RIP(K)ing away immunotherapy resistance

Mira A Patel; Sohail F Tavazoie

doi:10.1016/j.immuni.2022.03.010

RIP(K)ing away immunotherapy resistance

Immunity. 2022 Apr 12;55(4):580-582. doi: 10.1016/j.immuni.2022.03.010.

Authors

Mira A Patel¹, Sohail F Tavazoie²

Affiliations

¹ Laboratory of Systems Cancer Biology, The Rockefeller University, 1230 York Avenue, New York, NY 10065, USA. Electronic address: mpatel@rockefeller.edu.
² Laboratory of Systems Cancer Biology, The Rockefeller University, 1230 York Avenue, New York, NY 10065, USA. Electronic address: stavazoie@rockefeller.edu.

PMID: 35417670
DOI: 10.1016/j.immuni.2022.03.010

Abstract

Interferon signaling mediates resistance to immune checkpoint blockade therapy, but the underlying mechanisms are poorly understood. In this issue of Immunity, Cucolo et al. identify RIPK1 as an interferon-stimulated gene with potent effects on cell extrinsic and intrinsic immunotherapy resistance.

Publication types

Comment

MeSH terms

Drug Resistance, Neoplasm*
Humans
Immunologic Factors
Immunotherapy*
Interferons
Neoplasms*
Receptor-Interacting Protein Serine-Threonine Kinases*

Substances

Immunologic Factors
Interferons
RIPK1 protein, human
Receptor-Interacting Protein Serine-Threonine Kinases

Grants and funding

R35 CA274446/CA/NCI NIH HHS/United States