Antibodies that target self-antigens are an important component of certain autoimmune diseases and are sometimes used as a clinical marker for these syndromes.
A cardinal feature of the immune system is its ability to distinguish self from nonself. Although many early immunologists thought that its powerful defenses could rarely, if ever, be turned against the host, pioneering research on autoimmune diseases beginning in the early 1900s has documented a different reality. More than 80 different autoimmune disorders have now been described that may affect up to 5% of the population. Autoimmune diseases can be hereditary, triggered by infection and other environmental factors, or a mixture of the two. Practically any molecule, cell, tissue, or organ in the body can be a target. The immune system, it turns out, has a dark side.
This special issue surveys current progress in our understanding of autoimmunity and the regulation of immune tolerance. Recent work has elucidated how T cell tolerance is maintained in the periphery, how inborn errors of the innate immune system’s nucleic acid–sensing machinery can trigger autoimmune disease, how autoimmune disease genetics can inform the development of future therapies, and how autologous hematopoietic stem cell transplantation can “reset” the immune system and treat autoimmune disease.
Beyond spurring major advances in the fields of antiviral immunity, virology, and vaccinology, the COVID-19 pandemic continues to teach scientists about how the immune system’s delicate balancing act is regulated and how it sometimes goes awry. Autoantibodies against components of the antiviral immune response, for example, may underlie certain forms of severe disease. Furthermore, Long Covid is increasingly appreciated as a spectrum of virally induced autoimmune disorders. It is therefore contingent on us to better understand how the immune system is regulated and how a combination of inherited and outside forces can tip the scales.
Source: Science