Dermal Clusters of Mature Dendritic Cells and T Cells Are Associated with the CCL20/CCR6 Chemokine System in Chronic Psoriasis

Kim, Tae Kyun; Jee, Hyunseok; Fuentes‐Duculan, Judilyn; Wu, Wen‐guey; Byamba, Dashlkhumbe; Kim, Dae Suk; Kim, Do Young; Lew, Dae Hyun; Yang, Woo Ik; Krueger, James G.; Lee, Min Geol

doi:10.1038/jid.2013.534

Cited by 73 publications

(80 citation statements)

References 15 publications

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“…2F, G), constitute lymphoid tissuelike structures mimicking the T-cell areas of secondary lymphoid organs. 47,89,90 CCL19, a lymphoid-organizing chemokine, is selectively produced within dermal aggregates and recruits CCR7 1 (self-antigen-specific) T cells and DCs into this focus (see Fig. 2H).…”

Section: Immunologic Contributions To Histopathologic Changesmentioning

confidence: 99%

“…90 CCR6, a receptor for CCL20 attracting myeloid DCs and T cells, is also coexpressed in T cells and almost all the mature dermal myeloid DCs in the dermal aggregates. 89 These CCL19/CCR7 and CCL20/CCR6 chemokine systems may be crucial in selfmaintaining the interaction between lesional mature DCs and T cells where T cells are effectively activated in situ. 89,90 SUMMARY Clinical and translational research in human subjects has enabled a better understanding of the immunology of psoriasis, and subsequently the development of novel immune-targeted therapeutics.…”

Section: Immunologic Contributions To Histopathologic Changesmentioning

confidence: 99%

“…89 These CCL19/CCR7 and CCL20/CCR6 chemokine systems may be crucial in selfmaintaining the interaction between lesional mature DCs and T cells where T cells are effectively activated in situ. 89,90 SUMMARY Clinical and translational research in human subjects has enabled a better understanding of the immunology of psoriasis, and subsequently the development of novel immune-targeted therapeutics. IL-23/T17 is now recognized as the major axis of the psoriatic immune pathway, and antagonists to IL-23 or IL-17 result in the ability to control most of the signs and symptoms of clinical disease in approximately 80% of patients with psoriasis.…”

Section: Immunologic Contributions To Histopathologic Changesmentioning

confidence: 99%

See 2 more Smart Citations

The Immunopathogenesis of Psoriasis

Kim

Krueger

2015

Dermatologic Clinics

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281

227

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Section: Immunologic Contributions To Histopathologic Changesmentioning

confidence: 99%

Section: Immunologic Contributions To Histopathologic Changesmentioning

confidence: 99%

Section: Immunologic Contributions To Histopathologic Changesmentioning

confidence: 99%

See 1 more Smart Citation

The Immunopathogenesis of Psoriasis

Kim

Krueger

2015

Dermatologic Clinics

Self Cite

281

227

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“…The proportion of T-cells proliferating was clearly higher in the let-7a inhibitor group, while it was significantly lower in the let-7a mimics group, which might be due to the targeting of STAT3 by let-7a. A marked increase in the number of proliferating memory-type T-cells has been observed in lesional psoriasis due to the continuous activation of lesional antigen-presenting cells [37]. Moreover, psoriasis is a T-cell driven chronic inflammatory skin disease, and both T helper (Th) 1 and Th17 cells participate in psoriasis pathogenesis [38].…”

Section: Discussionmentioning

confidence: 99%

Let-7a Inhibits T-Cell Proliferation and IFN-γ Secretion by Down-Regulating STAT3 Expression in Patients with Psoriasis

