Effective Narrow-Band UVB Radiation Therapy Suppresses the IL-23/IL-17 Axis in Normalized Psoriasis Plaques

Johnson-Huang, Leanne M.; Suárez‐Fariñas, Mayte; Sullivan‐Whalen, Mary; Gilleaudeau, Patricia; Krueger, James G.; Lowes, Michelle A.

doi:10.1038/jid.2010.166

Cited by 141 publications

(132 citation statements)

References 49 publications

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“…Taken the available data on circulating T cells during biologics (39,40) and nb-UVB treatment (41,42) it is not possible to predict whether replenishment of skin T cells occur in the different treatments. The inflammatory profiles in epidermal T cells may seem contradictory to previous publications where expression analysis of full skin biopsies 6 wk after nb-UVB treatment suggested normalization of IL17A and IL22 gene expression (43,44) and highlights the importance of dissecting different T cell populations present within the different anatomical compartments of the skin.…”

Section: Discussioncontrasting

confidence: 52%

Epidermal Th22 and Tc17 Cells Form a Localized Disease Memory in Clinically Healed Psoriasis

Cheuk

Wikén

Blomqvist

et al. 2014

The Journal of Immunology

323

330

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Psoriasis is a common and chronic inflammatory skin disease in which T cells play a key role. Effective treatment heals the skin without scarring, but typically psoriasis recurs in previously affected areas. A pathogenic memory within the skin has been proposed, but the nature of such site-specific disease memory is unknown. Tissue-resident memory T (TRM) cells have been ascribed a role in immunity after resolved viral skin infections. Because of their localization in the epidermal compartment of the skin, TRM may contribute to tissue pathology during psoriasis. In this study, we investigated whether resolved psoriasis lesions contain TRM cells with the ability to maintain and potentially drive recurrent disease. Three common and effective therapies, narrowband-UVB treatment and long-term biologic treatment systemically inhibiting TNF-α or IL-12/23 signaling were studied. Epidermal T cells were highly activated in psoriasis and a high proportion of CD8 T cells expressed TRM markers. In resolved psoriasis, a population of cutaneous lymphocyte–associated Ag, CCR6, CD103, and IL-23R expressing epidermal CD8 T cells was highly enriched. Epidermal CD8 T cells expressing the TRM marker CD103 responded to ex vivo stimulation with IL-17A production and epidermal CD4 T cells responded with IL-22 production after as long as 6 y of TNF-α inhibition. Our data suggest that epidermal TRM cells are retained in resolved psoriasis and that these cells are capable of producing cytokines with a critical role in psoriasis pathogenesis. We provide a potential mechanism for a site-specific T cell–driven disease memory in psoriasis.

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Section: Discussioncontrasting

confidence: 52%

Epidermal Th22 and Tc17 Cells Form a Localized Disease Memory in Clinically Healed Psoriasis

Cheuk

Wikén

Blomqvist

et al. 2014

The Journal of Immunology

323

330

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“…UVB can inhibit the immune system from generating optimal responses to tumors, contact haptens, and various microbial antigens (Ags; viral, fungal, and parasitic) that can lead to exacerbated disease. Alternatively, immunosuppressive UVB can also be beneficial to control autoimmune diseases, such as psoriasis 1 and experimental autoimmune encephalomyelitis. 2 The epidermis of skin absorbs UVB through chromophores, including nuclear DNA, cytoplasmic tryptophan, and extracellular trans-urocanic acid (UCA).…”

mentioning

confidence: 99%

Systemic Low-Dose UVB Inhibits CD8 T Cells and Skin Inflammation by Alternative and Novel Mechanisms

