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Pregled bibliografske jedinice broj: 1050179

The Role of Cd8(+) T-Cells and their Cytokines in the Pathogenesis of Psoriasis


Volarić, Iva; Vičić, Marijana; Prpić-Massari, Larisa
The Role of Cd8(+) T-Cells and their Cytokines in the Pathogenesis of Psoriasis // Acta dermatovenerologica Croatica, 27 (2019), 3; 159-162 (međunarodna recenzija, pregledni rad, znanstveni)


CROSBI ID: 1050179 Za ispravke kontaktirajte CROSBI podršku putem web obrasca

Naslov
The Role of Cd8(+) T-Cells and their Cytokines in the Pathogenesis of Psoriasis

Autori
Volarić, Iva ; Vičić, Marijana ; Prpić-Massari, Larisa

Izvornik
Acta dermatovenerologica Croatica (1330-027X) 27 (2019), 3; 159-162

Vrsta, podvrsta i kategorija rada
Radovi u časopisima, pregledni rad, znanstveni

Ključne riječi
cytokines ; CD8(+) T-cells ; IFN-gamma ; TNF-alpha ; IL-17 ; IL-22

Sažetak
The important role of CD8(+) T-cells in the pathogenesis of psoriasis is well-determined. However, besides type 1 cytokines that were formerly known, it was recently found that these cells secrete type 17 and type 22 cytokines. The majority of IL-17A(+)CD8(+) T- cells in the blood belong to a subset of innate T-cells named mucosa-associated invariant T- cells (MAIT). However, the majority of IL- 17A(+)CD8(+) T-cells in psoriatic epidermis are conventional T-cells and are up-regulated in psoriasis. In contrast to Th17 cells that secrete only IL-17, Tc17 cells secrete IFN- gamma, TNF-alpha, CCL20, IL-22, and granzyme B as well. The key cytokine is IL-17A, which promotes keratinocyte hyperproliferation and stimulates them to produce other proinflammatory cytokines. These activities initiate and propagate the inflammation and architectural changes in the skin that clinically manifest as psoriatic lesions. However, a relatively novel cell subtype named Tc22 has been discovered in psoriasis that could secrete IL-22 in the absence of IL-17 and IFN-gamma. IL-22 stimulates proliferation and de-differentiation of keratinocytes, subsequently leading to epidermal acanthosis. As the understanding of the pathogenesis of psoriasis increases, the new selective therapies may offer an optimal balance between increased clinical benefit and reduced risk of side-effects.

Izvorni jezik
Engleski

Znanstvena područja
Kliničke medicinske znanosti



POVEZANOST RADA


Ustanove:
Medicinski fakultet, Rijeka,
Klinički bolnički centar Rijeka

Profili:

Avatar Url Marijana Vičić (autor)

Avatar Url Larisa Prpić Massari (autor)

Poveznice na cjeloviti tekst rada:

hrcak.srce.hr

Citiraj ovu publikaciju:

Volarić, Iva; Vičić, Marijana; Prpić-Massari, Larisa
The Role of Cd8(+) T-Cells and their Cytokines in the Pathogenesis of Psoriasis // Acta dermatovenerologica Croatica, 27 (2019), 3; 159-162 (međunarodna recenzija, pregledni rad, znanstveni)
Volarić, I., Vičić, M. & Prpić-Massari, L. (2019) The Role of Cd8(+) T-Cells and their Cytokines in the Pathogenesis of Psoriasis. Acta dermatovenerologica Croatica, 27 (3), 159-162.
@article{article, author = {Volari\'{c}, Iva and Vi\v{c}i\'{c}, Marijana and Prpi\'{c}-Massari, Larisa}, year = {2019}, pages = {159-162}, keywords = {cytokines, CD8(+) T-cells, IFN-gamma, TNF-alpha, IL-17, IL-22}, journal = {Acta dermatovenerologica Croatica}, volume = {27}, number = {3}, issn = {1330-027X}, title = {The Role of Cd8(+) T-Cells and their Cytokines in the Pathogenesis of Psoriasis}, keyword = {cytokines, CD8(+) T-cells, IFN-gamma, TNF-alpha, IL-17, IL-22} }
@article{article, author = {Volari\'{c}, Iva and Vi\v{c}i\'{c}, Marijana and Prpi\'{c}-Massari, Larisa}, year = {2019}, pages = {159-162}, keywords = {cytokines, CD8(+) T-cells, IFN-gamma, TNF-alpha, IL-17, IL-22}, journal = {Acta dermatovenerologica Croatica}, volume = {27}, number = {3}, issn = {1330-027X}, title = {The Role of Cd8(+) T-Cells and their Cytokines in the Pathogenesis of Psoriasis}, keyword = {cytokines, CD8(+) T-cells, IFN-gamma, TNF-alpha, IL-17, IL-22} }

Časopis indeksira:


  • Web of Science Core Collection (WoSCC)
    • Science Citation Index Expanded (SCI-EXP)
    • SCI-EXP, SSCI i/ili A&HCI
  • Scopus
  • MEDLINE





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