Advances in Arthritis: Focusing on Immune Cells and Targeted Therapy

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Immunology".

Deadline for manuscript submissions: closed (29 February 2024) | Viewed by 2202

Special Issue Editor


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Guest Editor
Barts and the London School of Medicine and Dentistry, Queen Mary University of London, Chaterhouse Square, London EC1M 6BQ, UK
Interests: arthropathies; type 1 diabetes; autoimmune condition; targeted immunotherapy
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Special Issue Information

Dear Colleagues,

Arthritis is a disease with a complex etiology, mainly related to infection, autoimmune reactions, trauma, metabolic disorder, degenerative diseases, and so on, which includes over 100 types including rheumatoid arthritis, osteoarthritis, psoriatic arthritis, and inflammatory arthritis. Among them, rheumatoid arthritis, as the most common inflammatory arthritis, has attracted widespread attention.

Rheumatoid arthritis is a systemic autoimmune disease that involves an influx of immune cells infiltrating the disease joints. Activated immune cells such as neutrophils, macrophages, lymphocytes, natural killer cells, mast cells, and innate lymphoid cells secrete different proinflammatory factors. It is of great interest to discuss the role of various immune cells and cytokines in arthritis, as well as the concept of defining therapeutic targets leading to novel targeted therapeutics.

Therefore, our Special Issue is intended to address broad aspects of arthritis, with a particular emphasis on inflammatory arthritis. We welcome researchers to submit original articles and state-of-the-art reviews to highlight current achievements linked to arthritis, but also to explore future directions in the novel therapeutic approaches of arthritis. 

Dr. Ahuva Nissim
Guest Editor

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Keywords

  • arthritis
  • rheumatoid arthritis
  • inflammatory arthritis
  • immune

Published Papers (2 papers)

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Research

13 pages, 1399 KiB  
Article
Examining the Relationship between Systemic Immune–Inflammation Index and Disease Severity in Juvenile Idiopathic Arthritis
by Delia-Maria Nicoară, Andrei-Ioan Munteanu, Alexandra-Cristina Scutca, Giorgiana-Flavia Brad, Iulius Jugănaru, Meda-Ada Bugi, Raluca Asproniu and Otilia Mărginean
Cells 2024, 13(5), 442; https://doi.org/10.3390/cells13050442 - 03 Mar 2024
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Abstract
Juvenile Idiopathic Arthritis (JIA), the leading childhood rheumatic condition, has a chronic course in which persistent disease activity leads to long-term consequences. In the era of biologic therapy and tailored treatment, precise disease activity assessment and aggressive intervention for high disease activity are [...] Read more.
Juvenile Idiopathic Arthritis (JIA), the leading childhood rheumatic condition, has a chronic course in which persistent disease activity leads to long-term consequences. In the era of biologic therapy and tailored treatment, precise disease activity assessment and aggressive intervention for high disease activity are crucial for improved outcomes. As inflammation is a fundamental aspect of JIA, evaluating it reflects disease severity. Recently, there has been growing interest in investigating cellular immune inflammation indices such as the neutrophil-to-lymphocyte ratio (NLR) and systemic immune inflammation index (SII) as measures of disease severity. The aim of this retrospective study was to explore the potential of the SII in reflecting both inflammation and disease severity in children with JIA. The study comprised 74 JIA patients and 50 healthy controls. The results reveal a notable increase in median SII values corresponding to disease severity, exhibiting strong correlations with traditional inflammatory markers, including CRP and ESR (ρ = 0.714, ρ = 0.661), as well as the JADAS10 score (ρ = 0.690). Multiple regression analysis revealed the SII to be independently associated with JADAS10. Furthermore, the SII accurately distinguished patients with high disease activity from other severity groups (AUC = 0.827, sensitivity 81.5%, specificity 66%). These findings suggest that integrating the SII as an additional measure holds potential for assessing disease activity in JIA. Full article
(This article belongs to the Special Issue Advances in Arthritis: Focusing on Immune Cells and Targeted Therapy)
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17 pages, 3207 KiB  
Article
A Peripheral Blood Signature of Increased Th1 and Myeloid Cells Combined with Serum Inflammatory Mediators Is Associated with Response to Abatacept in Rheumatoid Arthritis Patients
by Panagiota Goutakoli, Garyfalia Papadaki, Argyro Repa, Nestor Avgoustidis, Eleni Kalogiannaki, Irini Flouri, Antonios Bertsias, Jerome Zoidakis, Martina Samiotaki, George Bertsias, Maria Semitekolou, Panayotis Verginis and Prodromos Sidiropoulos
Cells 2023, 12(24), 2808; https://doi.org/10.3390/cells12242808 - 09 Dec 2023
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Abstract
Abatacept (CTLA4-Ig)—a monoclonal antibody which restricts T cell activation—is an effective treatment for rheumatoid arthritis (RA). Nevertheless, only 50% of RA patients attain clinical responses, while predictors of response are rather limited. Herein, we aimed to investigate for early biomarkers of response to [...] Read more.
Abatacept (CTLA4-Ig)—a monoclonal antibody which restricts T cell activation—is an effective treatment for rheumatoid arthritis (RA). Nevertheless, only 50% of RA patients attain clinical responses, while predictors of response are rather limited. Herein, we aimed to investigate for early biomarkers of response to abatacept, based on a detailed immunological profiling of peripheral blood (PB) cells and serum proteins. We applied flow cytometry and proteomics analysis on PB immune cells and serum respectively, of RA patients starting abatacept as the first biologic agent. After 6 months of treatment, 34.5% of patients attained response. At baseline, Th1 and FoxP3+ T cell populations were positively correlated with tender joint counts (p-value = 0.047 and p-value = 0.022, respectively). Upon treatment, CTLA4-Ig effectively reduced the percentages of Th1 and Th17 only in responders (p-value = 0.0277 and p-value = 0.0042, respectively). Notably, baseline levels of Th1 and myeloid cell populations were significantly increased in PB of responders compared to non-responders (p-value = 0.009 and p-value = 0.03, respectively). Proteomics analysis revealed that several inflammatory mediators were present in serum of responders before therapy initiation and strikingly 10 amongst 303 serum proteins were associated with clinical responses. Finally, a composite index based on selected baseline cellular and proteomics’ analysis could predict response to abatacept with a high sensitivity (90%) and specificity (88.24%). Full article
(This article belongs to the Special Issue Advances in Arthritis: Focusing on Immune Cells and Targeted Therapy)
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