Naslov
Damage and stress-associated signals as inducers of endoplasmic reticulum resident heat shock protein gp96, natural killer T and regulatory T cells

Autori
Radošević-Stašić, Biserka ; Jakovac, Hrvoje ; Mrakovčić-Šutić, Ines ; Grebić, Damir ; Rukavina, Daniel.

Vrsta, podvrsta i kategorija rada
Sažeci sa skupova, sažetak, znanstveni

Izvornik
Porto 08 Abstracts / Shoenfeld Yehuda - Ženeva : C/o Kenes International, 2008, 329-329

Skup
6th International Congress on Autoimmunity

Mjesto i datum
Porto, Portugal, 10.09.2008. - 14.09.2008

Vrsta sudjelovanja
Poster

Vrsta recenzije
Međunarodna recenzija

Ključne riječi
endoplasmic reticulum resident heat shock protein gp96; liver regeneration; stress; PGM-Zn; damage

Sažetak
Various kinds of tissue disintegration lead in the endoplasmic reticulum (ER) to activation of the ER stress response, which is directed to correction of unfolded proteins, to the activation of proteasome-dependent degradation of the misfolded proteins and to activation of protein translation that modulate the polypeptide traffic into the ER. A crucial role in these events plays gp96, which acts not only as a molecular chaperone, but also as an adjuvant, able to induce the specific immune response against some self and foreign antigens. response, which is directed to correction of unfolded proteins, to the activation of proteasome-dependent degradation of the misfolded proteins and to activation of protein translation that modulate the polypeptide traffic into the ER. A crucial role in these events plays gp96, which acts not only as a molecular chaperone, but also as an adjuvant, able to induce the specific immune response against some self and foreign antigens. Trying to estimate its possible link with the development of autoimmunity in this study we analyzed the interplay between the gp96, NKT and Treg in the conditions of: 1) normal growth, induced by partial hepatectomy, 2) psychosocial stress without the tissue lesions and 3) after the treatment with bacterial peptidoglycan-monomer. Tissue expression of gp96 protein and mRNA were estimated in liver, thymus and spleen and the data were correlated with phenotype and cytotoxicity of hepatic and splenic MNLC against the NK and NKT-sensitive targets. All procedures induced fast cytoplasmic overexpression of gp96 protein and mRNA in hepatocytes and in the thymus. Simultaneously, in the liver accumulated NKT and Treg cells, while hepatic and splenic MNLC became highly cytotoxic against syngeneic thymocytes and YAC-1, implying that during the disturbance of morphostasis gp96 acts as a natural adjuvant for chaperoning of self peptides into the immune surveillance pathway, leading to activation of autoreactive NKT and Treg cells that participate in reestablishment of self tolerance.

Izvorni jezik
Engleski

Znanstvena područja
Temeljne medicinske znanosti

POVEZANOST RADA