Coordinated induction by IL15 of a TCR-independent NKG2D signaling pathway converts CTL into lymphokine-activated killer cells in celiac disease

Bertrand Meresse, Zhangguo Chen, Cezary Ciszewski, Maria Tretiakova, Govind Bhagat, Thomas N. Krausz, David H. Raulet, Lewis L. Lanier, Veronika Groh, Thomas Spies, Ellen C. Ebert, Peter H. Green, Bana Jabri

Research output: Contribution to journalArticlepeer-review

715 Scopus citations

Abstract

A major function of NKG2D linking innate and adaptive immunity is to upregulate antigen-specific CTL-mediated cytotoxicity in tissues expressing stress-induced NKG2D ligands, such as MIC, by coactivating TCR signaling. Here, we show that, under conditions of dysregulated IL15 expression in vivo in patients with celiac disease and in vitro in healthy individuals, multiple steps of the NKG2D/DAP10 signaling pathway leading to ERK and JNK activation are coordinately primed to activate direct cytolytic function independent of TCR specificity in effector CD8 T cells. These findings may not only explain previous reports of transformation of CTL into NK-like "lymphokine- activated killers" (LAK cells) under high doses of IL2 (a substitute for IL15) but may also have significant implications for understanding and treating immunopathological diseases.

Original languageEnglish
Pages (from-to)357-366
Number of pages10
JournalImmunity
Volume21
Issue number3
DOIs
StatePublished - Sep 2004
Externally publishedYes

Fingerprint

Dive into the research topics of 'Coordinated induction by IL15 of a TCR-independent NKG2D signaling pathway converts CTL into lymphokine-activated killer cells in celiac disease'. Together they form a unique fingerprint.

Cite this