A skewed pool of resident T cells triggers psoriasis-associated tissue responses in never-lesional skin from patients with psoriasis

Sérézal, Irène Gallais; Hoffer, Elena; Ignatov, Borislav; Martini, Elisa; Zitti, Beatrice; Ehrström, Marcus; Eidsmo, Liv

doi:10.1016/j.jaci.2018.08.048

Cited by 68 publications

(54 citation statements)

References 56 publications

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“…At the same time psoriasis plaques showed IL-17-induced response patterns, indicating a relapse. The proportional amount of induced IFN-γ, IL-10e and IL-17A correlated with relapse time in patients after discontinuation of the treatment [38].…”

Section: Tissue Resident Memory Cells In Psoriasismentioning

confidence: 92%

“…Therefore, psoriatic lesions preferentially recur in previously affected areas of the skin, and pathogenic TRM cells exposed to IL-17A and IL-22 accumulate in resolved lesions [5,35]. In the study of Gallais Serezal et al [38], tissue responses after T cell stimulation in healthy and psoriatic lesions were analyzed. An increase in the number of epidermal IL-17 and IL-22-producing skin-resident T CCR6 + cells-may be a genetically predisposed reaction to microbial stimulation in never-lesional skin in patients with psoriasis.…”

Section: Tissue Resident Memory Cells In Psoriasismentioning

confidence: 99%

See 1 more Smart Citation

Immunological Memory of Psoriatic Lesions

Owczarczyk‐Saczonek

Krajewska–Włodarczyk

Kasprowicz-Furmańczyk

et al. 2020

IJMS

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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.

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Section: Tissue Resident Memory Cells In Psoriasismentioning

confidence: 92%

Section: Tissue Resident Memory Cells In Psoriasismentioning

confidence: 99%

Immunological Memory of Psoriatic Lesions

Owczarczyk‐Saczonek

Krajewska–Włodarczyk

Kasprowicz-Furmańczyk

et al. 2020

IJMS

View full text Add to dashboard Cite

show abstract

“…Keratinocytes in never-lesional skin, which has never experienced disease formation, of psoriasis patients are also reported to be involved in accumulation of T RM . Never-lesional keratinocytes are prone to upregulate CCL20 expression under stimulation with psoriasis-related cytokines, which leads to migration of CCR6expressing IL-17A-generating T cells [33]. Actually, psoriatic neverlesional epidermis is enriched with CD103 + CD8 T RM with the potential of producing IL-17A.…”

Section: Psoriasismentioning

confidence: 99%

Protective and pathogenic roles of resident memory T cells in human skin disorders

Watanabe

2019

Journal of Dermatological Science

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A B S T R A C TThe human skin is populated by recirculating T cells and skin-sessile resident memory T cells (T RM ). Skin T RM are constructed during immune responses against antigens that the host immune system encounters in the skin. T RM persist in the same sites for a long time and play important protective roles in skin immune responses in collaboration with other skin-composing cells such as dendritic cells and keratinocytes. These T RM with strong effector functions possibly also engender skin inflammatory disorders. Since human skin T cells, especially T RM , are phenotypically distinct from T cells in the blood circulation, T cells residing in the skin should be directly investigated, without presuming from the activities of blood T cells, in order to understand the functional characteristics of skin T cells in skin disorders. This review summarizes the features of human skin T RM and reviews the immunopathological involvement of T RM in human skin disorders such as infectious disease, inflammatory skin disease, and malignant skin tumors.

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“…Moreover, CCR6+ CD4+ T cells were capable of producing IFNγ and IL-17. These results suggested that pathogenic TRMs do exist in non-lesional skin [80].…”

Section: Cellular Scarmentioning

confidence: 79%

“…Moreover, pathogenic memory T cells seem to persist at sites of clinically resolved psoriatic lesions. Even after long-term therapy, these cells do not lose their ability to produce IL-17A [76,78], which can signal to keratinocytes and stimulate their proliferation [80]. Although the role of innate cells has not been studied extensively, Langerhans cells isolated from resolved psoriatic lesions can produce IL-23 after stimulation, which makes them another potential player in the restart of activation of "sleeping" TRMs [83] and possible reappearance of psoriatic lesions [76] (Fig.…”

Section: Conclusion and Open Questionsmentioning

confidence: 99%

Resolution of plaque-type psoriasis: what is left behind (and reinitiates the disease)

Benezeder

Wolf

2019

Semin Immunopathol

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Psoriasis is a chronic inflammatory skin disease that involves numerous types of immune cells and cytokines resulting in an inflammatory feedback loop and hyperproliferation of the epidermis. A more detailed understanding of the underlying pathophysiology has revolutionized anti-psoriatic treatment and led to the development of various new drugs targeting key inflammatory cytokines such as IL-17A and IL-23. Successfully treated psoriatic lesions often resolve completely, leaving nothing visible to the naked eye. However, such lesions tend to recur within months at the exact same body sites. What is left behind at the cellular and molecular levels that potentially reinitiates psoriasis? Here, we elucidate the cellular and molecular "scar" and its imprints left after clinical resolution of psoriasis treated with anti-TNFα, anti-IL-17, or anti-IL-23 antibodies or phototherapy. Hidden cytokine stores and remaining tissue-resident memory T cells (TRMs) might hold the clue for disease recurrence.

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A skewed pool of resident T cells triggers psoriasis-associated tissue responses in never-lesional skin from patients with psoriasis

Cited by 68 publications

References 56 publications

Immunological Memory of Psoriatic Lesions

Immunological Memory of Psoriatic Lesions

Protective and pathogenic roles of resident memory T cells in human skin disorders

Resolution of plaque-type psoriasis: what is left behind (and reinitiates the disease)

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