Articles tagged with T Cell Receptor Signaling
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Researchers developed a new AI model named BATMAN to improve T cell receptor therapy accuracy. The AI uses a vast database of over 22,000 TCR-peptide interactions to predict peptide binding and identify potential cancer treatments.
Combining PCSK9 inhibitors with anti-PD-1/PD-L1 treatment may improve antitumor effects. PCSK9 inhibition enhances antigen presentation, promoting T cell recognition and killing of tumor cells.
Researchers identified a method to enhance CAR-T cell therapy by modifying the CUL5 gene. This approach improves T cells' growth and longevity, making them more effective in fighting cancer. The study suggests a new way to create targeted cells using a virus to deliver genetic material.
Researchers at MD Anderson Cancer Center presented findings on novel treatments for MDS, including luspatercept, which significantly reduced the need for blood transfusions in lower-risk patients. Additionally, a triplet therapy regimen improved survival in older adults with FLT3-mutated AML.
A new DNA-powered signal amplification technology called ACE significantly enhances the sensitivity of mass cytometry, enabling the detection of multiple proteins in single cells. This breakthrough allows researchers to investigate complex biological processes and study immune cell functions with unprecedented depth.
A team of researchers has discovered a mechanism by which the liver's immune cells are suppressed in chronic hepatitis B, leading to organ damage. The 'sleep timer' function allows immune cells to weaken their activity over time, preventing them from proliferating excessively and causing further damage.
Researchers describe redundant innate immune pathways triggered by AAV vectors, including sensing of viral genome and cytoplasmic DNA sensors. The study highlights the need to understand complex biologic mechanisms underlying adverse reactions to AAV vectors in human gene therapy trials.
Researchers identified a fundamental imbalance in immune responses that patients with lupus make, leading to insufficient activation of the aryl hydrocarbon receptor pathway. This imbalance can be corrected by reprogramming disease-causing cells into Th22 cells promoting wound healing, offering a potential cure for lupus.
Researchers discovered how Vγ9Vδ2 T cells recognize pathogens and cancer cells by their altered cell metabolism. The study found that phosphoantigens bind to special molecules inside the cell, triggering a signal to kill. This finding can improve the clinical use of Vγ9Vδ2 T cells in tumor treatment.
A recent study found elevated TonEBP expression in patients with lupus nephritis, correlating with inflammatory cytokines and kidney damage. Suppressing TonEBP was shown to halt lupus progression and mitigate kidney damage in animal models.
Researchers at Gladstone Institutes identified conditions that enable gamma delta T cells to recognize cancer cells by disrupting energy production and causing cellular stress. This insight suggests that therapies manipulating butyrophilin abundance on the surface of cancer cells could boost gamma delta T cell effectiveness.
Researchers developed a new strategy for T-cell-based immunotherapy using aptamers, which directly activates immune cells against cancer cells without genetic modifications. The innovative regulatory circuit establishes an artificial interaction between T cells and cancer cells.
Researchers discovered cytoplasmic retinoic acid receptors, such as RARalpha, are essential for T cell linking sensing at the cell surface with downstream signaling cascades and gene expression programs. The study sheds new light on TCR signaling and its connection to cancer treatment.
A new CAR T cell design approach using machine learning and artificial intelligence is being developed to improve cancer treatment. The project aims to create a hybrid knowledge- and data-driven approach to guide the design of immunotherapeutic cells.
University of Pittsburgh researchers created a universal receptor system allowing T cells to recognize any cell surface target. This enables highly customizable CAR T cell and other immunotherapies for treating cancer and diseases, with potential applications in solid tumors.
A new study finds that rare helper T cells called Th9 can drive allergic disease and may hold the key to precision medicine approaches for treating severe allergies. Th9 cells are activated by specific transcription factors and can produce inflammatory cytokines without antigen stimulation.
Researchers at Georgia Institute of Technology developed a synthetic tumor model to understand the impact of microenvironment on targeted therapies for Activated B Cell-like Diffuse Large B cell lymphoma. The model showed promise in demonstrating how combining therapeutics can overcome tumor resistance to inhibitors.
Researchers have discovered that inhibiting conventional signalling pathway by disrupting LCK allows more efficient tumour cell killing, using FYN protein instead. This approach enhances T-cell function and reduces graft-versus-host disease, making CAR-T therapy more accessible to patients.
Researchers captured first image of antigen-bound T-cell receptor complex with bound antigen at atomic resolution. The study reveals no significant structural changes in the receptor after antigen binding, sparking further investigation into the signaling pathway activation mechanism.
Researchers at the University of Pittsburgh have discovered that even terminally exhausted T cells retain some capacity to function again. They identified approaches to overcome exhaustion by targeting co-stimulation pathways and reprogramming T cells to be resistant to hypoxia, a common tumor microenvironmental signal.
