[Role of IL-22 in the pathogenesis of skin diseases].

  title={[Role of IL-22 in the pathogenesis of skin diseases].},
  author={Hideki Fujita},
  journal={Nihon Rinsho Men'eki Gakkai kaishi = Japanese journal of clinical immunology},
  volume={35 3},
  • H. Fujita
  • Published 2012
  • Biology, Medicine
  • Nihon Rinsho Men'eki Gakkai kaishi = Japanese journal of clinical immunology
IL-22 is an IL-10 family cytokine that acts mainly on epithelial cells. It is produced by immune cell subsets, including CD4⁺ T cells, natural killer cells, and natural killer T cells. In the skin, IL-22 mediates keratinocyte proliferation and epidermal hyperplasia, inhibits terminal differentiation of keratinocytes, and induces the production of antimicrobial proteins. Although IL-22 production was initially linked with IL-17 expression in Th17 cells, IL-22 production can also occur in an… 

T‐helper 22 cells as a new player in chronic inflammatory skin disorders

The role of Th22 and its cytokine IL‐22 in the immunopathogenesis of inflammatory skin disorders such as psoriasis and atopic dermatitis is discussed.

AB0180 Plasma IL-22 Levels Correlate with Th22 Cells in Patients with New-Onset Systemic Lupus Erythematosus

Low plasma IL-22 levels may be a distinct feature in new-onset SLE and correlated with Th22 cell and SLE disease activity, and interleukin 22 serum levels are associated with radiographic progression in rheumatoid arthritis.

Impact of ROS-Dependent Lipid Metabolism on Psoriasis Pathophysiology

The analysis of the influence of oxidative stress and its consequences for metabolic changes, including lipidomic ones, in psoriasis may be of diagnostic and therapeutic importance.

Control of inflammation, helper T cell responses and regulatory T cell function by Bcl6

A key function for Bcl6 in repressing Gata3 function and miR-21 expression in Tregs is defined, and greater understanding of the control of Th2 inflammatory responses by Treg cells is provided.

Decreased Plasma IL‐22 Levels and Correlations with IL‐22‐Producing T Helper Cells in Patients with New‐Onset Systemic Lupus Erythematosus

Low plasma IL‐22 levels and correlation with Th22 cells may be distinct features in new‐onset SLE, and high frequencies of plasma IL-22 autoantibodies were detected in new-onsetSLE patients, while IL‐ 22 and Th22 cell correlated with SLE disease activity.

Bedside to bench: defining the immunopathogenesis of psoriatic arthritis

Data from clinical trials of novel targeted therapies for psoriatic arthritis and other autoimmune diseases, which have produced sometimes surprising results, can inform the understanding of the immunopathogenesis of these diseases and help to identify the most relevant therapeutic targets.

Cannabidiol Modifies the Formation of NETs in Neutrophils of Psoriatic Patients

It is suggested that psoriatic patients neutrophils are at a higher risk of NETosis both in vitro and in vivo, possibly due to its antioxidant properties.



Interleukin-22, a TH17 cytokine, mediates IL-23-induced dermal inflammation and acanthosis

The results suggest that TH17 cells, through the production of both IL-22 and IL-17, might have essential functions in host defence and in the pathogenesis of autoimmune diseases such as psoriasis.

Human Langerhans cells induce distinct IL-22-producing CD4+ T cells lacking IL-17 production

The ability of cutaneous resident dendritic cells (DCs) to differentiate IL-22-producing cells is investigated and indicates that cutaneous DCs, especially LCs, may control the generation of distinct IL- 22 producing Th22 cells infiltrating into the skin.

The Effects of IL-20 Subfamily Cytokines on Reconstituted Human Epidermis Suggest Potential Roles in Cutaneous Innate Defense and Pathogenic Adaptive Immunity in Psoriasis

It is shown that primary human keratinocytes express receptors for these cytokines and that IL-20 subfamily cytokines induce acanthosis in reconstituted human epidermis (RHE) in a dose-dependent manner.

IL-22 and IL-20 are key mediators of the epidermal alterations in psoriasis while IL-17 and IFN-γ are not

It is suggested that different cytokines are players in the psoriasis pathogenesis although only the IL-10 family members IL-22 and IL-20 directly cause the characteristic epidermal alterations.

IL-22 is required for Th17 cell-mediated pathology in a mouse model of psoriasis-like skin inflammation.

It is proposed that IL-22 antagonism might be a promising therapy for the treatment of human psoriasis, which is induced by the transfer of CD4(+)CD45RB(hi)CD25(-) cells to pathogen-free scid/scid mice.

Th17 cytokines stimulate CCL20 expression in keratinocytes in vitro and in vivo: implications for psoriasis pathogenesis.

It is shown that Th17 cytokines stimulate CCL20 production in vitro and in vivo, and thus provide a potential explanation of how CCR6-positive Th17 cells maintain their continual presence in psoriasis through a positive chemotactic feedback loop.

Low Expression of the IL-23/Th17 Pathway in Atopic Dermatitis Compared to Psoriasis1

Evidence is presented that the IL-23/Th17 axis is largely absent in atopic dermatitis, perhaps accounting for recurrent skin infections in this disease.

Possible pathogenic role of Th17 cells for atopic dermatitis.

Investigation of the involvement of T helper cell 17 (Th17) in atopic dermatitis (AD) found a significant correlation between the percentages of IL-17+ and IFN-gamma+ cells, although percentage of Th17 cells was not closely related to Th1/Th2 balance.

Th22 cells represent a distinct human T cell subset involved in epidermal immunity and remodeling.

A subset of human Th cells that infiltrates the epidermis in individuals with inflammatory skin disorders and is characterized by the secretion of IL-22 and TNF-alpha, but not IFN-gamma, IL-4, or IL-17 is identified.

A role for T cell‐derived interleukin 22 in psoriatic skin inflammation

The results reported in this study indicate that IL‐22 is a cytokine produced by skin‐infiltrating lymphocytes that is potentially involved in initiation and/or maintenance of the pathogenesis of psoriasis.