Advances are expected in the field of haematopoietic stem cell transplant (HSCT) as a therapeutic option for a subset of patients. Furthermore, some non-traditional immunomodulating therapies like statins, leflunomide and tacrolimus may prove useful as alternative or adjunct treatment in some patients. A better understanding of how current immunosuppressants act at the cellular and molecular level should guide the re-evaluation of the indications, doses and duration of therapy in clinical trials using these agents, many of which have not been subjected to proper double-blinded placebo-controlled studies. Research on triggers of SLE onset and flare of activity continues to yield information helpful in prevention. The evidence on the impact of psychosocial and economic factors on the outcome of SLE is overwhelming and the rheumatology community should enlist the assistance of other healthcare professionals, patient advocates and local health authorities to address these issues pertinent to good patient care and outcome. [source]

Regional Immunity of the Eye

ACTA OPHTHALMOLOGICA, Issue 3 2010
Manabu Mochizuki
Abstract. This article reviews molecular mechanism of intraocular inflammation in animal models and in humans, and the immunological defence system of the eye with particular attention to ocular pigment epithelium. In experimental autoimmune uveitis (EAU), T lymphocytes, particularly CD4+ T lymphocytes, play a central role in its immunopathogenic mechanisms. In humans, activated CD4+ T cells also play a central role in the immunopathogenic mechanisms. This notion is demonstrated in two human diseases: one is Vogt,Koyanagi,Harada disease, and the other is human T-cell leukemia virus type 1 (HTLV-1) uveitis. Activated CD4+ T cells infiltrating the eye are harmful to vision-related cells and tissues in the eye and cause sight-threatening conditions. However, the eye has regional defence systems to protect itself from these harmful activated T cells. We focus on ocular pigment epithelium (PE) and demonstrate immunoregulatory activity of iris PE and retinal PE. Iris PE suppresses activated CD4+ T cells by cell-to-cell contact with a crucial role played by B7-2 molecule on iris PE and CTLA4 on T cells. The actual immunosuppressive factor being membrane bound TGF-,. In contrast, retinal PE suppresses activated CD4+ T cells by soluble factors, such as soluble TGF-, and thrombospondin 1. In addition to the direct T-cell suppression by ocular PE, ocular PE has the capacity to promote activated T cells to regulatory T cells and use them as a tool to amplify the immune down regulation in the eye. The molecular mechanisms of generation of T regulatory cells by iris PE and retinal PE is also discussed. [source]