Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2015 Jun;73(2):342-50.
doi: 10.1016/j.cyto.2014.12.014. Epub 2015 Jan 10.

Cytokines in psoriasis

Jaymie Baliwag  1 , Drew H Barnes  1 , Andrew Johnston  2
Affiliations
Review

Cytokines in psoriasis

Jaymie Baliwag et al. Cytokine. 2015 Jun.

Abstract

Psoriasis is a common inflammatory skin disease with an incompletely understood etiology. The disease is characterized by red, scaly and well-demarcated skin lesions formed by the hyperproliferation of epidermal keratinocytes. This hyperproliferation is driven by cytokines secreted by activated resident immune cells, an infiltrate of T cells, dendritic cells and cells of the innate immune system, as well as the keratinocytes themselves. Psoriasis has a strong hereditary character and has a complex genetic background. Genome-wide association studies have identified polymorphisms within or near a number of genes encoding cytokines, cytokine receptors or elements of their signal transduction pathways, further implicating these cytokines in the psoriasis pathomechanism. A considerable number of inflammatory cytokines have been shown to be elevated in lesional psoriasis skin, and the serum concentrations of a subset of these also correlate with psoriasis disease severity. The combined effects of the cytokines found in psoriasis lesions likely explain most of the clinical features of psoriasis, such as the hyperproliferation of keratinocytes, increased neovascularization and skin inflammation. Thus, understanding which cytokines play a pivotal role in the disease process can suggest potential therapeutic targets. A number of cytokines have been therapeutically targeted with success, revolutionizing treatment of this disease. Here we review a number of key cytokines implicated in the pathogenesis of psoriasis.

Keywords: Cytokine; Inflammation; Interleukin; Psoriasis; Skin.

PubMed Disclaimer

Figures

Fig. 1
Fig. 1
Plaque psoriasis lesions. Characteristic well-demarcated skin lesions, common on the elbows, knees, trunk and extensor surfaces of the limbs (a). Immunofluorescent staining of a biopsy of lesional psoriasis skin showing infiltration of CD4+ T cells (red) in the dermis and CD8+ T cells (green) in the dermal and epidermal compartments. Cell nuclei counterstained with DAPI (blue). 100× original magnification. Photo courtesy of Dr. Johann E. Gudjonsson, University of Michigan Medical School. (For interpretation of the references to color in this figure legend, the reader is referred to the web version of this article.)
Fig. 2
Fig. 2
Psoriasis lesions contain multiple up-regulated cytokines. RNA-seq data [11] queried for transcripts of interleukins 1 through 38. Values calculated for the fold change in reads per kilobase of transcript per million mapped reads (RKPM) of involved skin vs. uninvolved skin.
Fig. 3
Fig. 3
Psoriasis is now regarded as a mixed Th1/Th17 disease as products of these cells dominate the cytokine network in psoriasis and drive the keratinocyte hyperproliferation and skin inflammation characteristic of this disease. Treatments targeting TNF-α (etanercept, adalimumab, infliximab), IL-12/23p40 (ustekinumab), and more recently IL-17A (secukinumab, ixekinumab), and the IL-17 receptor (brodalumab), are proving effective in decreasing psoriasis disease severity (indicated in green, for details see main text). On the other hand, inhibition of IL-1α/β, IL-6, IFN-γ have thus far proven ineffective (red). Other members of the cytokine network such as IL-19, 20, 22 (fezakinumab), IL-20R1 and IL-20R2, and IL-23p19 (CNTO1959), as well as the IL-36 cytokines and their receptor are now being explored as potential targets for new interventions (blue). The efficacy of any anti-psoriatic treatment likely depends on its ability to disassemble the inflammatory cytokine network, by targeting a critical component and also the remarkable synergies between component cytokines. (For interpretation of the references to color in this figure legend, the reader is referred to the web version of this article.)
See this image and copyright information in PMC

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Parisi R, Symmons DP, Griffiths CE, Ashcroft DM. Global epidemiology of psoriasis: a systematic review of incidence and prevalence. J Invest Dermatol. 2012 - PubMed
    1. Bata-Csorgo Z, Hammerberg C, Voorhees JJ, Cooper KD. Flow cytometric identification of proliferative subpopulations within normal human epidermis and the localization of the primary hyperproliferative population in psoriasis. J Exp Med. 1993;178:1271–81. - PMC - PubMed
    1. Di Cesare A, Di Meglio P, Nestle FO. The IL-23/Th17 axis in the immunopathogenesis of psoriasis. J Invest Dermatol. 2009;129:1339–50. - PubMed
    1. Zaba LC, Suarez-Farinas M, Fuentes-Duculan J, Nograles KE, Guttman-Yassky E, Cardinale I, et al. Effective treatment of psoriasis with etanercept is linked to suppression of IL-17 signaling, not immediate response TNF genes. J Allergy Clin Immunol. 2009;124:1022-10 e1–395. - PMC - PubMed
    1. Hijnen D, Knol EF, Gent YY, Giovannone B, Beijn SJ, Kupper TS, et al. CD8(+) T cells in the lesional skin of atopic dermatitis and psoriasis patients are an important source of IFN-gamma, IL-13, IL-17, and IL-22. J Invest Dermatol. 2013;133:973–9. - PMC - PubMed

Publication types