Developing a safe and efficacious vaccine that can induce broad and long-term immunity for SARS-CoV-2 infection is the most critical research to date. As the most potent APCs, dendritic cells (DCs)...

Current therapies for autoimmune diseases are immunosuppressant agents, which have many debilitating side effects. However, dendritic cells (DCs) can induce antigen-specific tolerance. Tolerance restoration mediated by ex vivo-generated DCs can be a therapeutic approach. Therefore, in this review, we summarize the conceptual framework for developing ex vivo-generated DC strategies for autoimmune diseases. First, we will discuss the role of DCs in developing immune tolerance as a foundation for developing dendritic cell-based immunotherapy for autoimmune diseases. Then, we also discuss relevant findings from pre-clinical and clinical studies of ex vivo-generated DCs for therapy of autoimmune diseases. Finally, we discuss problems and challenges in dendritic cell therapy in autoimmune diseases. Throughout the article, we discuss autoimmune diseases, emphasizing SLE.

A typical consequence of type 2 diabetes mellitus, diabetic kidney disease (DKD) is a significant risk factor for end-stage renal disease. The pathophysiology of diabetic kidney disease (DKD) is mainly associated with the immune system, which involves adhesion molecules and growth factors disruption, excessive expression of inflammatory mediators, decreased levels of anti-inflammatory mediators, and immune cell infiltration in the kidney. Dendritic cells are professional antigen-presenting cells acting as a bridge connecting innate and adaptive immune responses. The anti-inflammatory subset of DCs is also capable of modulating inflammation. Autologous anti-inflammatory dendritic cells can be made by in vitro differentiation of peripheral blood monocytes and utilized as a cell-based therapy. Treatment with anti-inflammatory cytokines, immunosuppressants, and substances derived from pathogens can induce tolerogenic or anti-inflammatory features in ex vivo–generated DCs. It has been established that targeting inflammation can alleviate the progression of DKD. Recent studies have focused on the potential of dendritic cell–based therapies to modulate immune responses favorably. By inducing a tolerogenic phenotype in dendritic cells, it is possible to decrease the inflammatory response and subsequent kidney damage. This article highlights the possibility of using anti-inflammatory DCs as a cell-based therapy for DKD through its role in controlling inflammation.

The prevalence of type 2 diabetes mellitus (T2DM) is increasing worldwide, leading to a higher incidence of diabetic kidney disease (DKD), a major risk factor for end-stage kidney disease (ESKD). This study investigates the effects of autologous dendritic cell (DC) therapy on albuminuria and inflammatory biomarkers (IL-6, IL-10, and TNF-α) in DKD patients. An open-label clinical trial was conducted with 69 DKD outpatients at the Gatot Soebroto Army Central Hospital (RSPAD GS). Each subject received a single DC injection, with evaluations of urinary albumin-creatinine ratio (UACR) and inflammatory biomarkers at baseline and 4 weeks post-intervention. UACR was measured weekly, while eGFR, IL-6, IL-10, and TNF-α levels were assessed at baseline and week 4. Results indicated a significant reduction in median UACR from 250 mg/g at baseline to 153 mg/g in week 1, with sustained lower levels over 4 weeks (p < 0.05). No significant change of eGFR was found (p = 0.478). TNF-α levels also significantly decreased from 2.16 pg/mL to 1.92 pg/mL (p = 0.03), while IL-6 (p = 0.83) and IL-10 (p = 0.11) showed no significant change. The reduction in UACR and TNF-α suggests that DC therapy may alleviate albuminuria through anti-inflammatory mechanisms primarily suppressing TNF-α. No significant change in IL-10 levels implies that the anti-inflammatory effect is not mediated by IL-10 enhancement. This study demonstrates the potential of DC therapy as adjunct therapy to reduce albuminuria in DKD patients, with further research needed to explore long-term efficacy, long-term safety, and dosing strategies.

Diabetic Kidney Disease (DKD) is a common complication of Type 2 Diabetes Mellitus and a major risk factor for end-stage kidney disease. The immune system plays a significant role in the pathogenesis of DKD, involving infiltration of immune cells in the kidney, upregulation of in-flammatory mediators, downregulation of anti-inflammatory mediators, and disturbance in ad-hesion molecules and growth factors. Dendritic cells are professional antigen-presenting cells acting as a bridge connecting innate and adaptive immune responses. DC is also capable of modulating inflammation. Autologous dendritic cells can be made by in vitro differentiation of peripheral blood monocytes and then utilized as a cell-based therapy. Cell-based therapy for DKD is currently focused on utilizing the anti-inflammatory properties of stem cells. However, research suggests unsatisfactory results due to several limitations. This article highlights the possibility of using DC as a cell-based therapy for DKD through its role in controlling inflammation.

This study aimed to evaluate the effects of autologous dendritic cell (DC) immunotherapy on clinical outcomes (glomerular filtration rate/GFR and urine creatinine albumin ratio/UACR) and endothelial dysfunction (ICAM, VCAM, VEGF) in patients with diabetic kidney disease (DKD). Endothelial dysfunction induced by inflammation is one of the key factors in the pathogenesis of DKD. In this one-group pretest–posttest quasi-experimental study, 69 subjects with DKD were administered a single dose of autologous DC immunotherapy ex vivo. UACR was measured at baseline and at weeks 1, 2, 3, and 4, while ICAM, VCAM, VEGF, and GFR were measured at baseline and at week 4 post-immunotherapy. The results showed a significant reduction in median UACR from 250 (IQR 71–668) mg/g at baseline to 164 (IQR 49–576) mg/g at week 4 (p < 0.05). GFR did not show any significant changes after immunotherapy. HbA1c (B = −33.270, p = 0.021) and baseline UACR (B = −0.185, p < 0.001) were identified as significant predictors of UACR change. Although there were no significant changes in ICAM, VCAM, and VEGF, subgroup analysis revealed a decrease in VCAM in macroalbuminuria patients and an increase in those with good glycemic control, suggesting differing endothelial responses. In conclusion, autologous DC immunotherapy effectively reduced UACR in DKD patients, and significant VCAM changes were found in macroalbuminuria and good glycemic control subjects. Further research is needed to understand the mechanisms behind UACR reduction and the long-term impact of this therapy.