Sökning: WFRF:(Karagianni M.) > Tumor Necrosis Fact...
Fältnamn | Indikatorer | Metadata |
---|---|---|
000 | 02558naa a2200469 4500 | |
001 | oai:DiVA.org:uu-220607 | |
003 | SwePub | |
008 | 140317s2013 | |||||||||||000 ||eng| | |
024 | 7 | a https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-2206072 URI |
040 | a (SwePub)uu | |
041 | a engb eng | |
042 | 9 SwePub | |
072 | 7 | a ref2 swepub-contenttype |
072 | 7 | a art2 swepub-publicationtype |
100 | 1 | a Kumari, S.4 aut |
245 | 1 0 | a Tumor Necrosis Factor Receptor Signaling in Keratinocytes Triggers Interleukin-24-Dependent Psoriasis-like Skin Inflammation in Mice |
264 | 1 | c 2013 |
338 | a print2 rdacarrier | |
520 | a Psoriasis is a common chronic inflammatory skin disease with a prevalence of about 2% in the Caucasian population. Tumor necrosis factor (TNF) plays an essential role in the pathogenesis of psoriasis, but its mechanism of action remains poorly understood. Here we report that the development of psoriasis-like skin inflammation in mice with epidermis-specific inhibition of the transcription factor NF-κB was triggered by TNF receptor 1 (TNFR1)-dependent upregulation of interleukin-24 (IL-24) and activation of signal transducer and activator of transcription 3 (STAT3) signaling in keratinocytes. IL-24 was strongly expressed in human psoriatic epidermis, and pharmacological inhibition of NF-κB increased IL-24 expression in TNF-stimulated human primary keratinocytes, suggesting that this mechanism is relevant for human psoriasis. Therefore, our results expand current views on psoriasis pathogenesis by revealing a new keratinocyte-intrinsic mechanism that links TNFR1, NF-κB, ERK, IL-24, IL-22R1, and STAT3 signaling to disease initiation. | |
653 | a Psoriasis | |
653 | a NFkappaB | |
653 | a TNF | |
653 | a inflammation | |
653 | a skin | |
653 | a IL-24 | |
653 | a Medical Science | |
653 | a Medicinsk vetenskap | |
700 | 1 | a Bonnet, M. C.4 aut |
700 | 1 | a Ulvmar, Maria Helena,d 1974-u Karolinska Institutet,Taija Mäkinen4 aut |
700 | 1 | a Wolk, K.4 aut |
700 | 1 | a Karagianni, N.4 aut |
700 | 1 | a Witte, E.4 aut |
700 | 1 | a Uthoff-Hachenberg, C.4 aut |
700 | 1 | a Renauld, J.-C.4 aut |
700 | 1 | a Kollias, G.4 aut |
700 | 1 | a Toftgard, R.4 aut |
700 | 1 | a Sabat, R.4 aut |
700 | 1 | a Pasparakis, M.4 aut |
700 | 1 | a Haase, I.4 aut |
710 | 2 | a Karolinska Institutetb Taija Mäkinen4 org |
773 | 0 | t Immunityg 5:39, s. 899-911q 5:39<899-911x 1074-7613x 1097-4180 |
856 | 4 8 | u https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-220607 |
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