A UCLA study has identified a synthetic IL-9 receptor that allows T cells to target cancerous tumors without the need for chemotherapy or radiation. The treatment showed promise in multiple systems and cured over half of mice with pancreatic cancer and melanoma.
Researchers have shed light on how immune checkpoint protein LAG3 modulates T cell activity, providing crucial information for the development of new LAG3-blocking therapies. The study found that LAG3 suppresses T cell activation by disrupting coreceptor-Lck association, even in the absence of MHC Class II molecules.
A new study from the La Jolla Institute for Immunology reveals that two groups of regulatory CD4+ T cells develop at different times to combat acute inflammation. The early Tregs reduce autoimmune damage, while the second wave shuts down the entire immune response to signal infection clearance.
Researchers found that interleukin-2 promotes the development of two subsets of CD8 T cells, one producing IL-2 and the other not, with distinct fates. The IL-2-producing cells develop into immune memory cells with long-term protection, while the non-IL-2-producing cells gain effector traits but lose memory formation.
A new study from Penn Medicine demonstrates that RN7SL1, a naturally occurring RNA, can activate the body's own natural T cells to seek out cancer cells that have escaped recognition by CAR T cells. This approach may help improve efforts to treat solid tumors.
Researchers from Monash University have made a fundamental advance in understanding how T cells become activated when encountering pathogens. The study found that T cells need to recognize pathogens in a particular orientation to receive a strong activating signal, revealing a critical mechanism for effective T cell immunity.
A research team at Pohang University of Science & Technology has uncovered the mechanism for regulating T cell differentiation via intestinal epithelial cells. This finding highlights the importance of intestinal immune homeostasis and suggests a new role for PD-1 signaling in CD4+ T cell differentiation into intraepithelial lymphocytes.
A novel T cell genetically engineered by University of Arizona Health Sciences researchers targets and attacks pathogenic T cells that cause Type 1 diabetes. The 5MCAR T cells, which mimic the evolutionary design of natural killer T cells, were tested in a non-obese diabetic mouse model with promising results.
Researchers at the University of Freiburg have identified a previously undiscovered domain of the T-cell receptor called RK motif. This discovery enables more precise control over T cells, potentially improving therapies for cancer and autoimmune diseases.
Researchers at UNSW achieved unprecedented resolution capabilities in single-molecule microscopy to detect interactions between individual molecules within intact cells. Their self-aligning microscope smashed the limits of existing super-resolution microscopy technology by measuring distances between proteins with nanometre precision.
Researchers discovered that angioimmunoblastic T-cell lymphoma (AITL) relies on T-cell receptor (TCR) signaling and dassatinib, a multi-kinase inhibitor, effectively treats this disease.
Researchers discovered two proteins that act like a 'clutch' in cells to activate the immune response. These protein condensates guide the movement of contents inside cells, much like switching gears in a car. The study sheds light on control mechanisms for immune activation and could lead to designing T cells with specific functions.
Researchers discovered two adaptor proteins that act as a 'clutch' to activate the immune response by moving protein condensates towards the center of cells. This discovery sheds light on the control mechanisms for immune response activation and could lead to designing immune cells to combat specific problems.
Researchers have unraveled the inner workings of a process that allows T cells to tune out fake signals, providing an enormous leap forward in understanding immune system fine-tuning. The discovery sheds light on why immune system activity sometimes goes awry and may provide insights into curing cancer.
Researchers discovered that second-generation CARs stimulate CD3 signaling more effectively than third-generation receptors and activate downstream signaling messengers. This may contribute to superior antitumor efficacy. The study aims to improve CAR designs and lead to better understanding of immunotherapy.
Researchers found that certain Gαs-coupled receptor agonists, including adrenaline and prostaglandin E2 and D2, prevent T cells from activating their integrins after recognizing their target. Sleep helps to decrease these molecules' levels, leading to higher integrin activation in T cells.
Researchers at Caltech have developed two new methods to determine T cell targets, which are critical for designing personalized treatments for cancers. The methods use a signaling domain attached to MHCs or trogocytosis to identify the correct antigen.
The study found a loop of physical signals, resembling a double-handed handshake, that encourages cell suicide. This discovery could lead to new immune-regulating therapies and understanding the mechanisms that ensure T cells aggressively pursue hordes of infectors but not damage healthy human tissue.
Researchers at Toronto General Hospital have identified a specific insulin signaling pathway that revs up the response of T cells in the immune system, enabling them to divide rapidly and secrete cytokines. This finding opens avenues for better regulating the immune system and potentially developing new therapies.
Researchers at Marshall University identified GPR68 as a target for studying T cell activation and pro-inflammatory functions. The study found that blocking the GPR68 pathway may be a potential therapy for chronic inflammatory diseases.
