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.

BACKGROUND: Analysis of chest X-ray images is one of the primary standards in diagnosing patients with COVID-19 and pneumonia, which is faster than using PCR Swab method. However, accuracy of using X-ray images needs to be improved. OBJECTIVE: To develop a new deep learning system of chest X-ray images and evaluate whether it can quickly and accurately detect pneumonia and COVID-19 patients. METHODS: The developed deep learning system (UBNet v3) uses three architectural hierarchies, namely first, to build an architecture containing 7 convolution layers and 3 ANN layers (UBNet v1) to classify between normal images and pneumonia images. Second, using 4 layers of convolution and 3 layers of ANN (UBNet v2) to classify between bacterial and viral pneumonia images. Third, using UBNet v1 to classify between pneumonia virus images and COVID-19 virus infected images. An open-source database with 9,250 chest X-ray images including 3,592 COVID-19 images were used in this study to train and test the developed deep learning models. RESULTS: CNN architecture with a hierarchical scheme developed in UBNet v3 using a simple architecture yielded following performance indices to detect chest X-ray images of COVID-19 patients namely, 99.6%accuracy, 99.7%precision, 99.7%sensitivity, 99.1%specificity, and F1 score of 99.74%. A desktop GUI-based monitoring and classification system supported by a simple CNN architecture can process each chest X-ray image to detect and classify COVID-19 image with an average time of 1.21 seconds. CONCLUSION: Using three hierarchical architectures in UBNet v3 improves system performance in classifying chest X-ray images of pneumonia and COVID-19 patients. A simple architecture also speeds up image processing time.

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.

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.