Jörg H. Fritz

ORCID: 0000-0003-3411-1238
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About
Contact & Profiles
Research Areas
  • Immune Cell Function and Interaction
  • Immune Response and Inflammation
  • IL-33, ST2, and ILC Pathways
  • Eosinophilic Esophagitis
  • T-cell and B-cell Immunology
  • Immunotherapy and Immune Responses
  • interferon and immune responses
  • Inflammasome and immune disorders
  • Pediatric health and respiratory diseases
  • Immune cells in cancer
  • Gut microbiota and health
  • Bacterial Infections and Vaccines
  • Immunodeficiency and Autoimmune Disorders
  • Asthma and respiratory diseases
  • Viral gastroenteritis research and epidemiology
  • Antimicrobial Peptides and Activities
  • Atherosclerosis and Cardiovascular Diseases
  • Influenza Virus Research Studies
  • Salmonella and Campylobacter epidemiology
  • Neutrophil, Myeloperoxidase and Oxidative Mechanisms
  • Dietary Effects on Health
  • HIV Research and Treatment
  • Invertebrate Immune Response Mechanisms
  • Autophagy in Disease and Therapy
  • Adipokines, Inflammation, and Metabolic Diseases

McGill University
2016-2025

McGill University Health Centre
2018-2025

University of Toronto
2006-2011

Memorial University of Newfoundland
2011

Hôpital Robert-Debré
2009

Freie Universität Berlin
2009

Canada Research Chairs
2007

University of New Brunswick
2007

Institut Pasteur
2005-2006

Innate immunity represents an important system with a variety of vital processes at the core many diseases. In recent years, central role Nod-like receptor (NLR) protein family became increasingly appreciated in innate immune responses. NLRs are classified as part signal transduction ATPases numerous domains (STAND) clade within AAA+ ATPase family. They typically feature N-terminal effector domain, nucleotide-binding domain (NACHT) and C-terminal ligand-binding region that is composed...

10.1371/journal.pone.0002119 article EN cc-by PLoS ONE 2008-04-29

Muropeptides are degradation products of bacterial peptidoglycan (PG) sensed by nucleotide-binding oligomerization domain 1 (NOD1) and NOD2, members a recently discovered family pattern recognition molecules (PRM). One these muropeptides, muramyl dipeptide (MDP) mediates cell signaling exerts adjuvant activity synergizes with lipopolysaccharide (LPS) to induce pro-inflammatory responses in vitro vivo. In contrast, few contradictory results exist about the stimulatory capacity NOD1 agonists....

10.1002/eji.200526286 article EN European Journal of Immunology 2005-07-14

Aspirin gained tremendous popularity during the 1918 Spanish Influenza virus pandemic, 50 years prior to demonstration of their inhibitory action on prostaglandins. Here, we show that influenza A (IAV) infection, prostaglandin E2 (PGE2) was upregulated, which led inhibition type I interferon (IFN) production and apoptosis in macrophages, thereby causing an increase replication. This role PGE2 not limited innate immunity, because both antigen presentation T cell mediated immunity were also...

10.1016/j.immuni.2014.02.013 article EN publisher-specific-oa Immunity 2014-04-01

Inborn errors of human IFN-γ-dependent macrophagic immunity underlie mycobacterial diseases, whereas inborn IFN-α/β-dependent intrinsic viral diseases. Both types IFNs induce the transcription factor IRF1. We describe unrelated children with inherited complete IRF1 deficiency and early-onset, multiple, life-threatening diseases caused by weakly virulent mycobacteria related intramacrophagic pathogens. These have no history severe disease, despite exposure to many viruses, including...

10.1016/j.cell.2022.12.038 article EN cc-by Cell 2023-02-01

Abstract While a number of microbial-associated molecular patterns have been known for decades to act as adjuvants, the mechanisms and signaling pathways underlying their action remained elusive. Here, we examined unfolding adaptive immune response induced by Nod2 in vivo upon activation its specific ligand, muramyl dipeptide, component peptidoglycan. Our findings demonstrate that this bacterial sensor triggers potent Ag-specific with Th2-type polarization profile, characterized induction...

