Cross-disease innate gene signature: emerging diversity and abundance in RA comparing to SLE and SSc
Identifikátory výsledku
Kód výsledku v IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00098892%3A_____%2F19%3AN0000028" target="_blank" >RIV/00098892:_____/19:N0000028 - isvavai.cz</a>
Nalezeny alternativní kódy
RIV/61989592:15110/19:73594630 RIV/61989100:27240/19:10244306
Výsledek na webu
<a href="https://www.hindawi.com/journals/jir/2019/3575803/" target="_blank" >https://www.hindawi.com/journals/jir/2019/3575803/</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1155/2019/3575803" target="_blank" >10.1155/2019/3575803</a>
Alternativní jazyky
Jazyk výsledku
angličtina
Název v původním jazyce
Cross-disease innate gene signature: emerging diversity and abundance in RA comparing to SLE and SSc
Popis výsledku v původním jazyce
Over-activation of the innate immune system together with impaired downstream pathway of type I interferon-responding genes are hallmarks of rheumatoid arthritis (RA), systemic lupus erythematosus (SLE) and systemic sclerosis (SSc). To date, limited data on the cross-disease innate gene signature exists among those diseases. We compared therefore an innate gene signature of Toll-like receptors (TLRs), seven key members of the interleukin (IL)-1/IL-1R family and CXCL8/IL8 in peripheral blood mononuclear cells from well-defined patients with active stages of RA (n=36, DAS28≥3.2), SLE (n=28, SLEDAI>6), and SSc (n=22, revised EUSTAR index>2.25). Emerging diversity and abundance of innate signature in RA patients was detected: RA was characterized by upregulation of TLR3, TLR5, IL1RAP/IL1R3, IL18R1, SIGIRR/IL1R8 when compared to SSc (Pcorr<0.02) and of TLR2, TLR5, SIGIRR/IL1R8 when compared to SLE (Pcorr<0.02). Applying association rule analysis, six rules (combinations and expression of genes describing disease) were identified in RA (most frequently included high TLR3 and/or IL1RAP/IL1R3), three rules for SLE (low IL1RN and IL18R1) and SSc (low TLR5 and IL18R1). This first cross-disease study identified emerging heterogeneity in innate signature of RA patients with many upregulated innate genes comparing to SLE and SSc.
Název v anglickém jazyce
Cross-disease innate gene signature: emerging diversity and abundance in RA comparing to SLE and SSc
Popis výsledku anglicky
Over-activation of the innate immune system together with impaired downstream pathway of type I interferon-responding genes are hallmarks of rheumatoid arthritis (RA), systemic lupus erythematosus (SLE) and systemic sclerosis (SSc). To date, limited data on the cross-disease innate gene signature exists among those diseases. We compared therefore an innate gene signature of Toll-like receptors (TLRs), seven key members of the interleukin (IL)-1/IL-1R family and CXCL8/IL8 in peripheral blood mononuclear cells from well-defined patients with active stages of RA (n=36, DAS28≥3.2), SLE (n=28, SLEDAI>6), and SSc (n=22, revised EUSTAR index>2.25). Emerging diversity and abundance of innate signature in RA patients was detected: RA was characterized by upregulation of TLR3, TLR5, IL1RAP/IL1R3, IL18R1, SIGIRR/IL1R8 when compared to SSc (Pcorr<0.02) and of TLR2, TLR5, SIGIRR/IL1R8 when compared to SLE (Pcorr<0.02). Applying association rule analysis, six rules (combinations and expression of genes describing disease) were identified in RA (most frequently included high TLR3 and/or IL1RAP/IL1R3), three rules for SLE (low IL1RN and IL18R1) and SSc (low TLR5 and IL18R1). This first cross-disease study identified emerging heterogeneity in innate signature of RA patients with many upregulated innate genes comparing to SLE and SSc.
Klasifikace
Druh
J<sub>imp</sub> - Článek v periodiku v databázi Web of Science
CEP obor
—
OECD FORD obor
30226 - Rheumatology
Návaznosti výsledku
Projekt
Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.
Návaznosti
P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)<br>I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace
Ostatní
Rok uplatnění
2019
Kód důvěrnosti údajů
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Údaje specifické pro druh výsledku
Název periodika
Journal of Immunology Research
ISSN
2314-8861
e-ISSN
2314-7156
Svazek periodika
2019
Číslo periodika v rámci svazku
July 2019
Stát vydavatele periodika
GB - Spojené království Velké Británie a Severního Irska
Počet stran výsledku
10
Strana od-do
3575803
Kód UT WoS článku
000477841500001
EID výsledku v databázi Scopus
2-s2.0-85071281960