A5068654921- Inflammasome and immune disorders
- Immune Response and Inflammation
- interferon and immune responses
- Immune Cell Function and Interaction
- Yersinia bacterium, plague, ectoparasites research
- RNA regulation and disease
- Gout, Hyperuricemia, Uric Acid
- Trace Elements in Health
- Toxoplasma gondii Research Studies
- Whipple's Disease and Interleukins
- Kawasaki Disease and Coronary Complications
- Cell death mechanisms and regulation
- Viral Infections and Immunology Research
- Endoplasmic Reticulum Stress and Disease
- NF-κB Signaling Pathways
- Calcium signaling and nucleotide metabolism
- T-cell and B-cell Immunology
- Leptospirosis research and findings
- Sepsis Diagnosis and Treatment
Tufts University
2020-2025
Stonehill College
2020
Significance While ZBP1 is well documented to drive cell death in response viruses, its role the context of Toll-like receptor (TLR)–mediated immune activation remains less defined. Here, we show that promotes inflammation bacterial lipopolysaccharide (LPS) or double-stranded RNA (dsRNA). In a dose dependent manner, recruitment RIPK1 TLR3/4 adaptor TRIF, activating downstream inflammatory signaling. plays crucial TRIF-dependent responses vivo , as Zbp1 −/− mice exhibited resistance...
Cell death and inflammation are interdependent host responses to infection. During pyroptotic cell death, interleukin-1β (IL-1β) release occurs through caspase-1 caspase-11-mediated gasdermin D pore formation. In vivo, lipopolysaccharide (LPS) result in IL-1β secretion. vitro, however, murine macrophages require a second "danger signal" for the inflammasome-driven maturation of IL-1β. Recent reports have shown caspase-8-mediated pyroptosis LPS-activated but provided conflicting evidence...
Abstract Inflammation and cell death are closely linked arms of the host immune response to infection, which when carefully balanced ensure survival. One example this balance is tightly regulated transition from TNFR1-associated pro-inflammatory complex I pro-death II. By contrast, here we show that a TRIF-dependent containing FADD, RIPK1 caspase-8 (that have termed TRIFosome) mediates in Yersinia pseudotuberculosis LPS. Furthermore, constitutive binding between ZBP1 essential for initiation...
TNF mediates a variety of biological processes including cellular proliferation, inflammatory responses, and cell death is therefore associated with numerous pathologies autoinflammatory diseases septic shock. The responses to have been studied extensively downstream TNF-R1 are believed rely on the formation proinflammatory complex I prodeath II, respectively. We recently identified similar multimeric TLR4, termed TRIFosome, that regulates inflammation in response LPS or Yersinia...
Abstract The life cycle of effector T cells is determined by signals downstream the cell receptor (TCR) that induce activation and proinflammatory activity, or death as part process to resolve inflammation. We recently reported myeloid differentiation primary response 88 (MyD88) tunes down TCR limits survival in cardiac tumor inflammatory environments, contrast its role upon toll-like (TLR) recognition pathogen- damage-associated molecular patterns. However, mechanism remains unknown. Here,...
Signaling through classical death receptor Fas was mainly appreciated as a pro-death pathway until recent reports characterized pro-inflammatory outcomes of Fas-mediated activation in pathological contexts. How signaling can switch to is poorly understood. Herein, we report that macrophages and neutrophils, the Toll-like (TLR) adapter CD14 determines inflammatory output signaling. Our findings propose crucial chaperone internalization resulting Cd14
Caspase-8-dependent pyroptosis has been shown to mediate host protection from Yersinia infection. For this mode of cell death, the kinase activity receptor-interacting protein 1 (RIPK1) is required, but autophosphorylation sites required drive caspase-8 activation have not determined. Here, we show that non-canonical RIPK1 at threonine 169 (T169) necessary for caspase-8-mediated pyroptosis. Mice with alanine in T169 position are highly susceptible dissemination. Mechanistically, delayed...
Introduction: Combined obesity and hypertension alter the endoplasmic reticulum (ER) stress response by downregulating X-box binding protein 1 ( Xbp1 ) in T cells, which heightens cell inflammatory potential persistence Heart Failure with Preserved Ejection Fraction (HFpEF), a prevalent syndrome no cure. The ER Stimulator of Interferon Genes (STING), concert , coordinates inflammation death other contexts, yet its role cardiometabolic HFpEF is unknown. Hypothesis: STING activation...