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Review
. 2020 Jan 17;21(2):625.
doi: 10.3390/ijms21020625.

Immunological Memory of Psoriatic Lesions

Agnieszka Owczarczyk Saczonek  1 , Magdalena Krajewska-Włodarczyk  2   3 , Marta Kasprowicz-Furmańczyk  1 , Waldemar Placek  1
Affiliations
Review

Immunological Memory of Psoriatic Lesions

Agnieszka Owczarczyk Saczonek et al. Int J Mol Sci. .

Abstract

The natural course of psoriasis is the appearance of new lesions in the place of previous ones, which disappeared after a successful therapy. Recent studies of psoriasis etiopathogenesis showed that after psoriatic plaques have disappeared, in healthy skin we can still find a trace of inflammation in the form of tissue resident memory cells (TRM). They are originally responsible for protection against viral and bacterial infections in non-lymphatic tissues. In psoriatic inflammation, they are characterized by heterogeneity depending on their origin. CD8+ T cells TRM are abundantly present in psoriatic epidermis, while CD4+ TRM preferentially populate the dermis. In psoriasis, epidermal CD8+ TRM cells express CLA, CCR6, CD103 and IL-23R antigen and produce IL-17A during ex vivo stimulation. However, CD4+ CD103+ TRM can also colonize the epidermis and produce IL-22 during stimulation. Besides T cells, Th22 and epidermal DCs proved that epidermal cells in healed skin were still present and functioning after several years of disease remission. It explains the clinical phenomenon of the tendency of psoriatic lesions to relapse in the same location and it allows to develop new therapeutic strategies in the future.

Keywords: IL-17; psoriasis; tissue resident memory cells.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
The relapse of psoriatic lesions in the same localization despite efficient treatment.
Figure 2
Figure 2
The receptors and secretory activity of tissue resident memory (TRM) CD8+ [5,22]
Figure 3
Figure 3
The role of TRM in psoriatic inflammation.
See this image and copyright information in PMC

References

    1. Diani M., Altomare G., Reali E. T helper cell subsets in clinical manifestations of psoriasis. J. Immunol. Res. 2016;2016:1–7. doi: 10.1155/2016/7692024. - DOI - PMC - PubMed
    1. Eberle F.C., Brück J., Holstein J., Hirahara K., Ghoreshi K. Recent advances in understanding psoriasis. F1000 Res. 2016;5:770. doi: 10.12688/f1000research.7927.1. - DOI - PMC - PubMed
    1. Matos T., O’Malley J.T., Lowry E.L., Hamm D., Kirsch I.R., Robins H.S., Kupper T.S., Krueger J.G., Clark R.A. Clinically resolved psoriatic lesions contain psoriasis-specific IL-17–producing αβ T cell clones. J. Clin. Invest. 2017;127:4031–4041. doi: 10.1172/JCI93396. - DOI - PMC - PubMed
    1. Watanabe R. Protective and pathogenic roles of resident memory T cells in human skin disorders. J. Dermatol. Sci. 2019;95:2–7. doi: 10.1016/j.jdermsci.2019.06.001. - DOI - PubMed
    1. Cheuk S., Wikén M., Blomqvist L., Nylén S., Talme T., Stàhle M., Eidsmo L. Epidermal Th22 and Tc17 cells form a localized disease memory in clinically healed psoriasis. J. Immunol. 2014;192:3111–3120. doi: 10.4049/jimmunol.1302313. - DOI - PMC - PubMed