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001-es BibID:BIBFORM032051
Első szerző:Fekete Tünde (immunológus, molekuláris biológus, mikrobiológus)
Cím:Constraints for monocyte-derived dendritic cell functions under inflammatory conditions / Fekete Tünde, Szabo Attila, Beltrame Luca, Vivar Nancy, Pivarcsi Andor, Lanyi Arpad, Cavalieri Duccio, Rajnavölgyi Eva, Rethi Bence
Dátum:2012
ISSN:0014-2980
Megjegyzések:The activation of TLRs expressed by macrophages or DCs, in the long run, leads to persistently impaired functionality. TLR signals activate a wide range of negative feedback mechanisms; it is not known, however, which of these can lead to long-lasting tolerance for further stimulatory signals. In addition, it is not yet understood how the functionality of monocyte-derived DCs (MoDCs) is influenced in inflamed tissues by the continuous presence of stimulatory signals during their differentiation. Here we studied the role of a wide range of DC-inhibitory mechanisms in a simple and robust model of MoDC inactivation induced by early TLR signals during differentiation. We show that the activation-induced suppressor of cytokine signaling 1 (SOCS1), IL-10, STAT3, miR146a and CD150 (SLAM) molecules possessed short-term inhibitory effects on cytokine production but did not induce persistent DC inactivation. On the contrary, the LPS-induced IRAK-1 downregulation could alone lead to persistent MoDC inactivation. Studying cellular functions in line with the activation-induced negative feedback mechanisms, we show that early activation of developing MoDCs allowed only a transient cytokine production that was followed by the downregulation of effector functions and the preservation of a tissue-resident non-migratory phenotype.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
DC
Endotoxin tolerance
IRAK-1
TLR
Megjelenés:European Journal of Immunology 42 : 2 (2012), p. 458-469. -
További szerzők:Szabó Attila (1981-) (molekuláris biológus, immunológus, filozófus) Beltrame, Luca Vivar, Nancy Pivarcsi Andor Lányi Árpád (1962-) (biológus, immunológus) Cavalieri, Duccio Rajnavölgyi Éva (1950-) (immunológus) Réthi Bence (1973-) (biológus, immunológus)
Pályázati támogatás:TORNADO 222720 (felhívás kód: FP7-KBBE-2007-2A)
FP7
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2.

001-es BibID:BIBFORM065601
Első szerző:Pivarcsi Andor
Cím:Expression and function of Toll-like receptors 2 and 4 in human keratinocytes / Andor Pivarcsi, Laszlo Bodai, Bence Réthi, Anna Kenderessy-Szabó, Andrea Koreck, Márta Széll, Zsuzsanna Beer, Zsuzsanna Bata-Csörgő, Mária Magócsi, Éva Rajnavölgyi, Attila Dobozy, Lajos Kemény
Dátum:2003
ISSN:1460-2377
Megjegyzések:Keratinocytes have the ability to kill pathogenic fungi and bacteria by producing antimicrobial substances. Recent studies suggest that microbial components use signaling molecules of the human Toll-like receptor (TLR) family to transduce signals in various cells. Here we provide evidence that keratinocytes express both TLR2 and TLR4 at the mRNA and protein levels, and show that TLR2 and TLR4 are present in the normal human epidermis in vivo and that their expression is regulated by microbial components. The expression of myeloid differentiation protein gene (MyD88), which is involved in the signaling pathway of many TLR, was also demonstrated in keratinocytes. LPS + IFN-gamma increased the expression of TLR2 and TLR4 50- and 5-fold respectively. Treatment of keratinocytes with Candida albicans, mannan, Mycobacterium tuberculosis or LPS with IFN-gamma resulted in the activation and nuclear translocation of NF-kappaB. Inhibition of NF-kappaB blocked the Candida-killing activity of keratinocytes, suggesting that the antimicrobial effect of keratinocytes requires NF-kappaB activation. LPS + IFN-gamma, C. albicans (4 Candida/KC), peptidoglycan (1 micro g/ml) or M. tuberculosis extract significantly increased IL-8 gene expression after 3 h of treatment (P < 0.05). The increases over the 0-h level were 15-, 8-, 10.8- and 7-fold, respectively. The microbial compound-induced increase in IL-8 gene expression could be inhibited by anti-TLR2 and anti-TLR4 neutralizing antibodies, suggesting that TLRs are involved in the pathogen-induced expression of this pro-inflammatory cytokine. Our findings stress the importance of the role of keratinocytes as a component of innate immunity.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
epidermis
host defense
IL-8
innate immunity
NF-kB
Megjelenés:International Immunology 15 : 6 (2003), p. 721-730. -
További szerzők:Bodai László Réthi Bence (1973-) (biológus, immunológus) Kenderessy Szabó Anna Koreck Andrea Széll Márta Beer Zsuzsanna Bata-Csörgő Zsuzsanna Magócsi Mária Rajnavölgyi Éva (1950-) (immunológus) Dobozy Attila Kemény Lajos
Pályázati támogatás:T 032496
OTKA
T 030749
OTKA
T 032498
OTKA
T 032494
OTKA
FKFP 1271
Egyéb
FKFP 0222
Egyéb
AKP grant 2000-151 3,2
Egyéb
EU5 QLK4-CT2001-00366
Egyéb
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DOI
Intézményi repozitóriumban (DEA) tárolt változat
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