Rana

Rogers

Halliday

2011

The American Journal of Pathology

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Exposure to UVB radiation before antigen delivery at an unirradiated site inhibits functional immunological responses. Mice treated dorsally with suberythemal lowdose UVB and immunized with ova in abdominal skin generated ova-specific CD8 T cells with a significantly decreased activation, expansion, and cytotoxic activity compared with unirradiated mice. UVB also impaired the delayed-type hypersensitivity (DTH) reaction to ova. Transfer of CD4 ؉ CD25 ؉ cells from UVB-exposed mice did not suppress the ova-specific CD8 T-cell response or DTH reaction in unexposed mice, confirming that systemic low-dose UVB does not induce long-lived functional regulatory CD4 ؉ CD25 ؉ T cells. Repairing cyclobutane pyrimidine dimer-type DNA damage and blocking aryl hydrocarbon receptor signaling also did not reverse the immunosuppressive effect of UVB on ova-specific CD8 T cells and DTH, suggesting that cyclobutane pyrimidine dimers and the aryl hydrocarbon receptor are not required in systemic low-dose UVBinduced immunosuppression. The known UVB chromophore, cis-urocanic acid, and reactive oxygen species triggered the inhibition of DTH caused by UVB, but they were not involved in the modulation of CD8 T cells. These findings indicate that systemic low-dose UVB impedes the primary response of antigen-specific CD8 T cells by a novel mechanism that is independent of pathways known to be involved in systemic suppression of DTH. UVB radiation (290 to 320 nm) in natural sunlight is a potent immunosuppressant. UVB can inhibit the immune system from generating optimal responses to tumors, contact haptens, and various microbial antigens (Ags; viral, fungal, and parasitic) that can lead to exacerbated disease. Alternatively, immunosuppressive UVB can also be beneficial to control autoimmune diseases, such as psoriasis 1 and experimental autoimmune encephalomyelitis. 2 The epidermis of skin absorbs UVB through chromophores, including nuclear DNA, cytoplasmic tryptophan, and extracellular trans-urocanic acid (UCA). The molecular processes that follow trigger a cascade of events that cumulates in the phenomenon of UVB-induced immunosuppression. Some of the hallmarks of this immunosuppression include UVB-induced genetic mutations in skin cells, circulation of cis-UCA from the isomerization of trans-UCA, production of reactive oxygen species (ROS), and generation of regulatory T and B cells that can transfer suppression into UVB-naïve mice. 3 Because UVB has both detrimental and beneficial effects on the immune system, it is critical to understand the mechanisms regulated by UVB so that effective prophylactic and palliative therapies can be designed for skin diseases, such as skin cancer, and immune-mediated diseases in internal organs, such as multiple sclerosis.A previous study 4 showed that UVB can inhibit CD8 and CD4 T-cell responses to haptens. In a model of contact hypersensitivity (CHS), we demonstrated that a low dose of UVB (approximately 5 minutes of summer sunlight in Sydney, Australia, at midday) is sufficient to inhibit the activati...

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“…UVB can improve the barrier function through increased expression of terminal differentiation proteins (filaggrin and involucrin) and antimicrobial peptides (AMPs) [41]. In addition, UVB has been shown to induce Tcell apoptosis in atopic skin lesions [42], and to suppress major T-cell pathways involved in AD pathogenesis namely the TH17/IL-23 and Th1 pathways [43][44][45][46]. UVB also suppresses the pro-inflammatory cytokines IL-12, IL-2 and IFN-γ, and to a lesser extent TNF-α [44].…”

Section: Groupmentioning

confidence: 99%

Estimation of Calcidiol Level in Serum of Atopic Dermatitis Patients before and after NB-UVB Phototherapy in Comparison to Oral Vitamin D Therapy

Youssef¹,

Dorgham²,

Hegazy³

et al. 2017

J Clin Exp Dermatol Res

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Effective Narrow-Band UVB Radiation Therapy Suppresses the IL-23/IL-17 Axis in Normalized Psoriasis Plaques

Cited by 141 publications

References 49 publications

Epidermal Th22 and Tc17 Cells Form a Localized Disease Memory in Clinically Healed Psoriasis

Epidermal Th22 and Tc17 Cells Form a Localized Disease Memory in Clinically Healed Psoriasis

Systemic Low-Dose UVB Inhibits CD8 T Cells and Skin Inflammation by Alternative and Novel Mechanisms

Estimation of Calcidiol Level in Serum of Atopic Dermatitis Patients before and after NB-UVB Phototherapy in Comparison to Oral Vitamin D Therapy

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