Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
7.8
5.6
Journals
IJMS
Special Issues
Spondyloarthritis: Molecular Mechanisms and Novel Therapies
ijms-logo
Submit to IJMS Review for IJMS Propose a Special Issue

Journal Menu

► Journal Menu

Journal Browser

► Journal Browser
share announcement

Spondyloarthritis: Molecular Mechanisms and Novel Therapies

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: closed (31 October 2023) | Viewed by 3699

Special Issue Editor

Dr. Marino Paroli

E-Mail Website
Guest Editor
Division of Clinical Immunology, Department of Clinical, Anesthesiologic and Cardiovascular Sciences, Sapienza University of Rome, 00185 Rome, Italy
Interests: inflammatory rheumatic diseases; autoimmunity; T-cell response
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Spondyloarthritis is a group of inflammatory rheumatic diseases that have a significant negative impact on human health and can cause severe disability. This family of diseases includes ankylosing spondylitis, non-radiographic axial spondyloarthritis, psoriatic arthritis, arthritis associated with inflammatory bowel disease, reactive arthritis, and undifferentiated forms. In recent years, several pathogenetic aspects of spondyloarthritis have been clarified. These include the role of HLA-B27 in the altered presentation of bacterial and viral antigens to T lymphocytes, the close relationship with the microbiota, the key role played by the interleukin-23–interleukin-17 axis, and the identification of inflammatory cells involved in pathogenesis. This knowledge has enabled the development of new therapeutic tools such as biologics, including anti-TNF-alpha, anti-interleukin-23, and anti-interleukin-17A. Recently, JAK inhibitors have also been successfully used in the treatment of spondyloarthritis. However, numerous aspects of the disease still need to be clarified. Therefore, the purpose of this Special Issue is to gather contributions from various experts in the field to shed light on the molecular and cellular mechanisms involved in the pathogenesis of spondyloarthritis, with the hope that they can help improve patient care in the future.

Dr. Marino Paroli
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • spondyloarthritis
  • T helper 17
  • innate lymphoid cells
  • HLA-B27

Published Papers (2 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

Jump to: Review

19 pages, 3124 KiB  
Article
ERAP1 and ERAP2 Haplotypes Influence Suboptimal HLA-B*27:05-Restricted Anti-Viral CD8+ T Cell Responses Cross-Reactive to Self-Epitopes
by Valentina Tedeschi, Giorgia Paldino, Josephine Alba, Emanuele Molteni, Fabiana Paladini, Rossana Scrivo, Mattia Congia, Alberto Cauli, Rosalba Caccavale, Marino Paroli, Manuela Di Franco, Loretta Tuosto, Rosa Sorrentino, Marco D’Abramo and Maria Teresa Fiorillo
Int. J. Mol. Sci. 2023, 24(17), 13335; https://doi.org/10.3390/ijms241713335 - 28 Aug 2023
Viewed by 1126
Abstract
The human leukocyte antigen (HLA)-B*27 family of alleles is strongly associated with ankylosing spondylitis (AS), a chronic inflammatory disorder affecting the axial and peripheral joints, yet some HLA-B*27 variants not associated with AS have been shown. Since no major differences in the ligandome [...] Read more.
The human leukocyte antigen (HLA)-B*27 family of alleles is strongly associated with ankylosing spondylitis (AS), a chronic inflammatory disorder affecting the axial and peripheral joints, yet some HLA-B*27 variants not associated with AS have been shown. Since no major differences in the ligandome of associated compared to not-associated alleles have emerged, a plausible hypothesis is that the quantity rather than the quality of the presented epitopes makes the difference. In addition, the Endoplasmic Reticulum AminoPeptidases (ERAPs) 1 and 2, playing a crucial role in shaping the HLA class I epitopes, act as strong AS susceptibility factors, suggesting that an altered peptidome might be responsible for the activation of pathogenic CD8+ T cells. In this context, we have previously singled out a B*27:05-restricted CD8+ T cell response against pEBNA3A (RPPIFIRRL), an EBV peptide lacking the B*27 classic binding motif. Here, we show that a specific ERAP1/2 haplotype negatively correlates with such response in B*27:05 subjects. Moreover, we prove that the B*27:05 allele successfully presents peptides with the same suboptimal N-terminal RP motif, including the self-peptide, pDYNEIN (RPPIFGDFL). Overall, this study underscores the cooperation between the HLA-B*27 and ERAP1/2 allelic variants in defining CD8+ T cell reactivity to suboptimal viral and self-B*27 peptides and prompts further investigation of the B*27:05 peptidome composition. Full article
(This article belongs to the Special Issue Spondyloarthritis: Molecular Mechanisms and Novel Therapies)
►▼ Show Figures

Figure 1

Review

Jump to: Research

15 pages, 1340 KiB  
Review
Janus Kinase Inhibitors: A New Tool for the Treatment of Axial Spondyloarthritis
by Marino Paroli, Rosalba Caccavale, Maria Pia Paroli, Luca Spadea and Daniele Accapezzato
Int. J. Mol. Sci. 2023, 24(2), 1027; https://doi.org/10.3390/ijms24021027 - 05 Jan 2023
Cited by 5 | Viewed by 2213
Abstract
Axial spondyloarthritis (axSpA) is a chronic inflammatory disease involving the spine, peripheral joints, and entheses. This condition causes stiffness, pain, and significant limitation of movement. In recent years, several effective therapies have become available based on the use of biologics that selectively block [...] Read more.
Axial spondyloarthritis (axSpA) is a chronic inflammatory disease involving the spine, peripheral joints, and entheses. This condition causes stiffness, pain, and significant limitation of movement. In recent years, several effective therapies have become available based on the use of biologics that selectively block cytokines involved in the pathogenesis of the disease, such as tumor necrosis factor-α (TNFα), interleukin (IL)-17, and IL-23. However, a significant number of patients show an inadequate response to treatment. Over 10 years ago, small synthetic molecules capable of blocking the activity of Janus kinases (JAK) were introduced in the therapy of rheumatoid arthritis. Subsequently, their indication extended to the treatment of other inflammatory rheumatic diseases. The purpose of this review is to discuss the efficacy and safety of these molecules in axSpA therapy. Full article
(This article belongs to the Special Issue Spondyloarthritis: Molecular Mechanisms and Novel Therapies)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-2
Back to TopTop