jcm-logo

Journal Browser

Journal Browser

Updates on Rheumatoid Arthritis: From Diagnosis to Treatment

A special issue of Journal of Clinical Medicine (ISSN 2077-0383). This special issue belongs to the section "Immunology".

Deadline for manuscript submissions: 25 August 2025 | Viewed by 546

Special Issue Editor


E-Mail Website
Guest Editor
Laboratory of Social Pharmacy and Public Health, School of Pharmacy, University of Coimbra, 3000-538 Coimbra, Portugal
Interests: pharmacoepidemiology; pharmacovigilance; effectiveness; post-marketing drug safety evaluation; observational studies; systematic review; meta-analysis; rheumatoid arthritis

Special Issue Information

Dear Colleagues,

Rheumatoid arthritis (RA) is an inflammatory autoimmune disease, causing symmetrical polyarthritis, typically resulting in swollen, stiff and painful joints. This condition affects approximatelly 5 in every 1000 adults worldwide. The pharmacological treatment of RA should start as soon as the diagnosis is made. Methotrexate is an effective conventional synthetic (cs) disease-modifying antirheumatic drug (DMARD) and it is the first-line treatment option. If the disease activity remains moderate to high, additional treatment with csDMARDs, biological DMARDs (bDMARDs) or targeted synthetic DMARDs (tsDMARDs) should be considered.

New treatments for RA have been introduced over the last few years, like Janus-Kinase (JAK) inhibitors or interleukin-6 (IL-6) inhibitors, which have demonstrated effectiveness in controlling the disease. Nonetheless, safety issues have also been recently identified, delaying or inhibiting the approval of new drugs.

There are agents being currently developed for RA treatment, like those targeting CD40 and CD40 ligand, programmed death protein 1 (PD-1), or granulocyte-macrophage colony-stimulating factor (GM-CSF).

The current Special Issue will focus on updated research addressing the effectiveness and safety of pharmacological alternatives for RA, aiming to improve the knowledge about clinical management and patients’ outcomes in the field.

Dr. Carlos Alves
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. Journal of Clinical Medicine is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). 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

  • rheumatoid arthritis
  • pharmacological intervention
  • treatment
  • clinical development
  • effectiveness
  • safety
  • immune therapy
  • biological disease-modifying antirheumatic drugs (bDMARDs)
  • synthetic disease-modifying antirheumatic drugs (sDMARDs)

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • Reprint: MDPI Books provides the opportunity to republish successful Special Issues in book format, both online and in print.

Further information on MDPI's Special Issue policies can be found here.

Published Papers (1 paper)

Order results
Result details
Select all
Export citation of selected articles as:

Other

9 pages, 639 KiB  
Brief Report
Recombinant IgG1 Fc-μTP-L309C Ameliorates Endogenous Rheumatoid Arthritis in the K/BxN Mouse Model by Decreasing Th1 and Th17 Cells in the Spleen, Lymph Nodes and Joint and Increasing T Regulatory Cells and IL-10 in the Joint
by Bonnie J. B. Lewis, Selena Cen, Ruqayyah J. Almizraq, Beth Binnington, Rolf Spirig, Fabian Käsermann and Donald R. Branch
J. Clin. Med. 2025, 14(13), 4509; https://doi.org/10.3390/jcm14134509 - 25 Jun 2025
Viewed by 188
Abstract
Background/Objectives: Recombinant Fc proteins have been produced that have a protective effect in mouse models of arthritis, such as the K/BxN rheumatoid arthritis model. We have previously shown that a recombinant human IgG1 Fc with a point mutation at position 309, replacing a [...] Read more.
Background/Objectives: Recombinant Fc proteins have been produced that have a protective effect in mouse models of arthritis, such as the K/BxN rheumatoid arthritis model. We have previously shown that a recombinant human IgG1 Fc with a point mutation at position 309, replacing a leucine with a cysteine, fused to the human IgM tailpiece to form a human IgG1 Fc hexamer, rFc-µTP-L309C, effectively prevents neutrophil infiltration into the joints and ameliorates arthritis in the K/BxN serum transfer model and in the endogenous chronic arthritis K/BxN model. We have now investigated the effect of rFc-µTP-L309C on T-cells in the K/BxN chronic arthritis mouse model. Methods: PBMCs were isolated from the spleen, lymph nodes and joint synovial fluid from K/BxN mice having severe chronic arthritis that had been treated with 200 mg/kg rFc-µTP-L309C or human serum albumin (HSA). Flow cytometry was used to isolate the activated CD4+CD44+ T-cells and T-regulatory cells (Tregs). Intracellular staining was used to identify Th1 and Th17 T-cell subsets, and CD4+CD25+FoxP3+ Tregs. ELISA was used to measure levels of IL-10 and TGF-β in synovial fluid. Results: We find that amelioration of the arthritis occurs after treatment with rFc-µTP-L309C and results in a decrease in Th1 cells’ production of IFNγ and Th17 cells’ production of IL-17. Amelioration also results in decreased production of GM-CSF. Moreover, amelioration results in increased Tregs and IL-10 production in the synovial fluid. Conclusions: rFc-µTP-L309C reduces the inflammatory T-cells and increases the regulatory anti-inflammatory T-cells in the chronic arthritis K/BxN mouse model. This effect explains, in part, the ability of rFc-µTP-L309C to ameliorate the arthritis and reduce damage on the articular cartilage of K/BxN mice. Full article
(This article belongs to the Special Issue Updates on Rheumatoid Arthritis: From Diagnosis to Treatment)
Show Figures

Figure 1

Back to TopTop