140,144 research outputs found
Smell and autoimmunity: a comprehensive review
No full textThe sense of smell is an ancient sensory modality vital for sampling and perceiving the chemical composition of surrounding environments. Olfaction involves a pathway of biochemical and electrophysiological processes, which allows the conversion of molecular information into sensations. Disturbances in the olfactory function have been investigated mainly in neurological/neurodegenerative disorders such as Alzheimer's and Parkinson's diseases; impaired sense of smell has been associated with depressed mood. Only recently, smell capability was tested in other diseases, particularly autoimmune diseases. Shoenfeld and colleagues opened this chapter showing that patients affected with systemic lupus erythematosus (SLE) have disturbances in their olfactory functions and revealed its association with neuropsychiatric manifestations of the disease. This evidence was confirmed in experimental models and replicated in other SLE populations. The connection between autoimmunity and the sense of smell was lately emphasized by studies on patients with Sjögren's syndrome and in patients with other autoimmune/immune-mediated diseases, such as polydermatomyositis, recurrent spontaneous abortion, and hereditary angioedema. Genetic susceptibility and hormonal and environmental factors may play a role in these conditions. Olfactory receptor gene clusters are located in proximity to key locus of susceptibility for autoimmune diseases such as the major histocompatibility complex, suggesting not only a physic linkage, but a functional association. Nonetheless, gender- and hormone-mediated effects are fundamental in the development of autoimmune diseases. The different connections between smell and autoimmunity, genes and hormones may suggest that this is another tessera of a mosaic which is waiting the answer of Oedipus
Autoimmunity and the endocrine system: Adrenal, Graves' disease, immune checkpoint
No full textNo abstract availabl
Predictive, protective, orphan autoantibodies : the example of anti-phospholipid antibodies
No full textAnti-phospholipid antibodies (aPL) are one of the most recent examples of autoantibodies that can appear even long time before any clinical manifestation can be associated with them. There is a general agreement that they may represent a strong risk factor for recurrent thrombosis and/or fetal losses. Anti-phospholipid antibodies represent a necessary but not sufficient factor (first hit) for thrombosis, and require additional triggering factors (second hit) to disclose the thrombogenic activity. Several factors may affect the predictive value of aPL, including titre, immunoglobulin isotype, fine antigenic specificity and affinity binding activity. Their careful evaluation is suggested in order to characterize the true predictive value of aPL
A new player in the antiphospholipid syndrome: the beta 2 glycoprotein I cofactor.
No full textThe study of antiphospholipid (aPL) antibodies has been greatly developed in recent years and conclusive evidence now exists concerning the correlation between aPL and clinical signs such as thrombosis, thrombocytopenia, abortion, and fetal loss. Several hypotheses have been put forward concerning the pathogenic mechanism of aPL, but none has received final confirmation from experimental data. Many studies have been devoted to characterizing the antigens recognized by the different aPL autoantibodies and to a cofactor involved in the binding of autoantibodies and phospholipids; this cofactor has been identified as an apolipoprotein, the beta 2 glycoprotein I (beta 2GPI) or APO-H. Direct evidence now exists which suggests that both the beta 2GPI and the phospholipid comprise the epitope to which aPL are directed. On the other hand anti-beta 2GPI antibodies have been identified in sera of patients suffering from SLE and primary Antiphospholipid Syndrome. beta 2GPI is normally present in human plasma/serum and possesses numerous inhibitory functions in multiple coagulation pathways. The amino acid sequence of beta 2GPI has been identified and found to consist of five repeating units that belong to the complement control protein (CCP) superfamily. This development of knowledge related to aPL has followed three steps respectively: 1. the standardization of the techniques of detection: 2. identification of the clinical signs related to the autoantibodies: and finally 3. the discovery of a new player, the beta 2GPI cofactor
Hepatitis B Vaccination and Undifferentiated Connective Tissue Disease Another Brick in the Wall of the Autoimmune/Inflammatory Syndrome Induced by Adjuvants(ASIA)
No full text- …
