Chronic inflammation in immune aging: role of pattern recognition receptor crosstalk with the telomere complex?
Identifikátory výsledku
Kód výsledku v IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00159816%3A_____%2F17%3A00067117" target="_blank" >RIV/00159816:_____/17:00067117 - isvavai.cz</a>
Nalezeny alternativní kódy
RIV/00216224:14110/17:00099687 RIV/65269705:_____/17:00067117
Výsledek na webu
<a href="http://journal.frontiersin.org/article/10.3389/fimmu.2017.01078/abstract" target="_blank" >http://journal.frontiersin.org/article/10.3389/fimmu.2017.01078/abstract</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.3389/fimmu.2017.01078" target="_blank" >10.3389/fimmu.2017.01078</a>
Alternativní jazyky
Jazyk výsledku
angličtina
Název v původním jazyce
Chronic inflammation in immune aging: role of pattern recognition receptor crosstalk with the telomere complex?
Popis výsledku v původním jazyce
Age-related decline in immunity is characterized by stem cell exhaustion, telomere shortening, and disruption of cell-to-cell communication, leading to increased patient risk of disease. Recent data have demonstrated that chronic inflammation exerts a strong influence on immune aging and is closely correlated with telomere length in a range of major pathologies. The current review discusses the impact of inflammation on immune aging, the likely molecular mediators of this process, and the various disease states that have been linked with immunosenescence. Emerging findings implicate NFkB, the major driver of inflammatory signaling, in several processes that regulate telomere maintenance and/or telomerase activity. While prolonged triggering of pattern recognition receptors is now known to promote immunosenescence, it remains unclear how this process is linked with the telomere complex or telomerase activity. Indeed, enzymatic control of telomere length has been studied for many decades, but alternative roles of telomerase and potential influences on inflammatory responses are only now beginning to emerge. Crosstalk between these pathways may prove to be a key molecular mechanism of immunosenescence. Understanding how components of immune aging interact and modify host protection against pathogens and tumors will be essential for the design of new vaccines and therapies for a wide range of clinical scenarios.
Název v anglickém jazyce
Chronic inflammation in immune aging: role of pattern recognition receptor crosstalk with the telomere complex?
Popis výsledku anglicky
Age-related decline in immunity is characterized by stem cell exhaustion, telomere shortening, and disruption of cell-to-cell communication, leading to increased patient risk of disease. Recent data have demonstrated that chronic inflammation exerts a strong influence on immune aging and is closely correlated with telomere length in a range of major pathologies. The current review discusses the impact of inflammation on immune aging, the likely molecular mediators of this process, and the various disease states that have been linked with immunosenescence. Emerging findings implicate NFkB, the major driver of inflammatory signaling, in several processes that regulate telomere maintenance and/or telomerase activity. While prolonged triggering of pattern recognition receptors is now known to promote immunosenescence, it remains unclear how this process is linked with the telomere complex or telomerase activity. Indeed, enzymatic control of telomere length has been studied for many decades, but alternative roles of telomerase and potential influences on inflammatory responses are only now beginning to emerge. Crosstalk between these pathways may prove to be a key molecular mechanism of immunosenescence. Understanding how components of immune aging interact and modify host protection against pathogens and tumors will be essential for the design of new vaccines and therapies for a wide range of clinical scenarios.
Klasifikace
Druh
J<sub>imp</sub> - Článek v periodiku v databázi Web of Science
CEP obor
—
OECD FORD obor
30102 - Immunology
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)
Ostatní
Rok uplatnění
2017
Kód důvěrnosti údajů
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Údaje specifické pro druh výsledku
Název periodika
Frontiers in Immunology
ISSN
1664-3224
e-ISSN
—
Svazek periodika
8
Číslo periodika v rámci svazku
SEP
Stát vydavatele periodika
CH - Švýcarská konfederace
Počet stran výsledku
10
Strana od-do
1078
Kód UT WoS článku
000409062200001
EID výsledku v databázi Scopus
—