Xie

Chen

et al. 2017

Cell Physiol Biochem

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Objective: This study aimed to explore the effects of STAT3 targeting by let-7a on T-cell proliferation and IFN-γ secretion in psoriasis. Methods: From January 2013 to January 2015, 40 patients with psoriasis (psoriasis group) and 38 volunteers undergoing plastic surgery (control group) were enrolled in this study. Pearson correlation analysis was performed to evaluate the correlation between let-7a and STAT3 expression. T-cells were isolated and subjected to different transfection methods. A dual luciferase reporter assay was carried out to confirm STAT3 as a target gene of let-7a. Let-7a, STAT3 and IFN-γ mRNA expression was detected by quantitative real-time fluorescent polymerase chain reaction (qRT-PCR), and pSTAT3 protein levels were determined by Western blot. T-cell proliferation was evaluated with a cell counting kit-8 (CCK-8) assay. Results: The level of STAT3 mRNA and pSTAT3 was higher, but let-7a expression was lower in the psoriasis group than the control group. Pearson correlation analysis indicated that STAT3 expression was negatively correlated with let-7a expression. T-cells transfected with inhibitors exhibited greater IFN-γ mRNA expression and T-cell proliferation than transfected T-cells and T-cells transfected with a non-sense sequence, while T-cells transfected with let-7a mimics exhibited lower IFN-γ mRNA expression and T-cell proliferation than transfected T-cells and T-cells transfected with a non-sense sequence. This suggested that siRNA-STAT3 could reverse the increase in IFN-y mRNA expression and T-cell proliferation induced by let-7a inhibitors. Conclusion: Our results demonstrated that let-7a inhibits T-cell proliferation and IFN-γ secretion by down-regulating STAT3 in psoriasis.

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“…More recently, dermal clusters of CD4+ T cells with DC and Mø were found in healthy skin at homeostasis [70], as well as in inflamed human skin, following infections [58,71], cutaneous adverse reactions [72,] and autoinflammatory skin diseases [73]. Clustered CD4+ T cells in the skin lesions of patients with genital herpes and in patients with psoriasis expressed CCR5, CCR6, and CCR4, thus suggesting that recruitment and retention of skin-tropic T cells through chemokines contributed to the formation of clusters [58,71,73]. Whether the protective T cell pool contained CD69+ Trm was, however, not investigated.…”

Section: Innate Immune Cell Determinants Of Cutaneous T Cell Responsesmentioning

confidence: 99%

Modulation of CD4+ T Helper Cell Memory Responses in the Human Skin

Padovan

2017

Int Arch Allergy Immunol

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Immunological memory is defined as the capacity to mount faster and more effective immune responses against antigenic challenges that have been previously encountered by the host. CD4+ T helper (Th) cells play central roles in the establishment of immunological memory as they assist the functions of other leukocytes. Th cells express polarized cytokine profiles and distinct migratory and seeding capacities, but also retain a certain functional plasticity that allows them to modulate their proliferation, activity, and homing behaviour upon need. Thus, in healthy individuals, T cell immunomodulation fulfils the task of eliciting protective immune responses where they are needed. At times, however, Th plasticity can lead to collateral tissue damage and progression to autoimmune diseases or, conversely, incapacity to reject malignant tissues and clear chronic infections. Furthermore, common immune players and molecular pathways of diseases can lead to different outcomes in different individuals. A mechanistic understanding of those pathways is therefore crucial for developing precise and curative medical interventions. Here, I focus on the skin microenvironment and comprehensively describe some of the cellular and molecular determinants of CD4+ T cell memory responses in homeostatic and pathological conditions. In discussing the cellular network orchestrating cutaneous immunity, I comprehensively describe the bidirectional interaction of skin antigen-presenting cells and mononuclear phagocytes with Th17 lymphocytes, and examine how the outcome of this interaction is influenced by endogenous skin molecules, including sodium salts and neuropeptides.

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Dermal Clusters of Mature Dendritic Cells and T Cells Are Associated with the CCL20/CCR6 Chemokine System in Chronic Psoriasis

Abstract: PLINK: a tool set for whole-genome association and population-based linkage analyses.

Cited by 73 publications

References 15 publications

The Immunopathogenesis of Psoriasis

The Immunopathogenesis of Psoriasis

Let-7a Inhibits T-Cell Proliferation and IFN-γ Secretion by Down-Regulating STAT3 Expression in Patients with Psoriasis

Modulation of CD4+ T Helper Cell Memory Responses in the Human Skin

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