Authors
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Abstract
Understanding the pathophysiology of antibody-driven autoimmune diseases (AAID) represents a major challenge for the biomedical community to develop innovative therapeutic strategies that are still lacking to control these diseases. If the reason why AAID are developing still needs to be defined, loss of tolerance to self-antigens leads to the development of an autoimmune chain reaction in some individuals. However, autoreactive antibodies are present in a large proportion of the general population without any associated pathological condition. The amplification of autoantibody production, circulating immune complex formation and innate immune system activation leading to this amplification are some central phenomena in AAID pathophysiology. In this review, we summarize the contribution of type 2 immunity, basophils and IgE in the initiation of some amplification loops that are pathogenic in some AAID, including systemic lupus erythematosus and mixed connective tissue disease.
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