Special Issue "Immune Mediated Inflammatory Diseases: From an Update on Molecular and Cellular Mechanisms to Biomarkers for Personalized Medicine"

A special issue of Biomedicines (ISSN 2227-9059).

Deadline for manuscript submissions: 30 June 2020.

Special Issue Editor

Prof. Frédérique Ponchel
Website
Guest Editor
University of Leeds, NIHR Leeds Musculoskeletal Biomedical Research Unit, Leeds, UK
Interests: arthritis; T-cells; Treg; Th17; inflammation; IL6; IL7; epigenetics

Special Issue Information

Dear Colleagues,

IMIDs are common conditions which cause pain, distress and loss of function, characterised by a burden of inflammatory leading to organ damage and increased morbidity and/or mortality. Inflammation may result from or be caused by an inadequate immune response for which an autoantigen has been identified in some conditions. An underlying manifestation of this shared immune dysregulation in clinically unrelated conditions is the inappropriate activation of inflammatory cytokines, notably, IL6 or TNF-alpha.

Although treatment of IMIDs has been revolutionised by the use of targeted biologic therapies with good efficacy, speed of onset and tolerability (such as cytokines blockade initially), response to therapies remains heterogeneous between patients, while the development of resistance to treatments over time is also a reason for inadequate response. This, nonetheless, has led to a shift in the management of these conditions from an organ‐based symptom relief approach to a disease mechanism modification-based treatment. As a result, tailored approaches are now possible and recognised as a high research priority in order to give the right drug to the right patient at the right time.

The Special Issue “Immune Mediated Inflammatory Diseases: From an Update on Molecular and Cellular Mechanisms to Biomarkers for Personalized Medicine” is related to new insight into the mechanism of in IMIDs from molecular and cellular events leading to the establishment of chronicity in these diseases, from epigenetics, gene expression, phenotyping or functional work, cytokine/chemokines networking ….etc. Research into biomarker for diagnostic, prognostic and prediction of response to treatment / relapse, are also invited from any stage of development from discovery to validation/replication studies. Both original research and comprehensive review are welcomed.

Prof. Frédérique Ponchel
Guest Editor

Manuscript Submission Information

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Keywords

  • IMIDs
  • molecular pathways
  • cellular immune mechanisms
  • inflammation
  • cyokine/chemokine networks
  • biomarker
  • diagnostic, prognostic
  • response to therapy

Published Papers (1 paper)

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Research

Open AccessArticle
Identification of Novel Native Autoantigens in Rheumatoid Arthritis
Biomedicines 2020, 8(6), 141; https://doi.org/10.3390/biomedicines8060141 (registering DOI) - 29 May 2020
Abstract
The majority of patients diagnosed with rheumatoid arthritis (RA) have developed autoantibodies against neoepitopes in proteins that have undergone post-translational modification, e.g., citrullination or carbamylation. There is growing evidence of their molecular relevance and their potential utility to improve diagnosis, patient stratification, and [...] Read more.
The majority of patients diagnosed with rheumatoid arthritis (RA) have developed autoantibodies against neoepitopes in proteins that have undergone post-translational modification, e.g., citrullination or carbamylation. There is growing evidence of their molecular relevance and their potential utility to improve diagnosis, patient stratification, and prognosis for precision medicine. Autoantibodies reacting to native proteins may also have a role in RA pathogenesis, however, their reactivity patterns remain much less studied. We hypothesized that a high-density protein array technology could shed light onto the normal and disease-related autoantibodies produced in healthy and RA patient subgroups. In an exploratory study, we investigated the global reactivity of autoantibodies in plasma pools from 15 anti-cyclic citrullinated peptide (CCP)-positive and 10 anti-CCP-negative RA patients and 10 healthy donors against more than 1600 native and unmodified human proteins using a high-density protein array. A total of 102 proteins recognized by IgG autoantibodies were identified, hereof 86 were recognized by antibodies from CCP-positive RA patients and 76 from anti-CCP-negative RA patients, but not by antibodies from healthy donors. Twenty-four of the identified autoantigens have previously been identified in synovial fluid. Multiple human proteins in their native conformation are recognized by autoantibodies from anti-CCP-positive as well as anti-CCP-negative RA patients. Full article
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