Could basement membrane alterations, resembling micro-wounds at the dermo-epidermal junction in psoriatic non-lesional skin, make the skin susceptible to lesion formation?
Current data suggest that tissue microenvironment control immune functions. Therefore, understanding the tissue environment in which immune activation occurs will enhance our capability to interfere with abnormal immune pathology. Here, we argue that studying the constitutively abnormal functions of...
Elmentve itt :
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| Dokumentumtípus: | Cikk |
| Megjelent: |
2020
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| Sorozat: | EXPERIMENTAL DERMATOLOGY
30 No. 6 |
| doi: | 10.1111/exd.14267 |
| mtmt: | 31798342 |
| Online Access: | http://publicatio.bibl.u-szeged.hu/20278 |
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| 040 | |a SZTE Publicatio Repozitórium |b hun | ||
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| 100 | 1 | |a Bozó Renáta | |
| 245 | 1 | 0 | |a Could basement membrane alterations, resembling micro-wounds at the dermo-epidermal junction in psoriatic non-lesional skin, make the skin susceptible to lesion formation? |h [elektronikus dokumentum] / |c Bozó Renáta |
| 260 | |c 2020 | ||
| 300 | |a 765-772 | ||
| 490 | 0 | |a EXPERIMENTAL DERMATOLOGY |v 30 No. 6 | |
| 520 | 3 | |a Current data suggest that tissue microenvironment control immune functions. Therefore, understanding the tissue environment in which immune activation occurs will enhance our capability to interfere with abnormal immune pathology. Here, we argue that studying the constitutively abnormal functions of clinically uninvolved psoriatic skin in patients with plaque type psoriasis is very important to better understand psoriasis pathobiology, because non-lesional skin provides the tissue environment in which the psoriatic lesion develops. A key question in psoriasis is what initiates the abnormal, uncontrolled immune activation in the first place and the answer may lie in the skin. In light of this concept, we summarize abnormalities at the dermal-epidermal junction region which shows a special "nonhealing-like" micro-wound phenotype in the psoriatic non-lesional skin that may act as a crucial susceptibility factor in the development of the disease. | |
| 700 | 0 | 1 | |a Flink Lili Borbála |e aut |
| 700 | 0 | 1 | |a Belső Nóra |e aut |
| 700 | 0 | 2 | |a Konczné Gubán Barbara |e aut |
| 700 | 0 | 2 | |a Széll Márta |e aut |
| 700 | 0 | 2 | |a Kemény Lajos |e aut |
| 700 | 0 | 2 | |a Csörgő Sándorné Bata Zsuzsanna |e aut |
| 856 | 4 | 0 | |u http://publicatio.bibl.u-szeged.hu/20278/1/3Br.exd.14267.pdf |z Dokumentum-elérés |