Correction to: Current Rheumatology Reports (2026) 28:2

In the original version of this article, the figure captions for Figures 1, 2 and 3 did not include the required credit statement. The captions have now been updated to include the following text: “Created with BioRender.com.”

This correction applies only to the figure captions. The figures themselves and their scientific content remain unchanged. All other elements of the figure captions remain the same. The publication licenses for these figures are attached separately.

The final caption for Figures 1, 2 and 3 should read as following:

Fig. 1 Overview pathophysiologic mechanisms and select novel therapeutic targets in rheumatoid arthritis. The physiology of rheumatoid arthritis is a complex interaction between various cell types, cytokines, and immunoglobulins. Novel targets in rheumatoid arthritis include inhibition of T cells through costimulatory molecules such as CD40/CD40L, modulation of lymphocyte trafficking via signaling molecule gradients, inhibition of B cells though bispecific T cell engagers, decrease in circulating IgG with FcRn receptor blockers, and fibroblast and myeloid cell inhibition. S1PR1 = Sphingosine-1-phosphate receptor-1, S1P = Sphingosine-1-phosphate, BTK = Bruton’s tyrosine kinase, CAR T cell = Chimeric antigen receptor T cell, CDK = cyclin dependent kinase, IRAK4 = interleukin-1 receptor-associated kinase 4, APC = antigen presenting cell, MMP = matrix metalloproteinases. Figure created with BioRender.com.

Fig. 2 Select T cell and lymphocyte trafficking investigational targets in rheumatoid arthritis. (A) PD1 agonism results in immune checkpoint stimulation and T cell anergy. (B) Antagonism of the CD40-CD40L costimulatory signal results in decreased CD4 + T cell activation. (C) Antagonism of the OX40-OX40L costimulatory signal results in decreased T cell activation utilizing nanovesicle delivery system. (D) S1PR1 modulators such as proximod lead to internalization and degradation of S1PR1, resulting in decreased lymphocyte trafficking via S1P gradients. (E) CXCR5 blockade reduces T cell response to CXCL13, which mitigates migration of T cells into B cell zones in lymphoid follicles. S1PR1 = Sphingosine-1-phosphate receptor-1, S1P = Sphingosine-1-phosphate, APC = antigen presenting cell. Figure created with BioRender.com.

Fig. 3 Select B cell, humoral immunity, fibroblast and myeloid investigational targets in rheumatoid arthritis. (A) B cell receptor signaling via Bruton’s tyrosine kinase activation of NF-kB leads to B cell maturation. (B) The FcRn receptor is responsible for recycling IgG taken up by endocytosis. FcRn-bound IgG is recycled and recirculated, whereas, IgG not bound to FcRn is degraded. (C) Activation of TLR or IL1-R leads to formation of an oligomeric complex including IRAK4 with downstream signaling causing production of inflammatory cytokines. (D) Multiple cyclin dependent kinases are responsible for progression through the fibroblast cell cycle. Additionally, MCL1 results in decreased apoptosis via stimulation by p21. (E) Bispecific T cell engagers rely on multiple mechanisms including stimulation of CD3 on T cells leading to B cell killing via interaction with CD19. BTK = Bruton’s tyrosine kinase, NF-kB = nuclear factor-kB, FcRn = neonatal Fc receptor, IRAK4 = Interleukin-1-associated kinase 4, IRAK1 = Interleukin-1-associated kinase 1, MyD88 = myeloid differentiation primary response protein 88, TRAF6 = Tumor Necrosis Factor Receptor-Associated Factor 6, IRF-5 = interferon regulatory factor-5, MAPK = mitogen-activated protein kinase, CDK = cyclin-dependent kinase, MCL1 = Induced myeloid leukemia cell differentiation protein Mcl-1. Figure created with BioRender.com.

The original version has been corrected.