Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004364 (autoimmune disease)
 24,845 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The initiation and progression of autoimmune diseases are complex processes that depend on a selective breakdown of tolerance and additional factors like genetic susceptibility and environmental factors, e.g. drugs, infections, toxins and UV light. The causative failure of the immune system to tolerate self can be initiated by molecular mimicry or polyclonal activation with the consequence of a breakdown of anergy or a failure of activation induced cell death. It presents itself in multiple forms including a disturbed balance between TH1 and TH2, alterations in the cytokine milieu and undue modulation of the expression of costimulatory molecules. Although all these features may vary between patients and within the individual patient depending on the state of disease, recent years have provided convincing evidence that, in particular, disease progression is markedly influenced by the expression profile of costimulatory molecules. Since in many forms of autoimmune diseases the causative self-antigen(s) are unknown, therapy largely depends on anti-inflammatory agents or in severe cases on a general immunosuppression. Increasing knowledge of the functional activities of costimulatory molecules in autoimmune disease now provides a new and promising therapeutic modality, which in a more selective way interferes with the pathological activities of immune cells. Here I discuss evidence for the involvement of costimulatory molecules, particularly of CD44 variant isoforms, in autoimmune diseases and their possible use as a therapeutic target. Due to the regulated and restricted expression of these molecules, treatment should not be burdened by severe side effects.
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PMID:Costimulatory molecules and their ligands as therapeutic targets in autoimmune disease. 1139 41

Immune thrombocytopenia (ITP) is an autoimmune disorder characterized by low platelet counts due to enhanced platelet clearance and compromised production. Traditionally, ITP was regarded a B cell mediated disorder as anti-platelet antibodies are detected in most patients. The very nature of self-antigens, evident processes of isotype switching and the affinity maturation of anti-platelet antibodies indicate that B cells in order to mount anti-platelet immune response require assistance of auto-reactive CD4+ T cells. For a long time, ITP pathogenesis has been exclusively reviewed through the prism of the disturbed balance between Th1 and Th2 subsets of CD4+ T cells, however, more recently new subsets of these cells have been described including Th17, Th9, Th22, T follicular helper and regulatory T cells. In this paper, we review the current understanding of the role and immunological mechanisms by which CD4+ T cells contribute to the pathogenesis of ITP.
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PMID:CD4+ T cell phenotypes in the pathogenesis of immune thrombocytopenia. 3219 87