Comparison of expression of heat‐shock protein 60, Toll‐like receptors 2 and 4, and T‐cell receptor γδ in plaque and guttate psoriasis

Seung, Na Reu; Park, Eun Joo; Kim, Chul Woo; Kim, Kwang Ho; Kim, Kwang Joong; Cho, Hee Jin; Park, Hye Rim

doi:10.1111/j.1600-0560.2007.00756.x

Cited by 77 publications

(52 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The association of this disease with streptococcal throat infections supports the hypothesis that pathogenic T cells are specific determinants common to streptococcal M protein and keratin (48), but this observation might only be relevant for a subset of patients. The role of gd T lymphocytes, which are activated by unconventional Ags, has been poorly studied in psoriasis, although there is evidence for local recruitment of these cells in psoriatic lesions (49). Interestingly, the Ags recognized by gd T cells include nonpeptide compounds associated with MHC-like molecules such as CD1 (50,51).…”

Section: Discussionmentioning

confidence: 99%

IL-22 Is Required for Imiquimod-Induced Psoriasiform Skin Inflammation in Mice

Belle

Heusch

Lemaire

et al. 2012

The Journal of Immunology

256

234

View full text Add to dashboard Cite

Psoriasis is a common chronic autoimmune skin disease of unknown cause that involves dysregulated interplay between immune cells and keratinocytes. IL-22 is a cytokine produced by the TH1, TH17, and TH22 subsets that are functionally implicated in the psoriatic pathology. We assessed the role of IL-22 in a mouse model where psoriasiform skin inflammation is triggered by topical application of the TLR7/8 agonist imiquimod. At the macroscopic level, scaly skin lesions induced by daily applications of imiquimod in wild-type mice were almost totally absent in IL-22–deficient mice or in mice treated with a blocking anti–IL-22 Ab. At the microscopic level, IL-22–deficient mice showed a dramatic decrease in the development of pustules and a partial decrease in acanthosis. At the molecular level, the absence or inhibition of IL-22 strongly decreased the expression of chemotactic factors such as CCL3 and CXCL3 and of biomarkers such as S100A8, S100A7, and keratin 14, which reflect the antimicrobial and hyperproliferative responses of keratinocytes. IL-22 also played a major role in neutrophil infiltration after imiquimod treatment. IL-23 was required for IL-22 production, and γδ TCR lymphocytes represented the major source of IL-22 in lymph nodes from imiquimod-treated mice. However, T cells were not absolutely required for IL-22 production because imiquimod-induced IL-22 expression in the skin is still preserved in Rag2−/− mice. Taken together, our data show that IL-22 is required for psoriasis-like lesions in the mouse imiquimod model and is produced by both T cells and innate immune cells.

show abstract

Section: Discussionmentioning

confidence: 99%

IL-22 Is Required for Imiquimod-Induced Psoriasiform Skin Inflammation in Mice

Belle

Heusch

Lemaire

et al. 2012

The Journal of Immunology

256

234

View full text Add to dashboard Cite

show abstract

“…Moreover, gd T cells, including those expressing the cutaneous lymphocyteassociated Ag, have been reported to be present in greater numbers in guttate and plaque psoriasis lesions (18,19). Interestingly, peripheral gd T cells express high levels of IL-23R and respond to IL-1b and IL-23 by producing IL-17 and IL-22 (7).…”

Section: Discussionmentioning

confidence: 99%

Epidermal CCR6+ γδ T Cells Are Major Producers of IL-22 and IL-17 in a Murine Model of Psoriasiform Dermatitis

Mabuchi

Takekoshi

Hwang

2011

The Journal of Immunology

144

138

View full text Add to dashboard Cite

Cytokine components of Th17 pathway play vital roles in human psoriasis. Although much is known about TCR αβ T cells in psoriasis, the role of unconventional T cells, including γδ T cells, is unclear. In this study, using an IL-23 skin injection model of psoriasiform dermatitis in mice, we demonstrate that IL-22, IL-17A, and the IL-23R were highly enriched in a population of CCR6+, TCR γδ-low expressing (GDL) T cells that accumulated in the epidermis after IL-23 injections. GDL cells were distinct from resident TCR γδ-high, Vγ3+,CCR6− T cells in the epidermis that did not change appreciably in numbers following IL-23 injection. Large numbers of CCR6+ cells were detected at or above the level of the epidermal basement membrane by confocal microscopy 5 d after repeated IL-23 injections at the same time GDL cells increased in numbers in the epidermis. TCR δ-deficient mice (lacking γδ T cells) exhibited decreased ear swelling and downregulated expression of IL-22 and IL-17A in the epidermis following IL-23 injection. Our data suggest that a subset of γδ T cells play a critical role in IL-23–mediated psoriasiform dermatitis.

show abstract

“…The actions of Hsp60 could lead to the modification of those proteins, and in this manner it could have a role in many diseases, including carcinogenesis. Heart Heart failure; Coronary vascular disease [137][138][139][140] Kidney Glomerulonephritis [141] Large bowel Inflammatory bowel diseases [19,142,143] Lung Chonic obstructive pulmonary disease [20] Oral cavity Periodontitis [144,145] Pancreas Type 1 diabetes [146][147][148][149][150][151] Skin Scleroderma, pemphigoid; Psoriasis; Dermatomyositis [152,153] Synovial joints Rheumatoid arthritis; Juvenile idiopathic arthritis [154][155][156][157] Vessels Vasculitis; Atherosclerosis [158][159][160][161][162][163][164][165][166][167] Adapted from [2]. Hsp60 seems to contribute to tumor cell survival, but this is controversial.…”

Section: Hsp60 Chaperonopathies and Chaperonotherapy: Targets And Agentsmentioning

confidence: 99%

Hsp60 chaperonopathies and chaperonotherapy: targets and agents

Cappello

Gammazza

Piccionello

et al. 2013

Expert Opinion on Therapeutic Targets

140

133

View full text Add to dashboard Cite

Comparison of expression of heat‐shock protein 60, Toll‐like receptors 2 and 4, and T‐cell receptor γδ in plaque and guttate psoriasis

Abstract: HSP60 may be related to the pathogenesis of both guttate and plaque psoriasis and TLR4 may be related to the pathogenesis of guttate psoriasis.

Cited by 77 publications

References 22 publications

IL-22 Is Required for Imiquimod-Induced Psoriasiform Skin Inflammation in Mice

IL-22 Is Required for Imiquimod-Induced Psoriasiform Skin Inflammation in Mice

Epidermal CCR6+ γδ T Cells Are Major Producers of IL-22 and IL-17 in a Murine Model of Psoriasiform Dermatitis

Hsp60 chaperonopathies and chaperonotherapy: targets and agents

Contact Info

Product

Resources

About