A new study by Sanford Burnham Prebys Medical Discovery Institute (SBP) researchers describes how nuclear pore component Nup210 is critical for the survival of circulating CD4+ T cells. The findings identify a new node of T cell receptor signaling and could pave the way for the development of future immunotherapies.
Early dysregulation of cellular energy metabolism appears characteristic of chronic hepatitis C infection. Gene expression patterns in HCV-specific CD8 T cells differentiate between chronic and resolving HCV infections, offering potential avenues for predicting disease outcome and intervening before failure.
Researchers have unveiled the molecular mechanism of T cell activation, a key step in the immune response. The study used nuclear magnetic resonance (NMR) to probe the interaction between a T cell receptor and an HIV protein, shedding light on the signaling process that triggers an immune response.
Researchers at Salk Institute have discovered that T cell receptors amplify 'invader' signals by producing and releasing ZAP70 protein, enabling rapid signal transmission throughout the cell. This finding could lead to the development of more effective treatments for cancer and autoimmune diseases.
Researchers discovered that a specific molecular pathway is responsible for the metabolic changes in exhausted T cells, which are crucial for effective immune response. By targeting this pathway, scientists may develop new cancer therapies to enhance treatment outcomes.
A team of scientists at the MBL Whitman Center successfully recreated a T-cell receptor signaling pathway, revealing novel insights into protein signaling and its role in the immune response. The study found that protein molecules separate into structures through phase separation, leading to efficient signal transduction.
Researchers at Monash University discovered that regulatory T cells can function even when their receptors bind to MHC in a completely different orientation, challenging established views on the immune system. This finding opens up new avenues for investigating and potentially treating autoimmune diseases like type 1 diabetes.
Researchers at TSRI found that interferon beta has an immune-suppressing effect that can help some viruses establish persistent infections, including HIV and hepatitis B and C. Blocking IFNβ signaling may lead to the development of new treatments for these infections.
Researchers found that blocking two pathways, PGE2 and PD-1, boosts T-cell function and enhances viral control in mice with chronic infections. Celecoxib, a non-steroidal anti-inflammatory drug, was also shown to improve T-cell responses.
Researchers at the La Jolla Institute for Allergy and Immunology report that Nuclear Factor of Activated T cells (NFAT) plays a key role in CD8 T cell exhaustion, leading to impaired immune responses. The study identifies NFAT as a molecular hub that orchestrates T cell activation and exhaustion.
Scientists discovered that Tregs need continuous contact with their environment to function correctly and require the T cell receptor for protection. The study showed that Tregs without the receptor lose their special ability to suppress excessive immune reactions.
Researchers discovered that integrin loss in dendritic cells leads to increased signaling through the GM-CSF receptor, reprogramming them into a mature phenotype. This activation triggers T cell immune response, offering insights into designing targeted therapies for autoimmunity and cancer treatments.
Scientists at ETH Zurich have identified a mechanism that protects immune cells from natural killer cells. Type I interferon receptors play a crucial role in this process, and its absence can lead to the elimination of healthy immune cells. This discovery may have implications for understanding autoimmune diseases.
Researchers at Berkeley Lab have developed a novel method to study the membranes of living cells by using size-based chromatography. This approach allows them to probe supramolecular structures in cell membranes at the nanometer length scales, providing insights into how spatial organization affects cellular function.
A protein complex named mTORC1 is essential for jumpstarting the immune response during the first 24 hours of an infection. It helps ensure that newly activated T cells have the energy needed to launch proliferation and produce specialized T cells.
Researchers at St. Jude Children's Research Hospital identified a 'rheostat' mechanism in T cell receptors that regulates the immune response, enabling cells to scale their response according to the threat. This finding offers insights into advancing understanding and treatment of problems like autoimmune disorders and cancer.
Researchers discovered a key interaction between skin cells and gamma delta T cells, revealing a molecular trigger for wound healing. The CD100 receptor plays a crucial role in signaling the activation of these immune cells, which then stimulate new epithelial cell production to repair damaged tissues.
Researchers have identified a novel genetic mechanism underlying idiopathic CD4 lymphopenia, an immunodeficiency characterized by low levels of CD4 T cells. The mutation affects Unc119's ability to activate T cells and reduce Lck signaling, leading to impaired T cell proliferation.
Researchers at The Wistar Institute have found that the protein Foxp1 actively maintains T cells in a 'quiescent state,' allowing them to work without antigenic triggers. Removing Foxp1 enables T cells to proliferate and become activated, which could lead to new treatments for diseases like cancer.
Researchers at Scripps Research Institute have discovered the underlying mechanisms that activate gamma delta T cells in the skin and other organs. These cells play a unique role in recognizing damage or disease in epithelial tissues, and their activation is crucial for wound healing.