The Imbalance of Th17 cells and <scp>CD</scp>4+<scp>CD</scp>25highFoxp3+ Treg cells in patients with atopic dermatitis

Ma, Lei; Xue, Haibo; Guan, Xiu-Hao; Shu, Chen; Wang, F.; Zhang, J.-H.; An, Rong‐Zhen

doi:10.1111/jdv.12288

Cited by 70 publications

(63 citation statements)

References 30 publications

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“…As compared with healthy controls (4.06% Tregs), significantly decreased levels of Tregs were recorded (1.6%) in eight individuals with skin sensitization to unspecified allergens, despite the fact that the average length of time since diagnosis was only 54 days. 27 Perhaps the most interesting report came from a study of melanoma patients who received an in vivo infusion of a recombinant IL-2-diphtheria toxin fusion protein, which depleted Tregs from~3% (3.5%-2%) to~2% (2.5%-1%) of CD4 + cells. Prior to depletion, only weak contact allergic responses were provoked by sensitization with the potent contact allergen diphencyprone, whereas, after depletion, very vigorous elicitation reactions to this allergen were recorded.…”

Section: Discussionmentioning

confidence: 99%

T lymphocyte phenotype of contact‐allergic patients: experience with nickel and p‐phenylenediamine

et al. 2019

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Background: There is considerable interest in understanding the immunological variables that have the greatest influence on the effectiveness of sensitization by contact allergens, particularly in the context of developing new paradigms for risk assessment of novel compounds.Objectives: To examine the relationship between patch test score for three different contact allergens and the characteristics of T cell responses.Methods: A total of 192 patients with confirmed nickel, p-phenylenediamine (PPD) or methylisothiazolinone (MI) allergy were recruited from the Contact Dermatitis Investigation Unit at Salford Royal Hospital. Severity of allergy was scored by the use of patch testing, peripheral blood lymphocytes were characterized for T cell phenotype by flow cytometry, and proliferative activity was characterized by radiolabelled thymidine incorporation. Comparisons were drawn with buffy coat samples from healthy volunteers.Results: Patch test positivity for nickel, PPD and MI was associated with changes in the phenotype of peripheral blood T cells: increases in naïve cells, decreases in regulatory T cell frequency and the CD4 + /CD8 hi ratio, and increased expression of the skin-homing marker cutaneous lymphocyte antigen (CLA), particularly for those patients with a +++ patch test score.Conclusions: This increased understanding of the characteristics of the T cell responses to contact allergens may provide parameters with which to better measure health risks associated with skin sensitization. K E Y W O R D SCD4, CD8, inverted CD4/CD8, skin-homing CLA, lymphocyte transformation test, T cell phenotype, RRID:SCR_001905

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Section: Discussionmentioning

confidence: 99%

T lymphocyte phenotype of contact‐allergic patients: experience with nickel and p‐phenylenediamine

et al. 2019

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“…Quantitative real-time PCR was performed on a CFX96 Real-Time PCR system (Bio-Rad), as per the manufacturer’s instructions, using gene-specific primers for human T-bet, GATA-3, RORγt, Foxp3, and GAPDH (as internal control) (see Table I for a list of all primers). Relative gene expression was quantified by normalizing Ct values with the corresponding GAPDH value (22–24). …”

Section: Methodsmentioning

confidence: 99%

Biotin Deficiency Induces Th1- and Th17-Mediated Proinflammatory Responses in Human CD4+ T Lymphocytes via Activation of the mTOR Signaling Pathway

