Primary Sjögren's syndrome (pSS) is a prototype of chronic autoimmune disease, the pathogenesis of which remains unclear and for which treatment does not exist.
Rheumatoid arthritis (RA) not only has a high prevalence but also represents the prototype of an autoimmune inflammatory joint disease that leads to progressive destruction of articular structures, particularly cartilage and bone [ 1].
Systemic lupus erythematosus (SLE) is the prototype of systemic autoimmune disease characterized by widespread immunologic abnormalities and multiorgan involvement including the skin, joints, lungs, heart, central and peripheral nervous system, and kidney [ 1].
Systemic lupus erythematosus (SLE), a prototype of human systemic autoimmune disease, is characterized by a wide variety of multi-organ damage (among which one of the hallmarks is glomerulonephritis), triggered by an autoantibody-mediated inflammation (Croker & Kimberly, 2005).
Systemic lupus erythematosus (SLE), the prototype of a systemic autoimmune disease, is characterized by the production of pathogenic autoantibodies that directly or indirectly contribute to the pathogenesis of SLE, resulting in cell destruction and inflammation [ 1, 2].
In this context, mixed cryoglobulinemia syndrome (MCs) represents the prototype of virus-related autoimmune-lymphoproliferative diseases.
Following the discovery of hepatitis C virus (HCV) in 1989 as the major etiological agent of non-A-non-B chronic hepatitis [ 1], some epidemiological studies suggested its possible role in the pathogenesis of mixed cryoglobulinemia syndrome (MCs), which now represents the prototype of HCV-associated autoimmune-lymphoproliferative disorders [ 1- 4].
Further elucidation of these pathways with studies in mouse models and human cells will shed light on the molecular complexity of this prototype autoimmune disease.
Systemic lupus erythematosus (SLE) is a prototype systemic autoimmune disease characterized by flares of high morbidity for which we have no predictors.
