Macrophage-Targeted Therapies for Rheumatoid Arthritis: Progress and Future Directions

Authors

  • Shilin Chen
  • Zhenxuan Hu

DOI:

https://doi.org/10.61173/ngnjjs37

Keywords:

Macrophages, rheumatoid arthritis, cytokine inhibition

Abstract

Considerable amounts of progress have been made to improve methods for treating RA within the past dozen of years. It is now clear that targeting macrophages in the development of RA is suitable for relieving symptoms or even for preventing them from developing. However, more research is to be done to promote the efficacy of current methods, as well as solving problems associated with frequent administration, sensitive reactions, and high doses. Treatment failures due to economical burdens are also problems to be solved. Macrophages are certainly linked with the progression of inflammation in the RA disease. In this article, we reviewed the role of macrophages and substances related to or secreted by them in the development of RA, and various treatments of RA targeting macrophages. Further research of macrophage behavior in inflamed joints with novel technologies may provide a better knowing of RA pathology, therefore helping develop RA therapies with less downsides.

References

[1] Maisha JA, El-Gabalawy HS, O’Neil LJ. Modifiable risk factors linked to the development of rheumatoid arthritis: evidence, immunological mechanisms and prevention. Front Immunol, 2023, 14: 1221125. Erratum in: Front Immunol, 2024, 15: 1370893.

[2] Deane KD, Demoruelle MK, Kelmenson LB, et al. Genetic and environmental risk factors for rheumatoid arthritis. Best Pract Res Clin Rheumatol, 2017, 31(1): 3-18.

[3] Rider P, Carmi Y, Guttman O, et al. IL-1α and IL-1β recruit different myeloid cells and promote different stages of sterile inflammation. J Immunol, 2011, 187(9): 4835-4843.

[4] Cohen I, Rider P, Carmi Y, et al. Differential release of chromatin-bound IL-1alpha discriminates between necrotic and apoptotic cell death by the ability to induce sterile inflammation. Proc Natl Acad Sci U S A, 2010, 107(6): 2574-2579.

[5] Ouyang T, Song L, Fang H, et al. Potential mechanistic roles of Interleukin-33 in rheumatoid arthritis. Int Immunopharmacol, 2023, 123: 110770.

[6] Kondo N, Kuroda T, Kobayashi D. Cytokine networks in the pathogenesis of rheumatoid arthritis. Int J Mol Sci, 2021, 22(20): 10922.

[7] Boutet MA, Courties G, Nerviani A, et al. Novel insights into macrophage diversity in rheumatoid arthritis synovium. Autoimmun Rev, 2021, 20(3): 102758.

[8] Huang QQ, Birkett R, Doyle RE, et al. Association of increased F4/80high macrophages with suppression of serumtransfer arthritis in mice with reduced FLIP in myeloid cells. Arthritis Rheumatol, 2017, 69(9): 1762-1771.

[9] Zhang W, Zhang Y, Zhang J, et al. Naringenin ameliorates collagen-induced arthritis through activating AMPK-mediated autophagy in macrophages. Immun Inflamm Dis, 2023, 11(10).

[10] Bilsborrow JB, Doherty E, Tilstam PV, et al. Macrophage migration inhibitory factor (MIF) as a therapeutic target for rheumatoid arthritis and systemic lupus erythematosus. Expert Opin Ther Targets, 2019, 23(9): 733-744.

[11] Umar S, Palasiewicz K, Volin MV, et al. IRAK4 inhibitor mitigates joint inflammation by rebalancing metabolism malfunction in RA macrophages and fibroblasts. Life Sci, 2021, 287: 120114.

[12] Wang Q, Zhou X, Zhao Y, et al. Polyphyllin I ameliorates collagen-induced arthritis by suppressing the inflammation response in macrophages through the NF-κB pathway. Front Immunol, 2018, 9: 2091.

[13] Sarsenova M, Issabekova A, Abisheva S, et al. Mesenchymal stem cell-based therapy for rheumatoid arthritis. Int J Mol Sci, 2021, 22(21): 11592.

[14] Zhang M, Hu W, Cai C, et al. Advanced application of stimuli-responsive drug delivery system for inflammatory arthritis treatment. Mater Today Bio, 2022, 14: 100223.

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Published

2024-12-31