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Scope
Excessive, unconstrained activation of the immune system has pathologic consequences. In some cases the unbridled activation is limited to innate immune cells leading to autoinflammatory diseases, in others, the adaptive immune response is tissue damaging. At times, both processes are dysregulated. In all cases, immune homeostasis and mechanisms that dampen either myeloid or lymphoid cells are impaired.
Scope
Excessive, unconstrained activation of the immune system has pathologic consequences. In some cases the unbridled activation is limited to innate immune cells leading to autoinflammatory diseases, in others, the adaptive immune response is tissue damaging. At times, both processes are dysregulated. In all cases, immune homeostasis and mechanisms that dampen either myeloid or lymphoid cells are impaired.
Recent discoveries of the genetic contributions to autoinflammatory and autoimmune diseases are providing unique insights into key immune pathways that, when dysregulated, drive pathologic human immune phenotypes. The study of these genetic mutations provides clues that have not only revealed targets for treatment, but also point to the intertwining and coordination of innate and adaptive immune processes in causing immune dysregulation and tissue pathology.
This section seeks contributions that characterize defects that cause autoinflammatory and autoimmune phenotypes which lead to tissue and organ damage. We welcome both basic and translational research contributions that aim to cover the following aspects in relation to autoimmunity and autoinflammatory diseases:
I) The role of adaptive and/or innate immune responses in autoimmunity/auto-inflammation II) The role of genetic and/or epigenetic alterations in disease pathogenesis. III) The role of environmental exposure in triggering autoimmunity/autoinflammatory diseases. IV) The role of metabolic dysregulation in immune and non-immune cells in autoimmunity/auto-inflammation. V) Dysregulation of signaling pathways that contribute to autoimmunity/auto-inflammation. VI) Novel strategies for the development of treatments for autoimmune/autoinflammatory diseases.
Studies in this field have fueled translational research and we hope to provide a forum that allows communication between basic, translational and clinical researchers which ultimately propels the translation of basic knowledge into early and improved treatments for these conditions.
Indexed in: PubMed, PubMed Central, Scopus, Web of Science, Google Scholar, DOAJ, CrossRef, Chemical Abstracts Service (CAS), EMBASE, Semantic Scholar, Ulrich's Periodicals Directory, CLOCKSS, EBSCO, OpenAIRE, Zetoc
PMCID: all published articles receive a PMCID
Autoimmune and Autoinflammatory Disorders welcomes submissions of the following article types: Addendum, Case Report, Classification, Clinical Study Protocol, Clinical Trial, Correction, Editorial, Erratum, General Commentary, Hypothesis and Theory, Methods, Mini Review, Opinion, Original Research, Perspective, Protocols, Review, Specialty Grand Challenge, Systematic Review and Technology Report.
All manuscripts must be submitted directly to the section Autoimmune and Autoinflammatory Disorders, where they are peer-reviewed by the Associate and Review Editors of the specialty section.
Articles published in the section Autoimmune and Autoinflammatory Disorders will benefit from the Frontiers impact and tiering system after online publication. Authors of published original research with the highest impact, as judged democratically by the readers, will be invited by the Chief Editor to write a Frontiers Focused Review - a tier-climbing article. This is referred to as "democratic tiering". The author selection is based on article impact analytics of original research published in all Frontiers specialty journals and sections. Focused Reviews are centered on the original discovery, place it into a broader context, and aim to address the wider community across all of Immunology.
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