Dendritic cells and their associated pro-inflammatory cytokines augment to the inflammatory milieu in vitiligo skin

Singh, Ankita; Das, Dayasagar; Kurra, Santosh; Arava, Sudheer; Gupta, Somesh; Sharma, Alpana

doi:10.1016/j.cyto.2021.155598

Cited by 6 publications

(8 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Furthermore, exogenous HSP70 can directly activate pDCs and induce IFN-α production, as demonstrated by the infiltrates of DCs and increased levels of IFN-α in the perilesional skin of patients with vitiligo [ 102 , 119 ]. However, a recent study found decreased levels of IFN-α in the circulation of patients with vitiligo, and increased levels of circulating DCs, IL-12, and TNF-α in patients with non-segmental vitiligo [ 120 ]. Another study demonstrated a relationship between the production of pro- and anti-inflammatory cytokines (IL-17A, IL-10, and IL-12p70) by DCs in both stable and active patients with vitiligo.…”

Section: Current Concepts In Immunopathogenesis Of Vitiligomentioning

confidence: 99%

Current Concepts of Vitiligo Immunopathogenesis

et al. 2022

View full text Add to dashboard Cite

Vitiligo is an acquired immune-mediated disorder of pigmentation clinically characterized by well-defined depigmented or chalk-white macules and patches on the skin. The prevalence of vitiligo varies by geographical area, affecting 0.5% to 2% of the population. The disease imposes a significant psychological burden due to its major impact on patients’ social and emotional aspects of life. Given its autoimmune background, vitiligo is frequently associated with other autoimmune diseases or immune-mediated diseases. Vitiligo is a multifaceted disorder that involves both genetic predisposition and environmental triggers. In recent years, major predisposing genetic loci for the development of vitiligo have been discovered. The current findings emphasize the critical role of immune cells and their mediators in the immunopathogenesis of vitiligo. Oxidative-stress-mediated activation of innate immunity cells such as dendritic cells, natural killer, and ILC-1 cells is thought to be a key event in the early onset of vitiligo. Innate immunity cells serve as a bridge to adaptive immunity cells including T helper 1 cells, cytotoxic T cells and resident memory T cells. IFN-γ is the primary cytokine mediator that activates the JAK/STAT pathway, causing keratinocytes to produce the key chemokines CXCL9 and CXCL10. Complex interactions between immune and non-immune cells finally result in apoptosis of melanocytes. This paper summarizes current knowledge on the etiological and genetic factors that contribute to vitiligo, with a focus on immunopathogenesis and the key cellular and cytokine players in the disease’s inflammatory pathways.

show abstract

Section: Current Concepts In Immunopathogenesis Of Vitiligomentioning

confidence: 99%

Current Concepts of Vitiligo Immunopathogenesis

et al. 2022

View full text Add to dashboard Cite

show abstract

“…SKL2001 (5‐furan‐2yl‐isoxazole‐3‐carboxylic acid (3‐imidazol‐1yl‐propyl)‐amide) is a Wnt agonist that disrupts Axin/β‐Catenin interaction in the β‐Catenin destruction complex and leads to inhibition of the phosphorylation of β‐catenin, increasing the cytoplasmic β‐catenin 100 . A recent study revealed that the frequency of DCs is significantly elevated in patients with vitiligo along with circulatory level of IL‐12 and TNF‐α, which may contribute to defective antigen presentation of DCs, inducing autoimmune response 101 . In vitro, the addition of β‐catenin agonist SKL2001 to Mycobacterium tuberculosis (Mtb)‐treated DCs significantly reduced pro‐inflammatory cytokines produced by DCs compared to Mtb‐treated DCs alone 102 .…”

Section: Agents and Nature Compounds Activating Wnt/β‐catenin Signall...mentioning

confidence: 99%

“…100 A recent study revealed that the frequency of DCs is significantly elevated in patients with vitiligo along with circulatory level of IL-12 and TNF-α, which may contribute to defective antigen presentation of DCs, inducing autoimmune response. 101 In vitro, the addition of βcatenin agonist SKL2001 to Mycobacterium tuberculosis (Mtb)-treated DCs significantly reduced pro-inflammatory cytokines produced by DCs compared to Mtb-treated DCs alone. 102 This suggests that the treatment of SKL2001 may attenuate autoimmune response in vitiligo.…”