10.4049/jimmunol.181.11.7925 article EN The Journal of Immunology 2008-12-01

Obesity is characterized by chronic systemic inflammation and enhances cancer metastasis mortality. promotes breast to lung in a neutrophil-dependent manner; however, the upstream regulatory mechanisms of this process remain unknown. Here, we show that obesity-induced monocytes underlie neutrophil activation metastasis. Using mass cytometry, obesity favors expansion myeloid lineages while restricting lymphoid cells within peripheral blood. RNA sequencing flow cytometry revealed...

10.1084/jem.20220509 article EN cc-by-nc-sa The Journal of Experimental Medicine 2023-05-11

Intestinal bacteria outnumber our own human cells in conditions of both health and disease. It has long been recognized that secretory antibody, particularly IgA, is produced response to these microbes hypothesized this must play an important role defining the relationship between a host its intestinal microbes. However, exact IgA mechanisms by which can act are only beginning be understood. In review we attempt unravel complex interaction so-called "natural," "primitive"...

10.3389/fimmu.2012.00100 article EN cc-by Frontiers in Immunology 2012-01-01

Abstract The T cell response to Shigella, the causative agent of bacillary dysentery, remains poorly understood. Using a murine model infection, we report that Shigella flexneri primes predominately IL-17A– and IL-22–producing Th17 cells. Shigella-specific Th1 cells are only significantly induced on secondary whereas specific Th2 CD8+ undetectable. Apart from primed in MHC class II- IL-6–dependent, but IL12/23p40-independent manner, identified γδ as an additional minor source IL-17A. Priming...

10.4049/jimmunol.0900978 article EN The Journal of Immunology 2010-01-20

Although a number of studies have examined the development T-helper cell type 2 (Th2) immunity in different settings, mechanisms underlying initiation this arm adaptive are not well understood. We exploited fact that immunization with antigen plus either nucleotide-binding oligomerization domain-containing proteins 1 (Nod1) or (Nod2) agonists drives Th2 induction to understand how these pattern-recognition receptors mediate systemic immune responses. Here, we show bone-marrow chimeric mice...

10.1073/pnas.1015063108 article EN Proceedings of the National Academy of Sciences 2011-08-19

ABSTRACT STING has emerged in recent years as a key player orchestrating innate immune responses to cytosolic DNA and RNA derived from pathogens. However, the regulation of still remains poorly defined. In present study, we investigated mechanism expression relation RIG-I pathway. Our data show that signaling through induces at both transcriptional protein levels various cell types. induction by agonist 5′triphosphorylated (5′pppRNA) was recognized be delayed event resulting an...

10.1128/jvi.00748-16 article EN Journal of Virology 2016-08-11

SummaryCD4+Foxp3+ regulatory T (TREG) cells are critical mediators of peripheral tolerance and modulators immune responses. Functional adaptation TREG cells, through acquisition secondary transcription factors is for their effector differentiation towards local inflammatory stimuli including infections. The drivers consequences this cell function remain largely unknown. Using an unbiased screen, we identified receptors the IL-1 family controlling cells. Through respiratory infection models,...

10.1038/s41385-019-0153-5 article EN cc-by Mucosal Immunology 2019-03-14

The Nod-like receptor proteins Nod1 and Nod2 participate in innate immune responses against bacteria through intracellular detection of peptidoglycan, a component bacterial cell wall. Recent evidence has demonstrated that stimulates the release chemokines attract neutrophils at site infection, such as CXCL8/IL-8 humans, CXCL1/keratinocyte-derived chemokine CXCL2/MIP-2 mice. We aimed to determine whether Nod could trigger CCL5/RANTES, known number cells, but not neutrophils. Our results...

10.1002/eji.200737069 article EN European Journal of Immunology 2007-08-17

Susceptibility to progressive infection with the fungus Cryptococcus neoformans is associated an allergic pattern of lung inflammation, yet factors that govern this host response are not clearly understood. Using a clinically relevant mouse model inhalational virulent C. H99, we demonstrate role for IL-33-dependent signaling in immune defense. Infection BALB/c mice 10(4) CFU H99 caused time-dependent induction IL-33 accumulation type 2 pulmonary innate lymphoid cells and alternatively...

10.4049/jimmunol.1300426 article EN The Journal of Immunology 2013-07-27
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