Aplikace anti-CD40 protilátky zvyšuje imunitní odpověď na slabé nádorové antigeny

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11120%2F07%3A00000465" target="_blank" >RIV/00216208:11120/07:00000465 - isvavai.cz</a>

Výsledek na webu

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DOI - Digital Object Identifier

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Jazyk výsledku

angličtina

Název v původním jazyce

Anti-CD40 conditioning enhances the T(CD8) response to a highly tolerogenic epitope and subsequent immunotherapy of simian virus 40 T antigen-induced pancreatic tumors

Popis výsledku v původním jazyce

Rapid loss of adoptively transferred tumor-specific CD8(+) T cells (T-CD8) following Ag recognition in the periphery and their limited accumulation within the tumor stroma reduces the effectiveness of T cell-based immunotherapy. To better understand therole of T-CD8 in the control of autochthonous tumors, we have used mice of the RIP1-Tag4 lineage that develop pancreatic beta cell tumors due to expression of the SV40 large T Ag from the rat insulin promoter. We previously showed that the kinetics of functional T-CD8 tolerance varies toward two distinct epitopes derived from T Ag. Epitope I ((206)SAINNYAQKL(215))-specific T-CD8 are rapidly deleted whereas T-CD8 targeting epitope IV (404VVYDFLKC411) persist over the lifetime of tumor-bearing animals. Inthis report, we show that the conditioning of tumor-bearing RIP1-Tag4 mice with agonistic anti-CD40 Ab induces extensive expansion of naive epitope I-specific TCR transgenic (TCR-I) T cells in this tolerogenic environment and delays thei

Název v anglickém jazyce

Anti-CD40 conditioning enhances the T(CD8) response to a highly tolerogenic epitope and subsequent immunotherapy of simian virus 40 T antigen-induced pancreatic tumors

Popis výsledku anglicky

Rapid loss of adoptively transferred tumor-specific CD8(+) T cells (T-CD8) following Ag recognition in the periphery and their limited accumulation within the tumor stroma reduces the effectiveness of T cell-based immunotherapy. To better understand therole of T-CD8 in the control of autochthonous tumors, we have used mice of the RIP1-Tag4 lineage that develop pancreatic beta cell tumors due to expression of the SV40 large T Ag from the rat insulin promoter. We previously showed that the kinetics of functional T-CD8 tolerance varies toward two distinct epitopes derived from T Ag. Epitope I ((206)SAINNYAQKL(215))-specific T-CD8 are rapidly deleted whereas T-CD8 targeting epitope IV (404VVYDFLKC411) persist over the lifetime of tumor-bearing animals. Inthis report, we show that the conditioning of tumor-bearing RIP1-Tag4 mice with agonistic anti-CD40 Ab induces extensive expansion of naive epitope I-specific TCR transgenic (TCR-I) T cells in this tolerogenic environment and delays thei

Druh

J_x - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)

CEP obor

FN - Epidemiologie, infekční nemoci a klinická imunologie

OECD FORD obor

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Projekt

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Návaznosti

V - Vyzkumna aktivita podporovana z jinych verejnych zdroju

Rok uplatnění

2007

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Journal of Immunology

ISSN

0022-1767

e-ISSN

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Svazek periodika

179

Číslo periodika v rámci svazku

10

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

10

Strana od-do

6686-6695

Kód UT WoS článku

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EID výsledku v databázi Scopus

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