Imperial College London

Avinash R. Shenoy

Faculty of MedicineDepartment of Medicine

Non-Clinical Lecturer in Molecular Microbiology



+44 (0)20 7594 3785a.shenoy Website




4.40AFlowers buildingSouth Kensington Campus






BibTex format

author = {Matsuzawa, T and Kim, B-H and Shenoy, AR and Kamitani, S and Miyake, M and Macmicking, JD},
doi = {10.4049/jimmunol.1102041},
journal = {J Immunol},
pages = {813--818},
title = {IFN-γ elicits macrophage autophagy via the p38 MAPK signaling pathway.},
url = {},
volume = {189},
year = {2012}

RIS format (EndNote, RefMan)

AB - Autophagy is a major innate immune defense pathway in both plants and animals. In mammals, this cascade can be elicited by cytokines (IFN-γ) or pattern recognition receptors (TLRs and nucleotide-binding oligomerization domain-like receptors). Many signaling components in TLR- and nucleotide-binding oligomerization domain-like receptor-induced autophagy are now known; however, those involved in activating autophagy via IFN-γ remain to be elucidated. In this study, we engineered macrophages encoding a tandem fluorescently tagged LC3b (tfLC3) autophagosome reporter along with stably integrated short hairpin RNAs to demonstrate IFN-γ-induced autophagy required JAK 1/2, PI3K, and p38 MAPK but not STAT1. Moreover, the autophagy-related guanosine triphosphatase Irgm1 proved dispensable in both stable tfLC3-expressing RAW 264.7 and tfLC3-transduced Irgm1(-/-) primary macrophages, revealing a novel p38 MAPK-dependent, STAT1-independent autophagy pathway that bypasses Irgm1. These unexpected findings have implications for understanding how IFN-γ-induced autophagy is mobilized within macrophages for inflammation and host defense.
AU - Matsuzawa,T
AU - Kim,B-H
AU - Shenoy,AR
AU - Kamitani,S
AU - Miyake,M
AU - Macmicking,JD
DO - 10.4049/jimmunol.1102041
EP - 818
PY - 2012///
SP - 813
TI - IFN-γ elicits macrophage autophagy via the p38 MAPK signaling pathway.
T2 - J Immunol
UR -
UR -
VL - 189
ER -