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Literature summary for 3.4.21.78 extracted from

  • Cheuk, S.; Martini, E.; Bergh, K.; Chang, D.; Rethi, B.; Staehle, M.; Eidsmo, L.
    Granzyme A potentiates chemokine production in IL-17-stimulated keratinocytes (2017), Exp. Dermatol., 26, 824-827 .
    View publication on PubMed
Search for more literature for 3.4.21.78

Organism

Organism UniProt Comment Textmining
Homo sapiens P12544
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Source Tissue

Source Tissue Comment Organism Textmining
keratinocyte
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 Homo sapiens
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neutrophil
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 Homo sapiens
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skin
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 Homo sapiens
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T-lymphocyte CD8+ cell Homo sapiens
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Synonyms

Synonyms Comment Organism
Gzma
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 Homo sapiens

General Information

General Information Comment Organism
metabolism CD8 T cells in psoriasis skinlesions display a dominant expression of granzyme A (GzmA) over granzyme B in the absence of perforin expression. Signals recruiting GzmA+ T cells into the skin and triggers of GzmA expression in the context of chronic inflammation, Tc17-polarizing conditions favour development of GzmA+GzmB-Prf-CD8 T-cells in the context of psoriasis Homo sapiens
physiological function interleukin-17 induced secretion of the cytokines interleukin-6, interleukin-8 and interleukin-23, whereas GzmA treatment alone does not induce secretion of inflammatory mediators. The combination of GzmA and interleukin-17 significantly increases the release of the proinflammatory chemokines CXCL 1, CXCL 12, and CCL 4 compared to interleukin-17 stimulation alone, but does not alter the levels of interleukin-17-induced cytokines interleukin-6, interleukin-8 and interleukin-23. GzmA neither promotes proliferation nor affects interleukin-17-induced keratinocyte differentiation status as measured by gene expression of MKI67, IVL, KRT16 or KRT10 Homo sapiens