학술논문

ILC1 Confer Early Host Protection at Initial Sites of Viral Infection
Document Type
article
Source
Cell. 171(4)
Subject
Medical Microbiology
Biomedical and Clinical Sciences
Immunology
Infectious Diseases
HIV/AIDS
Digestive Diseases
2.1 Biological and endogenous factors
Underpinning research
1.1 Normal biological development and functioning
Aetiology
Infection
Inflammatory and immune system
Animals
Herpesviridae Infections
Immunity
Innate
Immunologic Surveillance
Inflammation
Interferon-gamma
Killer Cells
Natural
Liver
Lymphocytes
Mice
Inbred C57BL
Muromegalovirus
Peritoneal Cavity
Virus Replication
ILC1
MCMV
cDC1
infection
influenza
innate immunity
sendai virus
tissue-resident
Biological Sciences
Medical and Health Sciences
Developmental Biology
Biological sciences
Biomedical and clinical sciences
Language
Abstract
Infection is restrained by the concerted activation of tissue-resident and circulating immune cells. Whether tissue-resident lymphocytes confer early antiviral immunity at local sites of primary infection prior to the initiation of circulating responses is not well understood. Furthermore, the kinetics of initial antiviral responses at sites of infection remain unclear. Here, we show that tissue-resident type 1 innate lymphoid cells (ILC1) serve an essential early role in host immunity through rapid production of interferon (IFN)-γ following viral infection. Ablation of Zfp683-dependent liver ILC1 lead to increased viral load in the presence of intact adaptive and innate immune cells critical for mouse cytomegalovirus (MCMV) clearance. Swift production of interleukin (IL)-12 by tissue-resident XCR1+ conventional dendritic cells (cDC1) promoted ILC1 production of IFN-γ in a STAT4-dependent manner to limit early viral burden. Thus, ILC1 contribute an essential role in viral immunosurveillance at sites of initial infection in response to local cDC1-derived proinflammatory cytokines.