Elahi

Sabui

Narasappa

et al. 2018

The Journal of Immunology

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Biotin (vitamin B7) is essential for human health because of its involvement, as a cofactor, in a variety of critical cellular metabolic reactions. Previous studies have shown that biotin deficiency enhances inflammation, and certain chronic inflammatory diseases are associated with biotin deficiency; however, the mechanisms that mediate the association between biotin status and inflammation are not well understood. In this study, we examined the effect of biotin deficiency on human CD4+ T cell responses to determine their role in biotin deficiency–associated inflammation. Our investigations revealed that anti-CD3/CD28–stimulated CD4+ T cells cultured in biotin-deficient medium secreted significantly enhanced levels of the proinflammatory cytokines IFN-γ, TNF, and IL-17. Expression of the transcription factors T-bet and RORγt was increased, whereas Foxp3 expression was decreased, in biotin-deficient CD4+ T cells. The percentage of T regulatory cells was also decreased under biotin-deficient condition. A similar increase in T-bet, RORγt, and proinflammatory cytokine levels, as well as a decrease in Foxp3, was observed in inguinal lymph nodes of mice fed a biotin-deficient diet relative to pair-fed controls. Furthermore, differentiation of CD4+ T cells toward Th1 and Th17 cells was also enhanced. In vitro and in vivo investigations indicated that the increased inflammatory response was due to enhanced activation of the mammalian target of rapamycin signaling pathway in biotin-deficient CD4+ T cells. In summary, these results demonstrate that biotin deficiency enhances the inflammatory responses in CD4+ T cells, which may contribute to inflammation associated with biotin deficiency.

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“…108 Th17 cells are increased in both skin 52e54 and blood of patients with AD. 109 In a mouse model of AD deficiency of filaggrin appeared to be a driver of increased peripheral levels of Th17 cells. The authors hypothesized that this increase must be acquired as peripheral Th17 cells were found only in adult mice indicating involvement of exogenous factors.…”

Section: Il-17 and Neutrophilic Endotypementioning

confidence: 99%

Endotypes of allergic diseases and asthma: An important step in building blocks for the future of precision medicine

Agache

Akdiş

2016

Allergology International

163

140

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Discoveries from basic science research in the last decade have brought significant progress in knowledge of pathophysiologic processes of allergic diseases, with a compelling impact on understanding of the natural history, risk prediction, treatment selection or mechanism-specific prevention strategies. The view of the pathophysiology of allergic diseases developed from a mechanistic approach, with a focus on symptoms and organ function, to the recognition of a complex network of immunological pathways. Several subtypes of inflammation and complex immune-regulatory networks and the reasons for their failure are now described, that open the way for the development of new diagnostic tools and innovative targeted-treatments. An endotype is a subtype of a disease condition, which is defined by a distinct pathophysiological mechanism, whereas a disease phenotype defines any observable characteristic of a disease without any implication of a mechanism. Another key word linked to disease endotyping is biomarker that is measured and evaluated to examine any biological or pathogenic processes, including response to a therapeutic intervention. These three keywords will be discussed more and more in the future with the upcoming efforts to revolutionize patient care in the direction of precision medicine and precision health. The understanding of disease endotypes based on pathophysiological principles and their validation across clinically meaningful outcomes in asthma, allergic rhinitis, chronic rhinosinusitis, atopic dermatitis and food allergy will be crucial for the success of precision medicine as a new approach to patient management.

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The Imbalance of Th17 cells and CD4⁺CD25^highFoxp3⁺ Treg cells in patients with atopic dermatitis

Abstract: In AD, there exists an immune imbalance in Th17 and Treg cells, which may contribute to its pathogenesis and development.

Cited by 70 publications

References 30 publications

T lymphocyte phenotype of contact‐allergic patients: experience with nickel and p‐phenylenediamine

T lymphocyte phenotype of contact‐allergic patients: experience with nickel and p‐phenylenediamine

Biotin Deficiency Induces Th1- and Th17-Mediated Proinflammatory Responses in Human CD4+ T Lymphocytes via Activation of the mTOR Signaling Pathway

Endotypes of allergic diseases and asthma: An important step in building blocks for the future of precision medicine

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The Imbalance of Th17 cells and CD4+CD25highFoxp3+ Treg cells in patients with atopic dermatitis

Abstract: In AD, there exists an immune imbalance in Th17 and Treg cells, which may contribute to its pathogenesis and development.

Cited by 70 publications

References 30 publications

T lymphocyte phenotype of contact‐allergic patients: experience with nickel and p‐phenylenediamine

T lymphocyte phenotype of contact‐allergic patients: experience with nickel and p‐phenylenediamine

Biotin Deficiency Induces Th1- and Th17-Mediated Proinflammatory Responses in Human CD4+ T Lymphocytes via Activation of the mTOR Signaling Pathway

Endotypes of allergic diseases and asthma: An important step in building blocks for the future of precision medicine

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The Imbalance of Th17 cells and CD4⁺CD25^highFoxp3⁺ Treg cells in patients with atopic dermatitis