Gretchen E. Diehl

ORCID: 0000-0002-1841-2842
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About
Contact & Profiles
Research Areas
  • Immune Cell Function and Interaction
  • Gut microbiota and health
  • IL-33, ST2, and ILC Pathways
  • T-cell and B-cell Immunology
  • Inflammatory Bowel Disease
  • Eosinophilic Esophagitis
  • Immunotherapy and Immune Responses
  • Cancer Immunotherapy and Biomarkers
  • Clostridium difficile and Clostridium perfringens research
  • Immune Response and Inflammation
  • Immune cells in cancer
  • Pancreatitis Pathology and Treatment
  • Helicobacter pylori-related gastroenterology studies
  • Cell death mechanisms and regulation
  • Microscopic Colitis
  • Phagocytosis and Immune Regulation
  • Immune responses and vaccinations
  • Dermatology and Skin Diseases
  • Asthma and respiratory diseases
  • Diabetes and associated disorders
  • Immunodeficiency and Autoimmune Disorders
  • Cancer, Stress, Anesthesia, and Immune Response
  • Inflammasome and immune disorders
  • Digestive system and related health
  • Alzheimer's disease research and treatments

Kettering University
2021-2024

Memorial Sloan Kettering Cancer Center
2020-2023

Baylor College of Medicine
2015-2022

Cornell University
2021-2022

Children's Cancer Center
2019

New York University
2006-2016

York University
2016

Howard Hughes Medical Institute
2014

University of California, Berkeley
1999-2010

Ontario Institute for Cancer Research
2010

Interleukin (IL)-22–producing group 3 innate lymphoid cells (ILC3) promote mucosal healing and maintain barrier integrity, but how microbial signals are integrated to regulate protection offered by these remains unclear. Here, we show that in vivo depletion of CX3CR1+ mononuclear phagocytes (MNPs) resulted more severe colitis death after infection with Citrobacter rodentium. This phenotype was rescued exogenous IL-22, which endogenously produced ILC3 close spatial proximity MNPs were...

10.1084/jem.20140678 article EN cc-by-nc-sa The Journal of Experimental Medicine 2014-07-14

TRAIL (tumor necrosis factor-related apoptosis-inducing ligand) is a member of the tumor factor family that can kill wide variety cells but not normal cells. TRAIL-induced apoptosis in humans mediated by its receptors DR4 (TRAIL-R1) and DR5 (TRAIL-R2). What constitutes signaling molecules downstream these receptors, however, remains highly controversial. Using FADD dominant negative molecule, several groups have reached different conclusions with respect to role apoptosis. More recently,...

10.1074/jbc.c000284200 article EN cc-by Journal of Biological Chemistry 2000-08-01

Cell death is an important mechanism to limit uncontrolled T-cell expansion during immune responses. Given the role of death-receptor adapter protein Fas-associated domain (FADD) in apoptosis, it intriguing that receptor (TCR)–induced proliferation blocked FADD-defective T cells. Necroptosis alternate form can be induced by receptors and linked autophagy. It requires domain-containing kinase RIP1 and, certain instances, RIP3. FADD its apoptotic partner, Caspase-8, have also been implicated...

10.1073/pnas.1005997107 article EN Proceedings of the National Academy of Sciences 2010-07-06

Retinol plays a vital role in the immune response to infection, yet proteins that mediate retinol transport during infection have not been identified. Serum amyloid A (SAA) are strongly induced liver by systemic and intestine bacterial colonization, but their exact functions remain unclear. Here we show mouse human SAAs binding proteins. Mouse bound with nanomolar affinity, were associated vivo, limited burden tissues after acute infection. We determined crystal structure of SAA3 at...

10.7554/elife.03206 article EN cc-by eLife 2014-07-29

Inflammatory bowel disease (IBD) is a chronic life-long inflammatory affecting almost 2 million Americans. Although new biologic therapies have been developed, the standard medical treatment fails to selectively control dysregulated immune pathways involved in colonic inflammation. Further, IBD patients with uncontrolled inflammation are at higher risk for developing colorectal cancer (CRC). Intestinal microbes can impact many functions, and here we asked if they could be used improve...

10.1080/19490976.2022.2119054 article EN cc-by-nc Gut Microbes 2022-09-04

The gut microbiota is essential for maintenance and repair of the intestinal epithelial barrier. As shifts in both barrier function composition are found inflammatory bowel disease patients, it critical to understand role distinct bacteria regulating repair. We identified a mouse commensal E. coli isolate, GDAR2-2, that protects mice from Citrobacter rodentium infection dextran sulfate sodium-induced colitis. Colonization with GDAR2-2 resulted expansion CX3CR1+ mononuclear phagocytes,...

10.1080/19490976.2021.2014772 article EN cc-by Gut Microbes 2022-01-06

Immune checkpoint blockade (ICB) has revolutionized cancer treatment, yet quality of life and continuation therapy can be constrained by immune-related adverse events (irAEs). Limited understanding irAE mechanisms hampers development approaches to mitigate their damage. To address this, we examined whether mice gained sensitivity anti-CTLA-4 (αCTLA-4)–mediated toxicity upon disruption gut homeostatic immunity. We found αCTLA-4 drove increased inflammation colonic tissue damage in with...

10.1084/jem.20221333 article EN cc-by-nc-sa The Journal of Experimental Medicine 2022-11-11

Epidemiological evidence finds cigarette smoking is a common risk factor for number of diseases, not only in the lung but also other tissues such as gastrointestinal tract. While it well documented that directly drives inflammatory disease, how promotes disease peripheral incompletely understood. In this study, we utilized mouse model short-term smoke exposure and found increased Th17 cells neutrophilia circulation. Following intestinal challenge, exposed mice showed pathology which...

10.3389/fimmu.2019.00075 article EN cc-by Frontiers in Immunology 2019-01-29

Alteration of innate immune cells in the lungs can promote loss peripheral tolerance that leads to autoimmune responses cigarette smokers. Development autoimmunity smokers with emphysema is also strongly linked expansion autoreactive T helper (Th) expressing interferon gamma (Th1), and interleukin 17A (Th17). However, mechanisms responsible for enhanced self-recognition reduced smoker remain less clear. Here we show C1q, a component complement protein 1 complex (C1), downregulated lung CD1a+...

10.1172/jci.insight.124317 article EN JCI Insight 2019-05-21

Abstract Somatic mutations can promote malignant transformation of airway epithelial cells and induce inflammatory responses directed against resultant tumors. Tumor-infiltrating T lymphocytes (TIL) in early-stage non–small cell lung cancer (NSCLC) secrete distinct proinflammatory cytokines, but the contribution these TILs to tumor development metastasis remains unknown. We show here that NSCLC are biased toward IL17A expression (Th17) when compared with adjacent tumor-free tissue, whereas...

10.1158/2326-6066.cir-17-0554 article EN Cancer Immunology Research 2018-04-13

This report describes the production of a monoclonal antibody raised against Bcl-xl, and includes an initial study bcl-xl expression in neuropathology including Alzheimer's disease (AD). Bcl-xl is potent apoptotic inhibitor known to be predominant Bcl-x isoform brain. To examine aged brain neurodegenerative disease, we Bcl-xl-specific antibody. In human brain, highest was observed cerebellum. By immunohistochemistry, significant detected reactive microglia patients with AD other neurological...

10.1002/(sici)1097-4547(19970101)47:1<98::aid-jnr11>3.0.co;2-6 article EN Journal of Neuroscience Research 1997-01-01
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