Section: Skl2001mentioning

confidence: 99%

The possible role of Wnt/β‐catenin signalling in vitiligo treatment

Lin

Meng

Lin

2023

Acad Dermatol Venereol

View full text Add to dashboard Cite

Vitiligo is a common chronic skin disease which has an adverse impact on patients' life. Its pathogenesis is complex, involving autoimmunity and oxidative stress (OS). Autoimmunity leads to the loss of epidermal melanocytes and the formation of the depigmented patches of the disease. Treatment of vitiligo should control the exaggerated immune response to arrest the progress of active disease, and then promote melanocytes to repigmentation. Wnt/β‐catenin signalling pathway has been of recent interest in vitiligo. Wnt/β‐catenin signalling pathway is downregulated in vitiligo. Upregulation of Wnt/β‐catenin signalling possibly control vitiligo autoimmune response by protecting melanocyte from OS damage, inhibiting CD8+ T cell effector cell differentiation and enhancing Treg. Wnt/β‐catenin signalling plays a critical role in the melanocyte regeneration by driving the differentiation of melanocyte stem cells (McSCs) into melanocytes. Promoting Wnt/β‐catenin signalling can not only arrest the progress of active disease of vitiligo but also promote repigmentation. Some of the main effective therapies for vitiligo are likely to work by activating Wnt/β‐catenin signalling. Agents that can enhance the effect of Wnt/β‐catenin signalling may become potential candidates for the development of new drugs for vitiligo treatment.

show abstract

“…11,12 Upon encountering external antigenic stimuli, immature DCs undergo changes in surface markers and differentiate into mature DCs (mDCs). This maturation process involves upregulation of co-stimulatory proteins (such as CD80, CD86) and maturation receptors (such as CD83, MHCII), along with the secretion of pro-inflammatory or anti-inflammatory cytokines 13 (such as IL-6, IL-12, IL-23, TNF-a, or IL-10). In order to accomplish the maturation process, DCs enhance their ability to migrate from lymph nodes to peripheral tissues by upregulating the chemokine receptor CCR7, 14 thereby providing antigens to T-cells, activating T lymphocytes to exert immune responses.…”

Section: Introductionmentioning

confidence: 99%

Tolerogenic CD11c⁺dendritic cells regulate CD4⁺Tregs in replacing delayed ischemic preconditioning to alleviate ischemia–reperfusion acute kidney injury

Wang,

Li,

Peng

et al. 2024

The FASEB Journal

View full text Add to dashboard Cite

Ischemia–reperfusion injury (IRI) is one of the primary clinical causes of acute kidney injury (AKI). The key to IRI lies in immune‐inflammatory damage, where dendritic cells (DCs) play a central role in eliciting immune responses within the context of inflammation induced by ischemia–reperfusion. Our previous study has confirmed that delayed ischemic preconditioning (DIPC) can reduce the kidney injury by mediating DCs to regulate T‐cells. However, the clinical feasibility of DIPC is limited, as pre‐clamping of the renal artery is not applicable for the prevention and treatment of ischemia–reperfusion acute kidney injury (I/R‐AKI) in clinical patients. Therefore, the infusion of DCs as a substitute for DIPC presents a more viable strategy for preventing renal IRI. In this study, we further evaluated the impact and mechanism of infused tolerogenic CD11c+DCs on the kidneys following IRI by isolating bone marrow‐derived dendritic cells and establishing an I/R‐AKI model after pre‐infusion of DCs. Renal function was significantly improved in the I/R‐AKI mouse model after pre‐infused with CD11c+DCs. The pro‐inflammatory response and oxidative damage were reduced, and the levels of T helper 2 (Th2) cells and related anti‐inflammatory cytokines were increased, which was associated with the reduction of autologous DCs maturation mediated by CD11c+DCs and the increase of regulatory T‐cells (Tregs). Next, knocking out CD11c+DCs, we found that the reduced immune protection of tolerogenic CD11c+DCs reinfusion was related to the absence of own DCs. Together, pre‐infusion of tolerogenic CD11c+DCs can replace the regulatory of DIPC on DCs and T‐cells to alleviate I/R‐AKI. DC vaccine is expected to be a novel avenue to prevent and treat I/R‐AKI.

show abstract

Dendritic cells and their associated pro-inflammatory cytokines augment to the inflammatory milieu in vitiligo skin

Cited by 6 publications

References 34 publications

Current Concepts of Vitiligo Immunopathogenesis

Current Concepts of Vitiligo Immunopathogenesis

The possible role of Wnt/β‐catenin signalling in vitiligo treatment

Tolerogenic CD11c⁺dendritic cells regulate CD4⁺Tregs in replacing delayed ischemic preconditioning to alleviate ischemia–reperfusion acute kidney injury

Contact Info

Product

Resources

About

Dendritic cells and their associated pro-inflammatory cytokines augment to the inflammatory milieu in vitiligo skin

Cited by 6 publications

References 34 publications

Current Concepts of Vitiligo Immunopathogenesis

Current Concepts of Vitiligo Immunopathogenesis

The possible role of Wnt/β‐catenin signalling in vitiligo treatment

Tolerogenic CD11c+dendritic cells regulate CD4+Tregs in replacing delayed ischemic preconditioning to alleviate ischemia–reperfusion acute kidney injury

Contact Info

Product

Resources

About

Tolerogenic CD11c⁺dendritic cells regulate CD4⁺Tregs in replacing delayed ischemic preconditioning to alleviate ischemia–reperfusion acute kidney injury