Lack of association between cytotoxic T-lymphocyte antigen-4+49A/G polymorphism and psoriasis and vitiligo: A meta-analysis of case–control studies

Liang, Jingyao; Zhang, Sanquan; Luo, Quan; Li, Wei; Xiang, Tian; Zhang, Fang; Tian, Zhong; Chen, Xiaoxiao; Zhang, Xibao

doi:10.1016/j.gene.2015.05.051

Cited by 12 publications

(9 citation statements)

References 26 publications

(47 reference statements)

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“…CTLA4 is a critical negative regulator of T-cell activation and induces an inhibitory effect on B-cell inactivity, with a consequent decrease in autoantibody formation, decrease in macrophage activation, and reduction in pro-inflammatory cytokines [66, 67]. We observed higher ( p < 0.05) CTLA-4 expression in psoriatic lesions, especially in the papillary layer.…”

Section: Discussionmentioning

confidence: 65%

Evaluation of selected mechanisms of immune tolerance in psoriasis

Owczarczyk‐Saczonek¹,

Czerwińśka²,

Orylska³

et al. 2019

pdia

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Introduction Psoriasis is an autoimmune disease with an excessively aberration of the Th17/Treg balance and deficiency of anti-inflammatory cytokines. Aim Evaluation of Treg markers expression in the lesional and perilesional psoriatic skin and serum anti-inflammatory cytokines in male psoriatic patients compared to healthy men. Material and methods Treg markers (FoxP3+, CD4, CTLA-4, CD25/IL-2R, CD39/ENTPD1, IL-7R/CD127, CD3) and tissue expression of protective cytokines (IL-10, IL-35, TGF-β) in the lesional and perilesional psoriatic skin from 33 male patients compared to 6 healthy skin samples were evaluated by immunohistochemistry. ELISA was used to assess serum IL-10, IL-35 and TGF-β levels. Results The serum levels of IL-35, IL-10 and TGF-β1 were higher in psoriatic patients than in controls but without any statistically significant relationship with PASI. The expressions of IL-35, CD4, IL-10, TGF-β1, CD3, FOXP3 and CD25/IL-2R were varied in different experimental groups ( p < 0.05). The level of IL-35 was the lowest in psoriatic lesions ( p < 0.05) compared to perilesional skin and to controls. CD4, IL-10 and TGF-β1 expressions were higher ( p < 0.05) in perilesional skin than in lesions. TGF-β1 expression was decreased in psoriatic lesions compared to controls ( p < 0.05). CD25/IL2R expression was increased in healthy skin compared to psoriatic skin ( p < 0.05). FOXP3 expression was elevated in psoriatic skin compared to healthy and perilesional one. There was no difference between experimental groups in CTLA-4, IL7R/CD127 and CD39/ENTPD1 expression. Conclusions The differences between the levels of protective cytokines and expression of Treg markers might explain the inflammation development in psoriasis.

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Section: Discussionmentioning

confidence: 65%

Evaluation of selected mechanisms of immune tolerance in psoriasis

Owczarczyk‐Saczonek¹,

Czerwińśka²,

Orylska³

et al. 2019

pdia

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“…In addition, a recent study has shown that the gene for Forkhead box protein 3 (FOXP3), which is important for cellular proliferation and functions of the CD4+ and CD25+ regulatory T cells, play a role in the pathogenesis of vitiligo as an immunoregulator (Jahan P, 2015). In another study, cytotoxic T lymphocyte antigen-4 (CTLA-4) gene polymorphism was not found to contribute to the pathogenesis of vitiligo (Liang J, et al 2015). In another genetic research, a family has been defined with the heterozygous mutation for the suppressor gene of cytokine signaling-4 (SOCS4), and having autoimmune diseases like vitiligo, alopecia, and hypothyroidism (Arts P, et al 2015).…”

Section: Discussionmentioning

confidence: 99%

Research Article IGF2BP2 gene polymorphism in the pathogenesis of vitiligo

Kargün¹,

Demir²,

Çiçek³

et al. 2017

Genet. Mol. Res.

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Vitiligo is a disorder of pigmentation presenting with loss of melanocytes in the epidermis and hair follicles. The gene for insulin-like growth factor binding protein 2 (IGF2BP2) is located on the third chromosome and it plays role in growth, development, cellular differentiation, and metabolism. In the present study, we aimed to investigate the rs1470579 and rs4402960 gene polymorphisms of IGF2BP2 in the patients with vitiligo, which were confirmed to have a relationship with insulin resistance. The study was conducted with a total of 100 patients with vitiligo between the ages of 18 to 60 years and 100 healthy controls. Gene polymorphism was investigated in deoxyribonucleic acid (DNA) samples isolated from blood cells using the real-time polymerase chain reaction (PCR) method. There was no statistically significant difference in the genotype and allele frequencies of the rs1470579 and rs4402960 polymorphisms on IGF2BP2 between the groups (p>0.05). Our study results show that the IGF2BP2 gene has no significant role in the pathogenesis of vitiligo.

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“…Some polymorphisms in the CTLA‐4 gene have been investigated in vitiligo, but a meta‐analysis could not find a significant involvement of the CTLA‐4 +49A/G polymorphism in vitiligo. Nonetheless, such polymorphism analyses may require a large patient size in diseases with a multigenetic involvement …”

Section: Implications For Vitiligomentioning

confidence: 99%

“…CD11b+ cells are known to be able to express IDO, and IDO+CD11b+ cells are associated with increased skin graft survival . In the light of the preliminary report of successful repigmentation using tofacitinib, it should be noted that JAK1/3 inhibition was also reported to induce IDO expression in dendritic cells . This might be surprising as JAK1 inhibits IFNγ which is a major inducer of IDO.…”

Section: Preclinical Studies and Clinical Trials Influencing The Ctlamentioning

confidence: 99%

Targeting CTLA‐4, PD‐L1 and IDO to modulate immune responses in vitiligo

Speeckaert

Geel

2016

Experimental Dermatology

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For decades, an extensive debate is continued on the pathophysiology of vitiligo. Numerous hypotheses have been put forward, and many supported by well-documented arguments. Regardless of the initiating steps, most experts agree that an immune-based melanocyte destruction is responsible for the final steps leading to epidermal depigmentation. It is remarkable that currently the only therapeutic approach to counter this phenomenon consists of non-specific local and systemic immunosuppressants. Immunotherapy for melanoma reveals that targeting factors involved in peripheral tolerance are sufficient to break the natural defense mechanisms to develop skin depigmentations. Therapeutically enhancing these immune checkpoints seems therefore a promising long-term therapy for vitiligo. In this viewpoint, we propose this strategy as a promising therapeutic option for vitiligo. Several approaches are proposed with a focus on cytotoxic T-lymphocyte-associated protein 4, programmed death ligand-1 and indoleamine 2,3-dioxygenase.

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Lack of association between cytotoxic T-lymphocyte antigen-4+49A/G polymorphism and psoriasis and vitiligo: A meta-analysis of case–control studies

Cited by 12 publications

References 26 publications

Evaluation of selected mechanisms of immune tolerance in psoriasis

Evaluation of selected mechanisms of immune tolerance in psoriasis

Research Article IGF2BP2 gene polymorphism in the pathogenesis of vitiligo

Targeting CTLA‐4, PD‐L1 and IDO to modulate immune responses in vitiligo

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