From autoinflammation to autoimmunity: old and recent findings
Francesco Caso1, Luisa Costa1, Valeria Nucera2
1Rheumatology Unit, Department of Clinical Medicine and Surgery, University Federico II, Via Sergio Pansini, 5, Naples, Italy.
Clinical Rheumatology
|July 18, 2018
Summary
Autoimmune diseases (ADs) involve both innate and adaptive immunity. Interleukin-1 beta (IL-1ß) is key in linking these systems, suggesting inflammasomes play a role in ADs.
Area of Science:
- Immunology
- Pathogenesis of Autoimmune Diseases
Background:
- Autoimmune diseases (ADs) and autoinflammatory diseases share genetic and clinical traits, including inflammatory flares.
- Both disease types involve complex interactions between innate and adaptive immune responses.
Purpose of the Study:
- To elucidate the interconnectedness of innate and adaptive immune mechanisms in autoimmune diseases.
- To highlight the role of inflammasomes and IL-1ß in the pathogenesis of ADs.
Main Methods:
- Review of current literature on the immunopathogenesis of ADs.
- Analysis of the roles of Toll-like receptors (TLRs), inflammasomes, and cytokines like IL-1ß.
Main Results:
- The initial phase of ADs involves innate immunity, including TLRs and autoantibody synthesis.
- The second phase involves adaptive immunity, with autoantibodies and nucleic acids driving inflammation.
- Interleukin-1 beta (IL-1ß) acts as a critical link between innate (NLR activation) and adaptive immune responses.
Conclusions:
- While traditionally viewed as adaptive immunity disorders, ADs increasingly show involvement of innate immunity and inflammasomes.
- Understanding the interplay between innate and adaptive immunity is crucial for comprehending AD pathogenesis.
- IL-1ß is a central mediator connecting innate and adaptive immune pathways in ADs.
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