A new study identifies Th17 cells as drivers of periodontitis, a common disorder affecting nearly half of American adults over age 30. The research found that an unhealthy oral microbiome triggers the accumulation of these immune cells, leading to inflammation and bone loss.
A subset of T cells known as Th17 cells contribute to periodontitis, a severe form of gum disease. The study identifies these cells as key mediators of the condition and finds that inhibiting their development holds promise as a new therapeutic approach.
Researchers at the University of Alabama at Birmingham have described a key immune response mechanism that determines the fate of T cells. This knowledge can aid in the development of better vaccines, treatments for infections, and moderation of autoimmune diseases.
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Scientists at Johns Hopkins Kimmel Cancer Center discovered that inhibiting the Yes-associated protein (YAP) reduces tumor burdens and enhances the effectiveness of immunotherapy treatments. YAP plays a role in suppressing antitumor immunity by regulatory T-cells, which can dampen immune responses to tumors.
Scientists found that damage from chronic inflammation induces the death of white blood cells essential to eliminating the parasite, allowing it to sustain the infection. The findings may lead to possible treatment and shed light on a phenomenon shared by other chronic infections.
AEP enhances checkpoint inhibitor drug effects on cancer cells and autoimmune diseases; measuring AEP levels may help identify patients responding to treatment with PD-1 inhibitors.
Researchers at FAU found that immune cells in Parkinson's patients, specifically T-cells, kill nerve cells producing dopamine. Antibodies blocking Th17 cells offer hope for new treatment methods.
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Researchers at Boston Children's Hospital have discovered a new way to enhance the immune system's tolerance for organ transplants. By increasing the activity of a regulatory protein called DEPTOR in immune cells, heart transplants were able to survive for an average of 35 days, compared to just 7 days without immunosuppressive drugs.
This review discusses immune-suppressive mechanisms in oral cancer, including regulatory T cells, myeloid-derived suppressor cells, and cancer-associated fibroblasts. The complexity of these mechanisms is explored, with a focus on identifying potential therapeutic targets for oral squamous cell carcinoma development.
The NIH has awarded a $2 million grant to Ken Oestreich at the Virginia Tech Carilion Research Institute to study immunological memory. The research aims to understand how immune cells form and transition into memory cells, which can recognize and respond to pathogens more efficiently.
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Researchers from Turku Centre for Biotechnology and Aalto University used label-free quantitative proteomics to identify over 4000 proteins expressed in Th17 and iTreg cells. The study, published in PLoS Biology, reveals protein expression changes that may be targeted in immunotherapy for diseases like cancer and autoimmunity.
Research finds higher Treg lymphocyte levels in uninfected babies born to mothers with HIV, suggesting a protective mechanism against infection. This discovery could pave the way for vaccine or immune-based therapies to prevent HIV transmission from mothers to their babies.
Researchers analyzed blood and tissue samples from kidney transplant recipients to understand how immunosuppressive drug tacrolimus works. They found that it reduces the number of T follicular helper cells, a key player in antibody production.
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Researchers at Osaka University identified a cellular network involving Th17 cells and stromal cells that secretes inflammatory cytokines to initiate and maintain rheumatoid arthritis. By targeting this network, a novel immunotherapeutic approach has been proposed to reduce chronic joint inflammation.
Researchers found that infusions of properly functioning Tregs significantly slowed ALS disease progression in patients. The treatment increased Treg levels by 30-40% and showed promise as a potential treatment for the debilitating disease.
Researchers at FAU have discovered a special mechanism that regulates tumour growth in lung cancer, opening up new possibilities in the treatment of lung cancer patients. The discovery reveals that lung tumours can reprogram the immune response, leading to the suppression of anti-tumour cells and promoting tumour growth.
A team of Osaka University researchers identified a specific subset of B cells with higher affinity that preferentially commit to plasma cell fate. The study suggests that stable Tfh-GC B cell contacts are key for plasma cell-prone GC cell formation, providing valuable insights for vaccine development.
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A study found that tumors may overcome immunotherapy by increasing TIM3 and regulatory T cells, which inactivate immune killer T cells. Adding a TIM3 inhibitor to radiotherapy/immunotherapy increased response duration, but tumors still relapsed. Researchers also discovered that Tregs contribute to cancer regrowth.
A new study reveals that HIV-infected patients experience dysfunction in follicular helper T cells, which typically help fight off infection. The researchers found that these cells are not playing their usual role to defend against viral infections.
A new study reveals that non-specific bystander T cells can counteract type 1 diabetes by limiting access to beta cells and interfering with inflammatory signals. This challenge to the traditional notion of regulatory T cells' anti-inflammatory effects opens up new avenues for treatment.
New research reveals that CD4+Foxp3+ regulatory T-cells (Tregs) are closely linked to ALS progression, with patients having higher numbers of Tregs experiencing slower disease progression. This discovery provides a promising approach for developing new therapies to treat ALS.
A high-fat, high-cholesterol Western diet reprograms protective immune cells called regulatory T cells into follicular helper T cells that promote inflammation and atherosclerosis. HDL 'good cholesterol' helps shield these protective cells from this transformation.
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Researchers discovered that retinoid-related orphan receptor alpha (RORα) in skin Tregs regulates immune response. Removing RORα from Tregs led to an increase in inflammatory cells and worsened eczema symptoms. The study suggests boosting RORα or targeting related pathways may be effective treatments.
Researchers at Johns Hopkins Medicine have invented a new class of immunotherapy drugs called Y-traps, which target and disable key immune suppressors in tumors. The treatment has been shown to significantly decrease tumor growth and even work against cancers that do not respond to existing immunotherapy.
A new regulator of the immune system has been identified by a Finnish research group, with potential implications for treating both cancer and immune-mediated diseases. HIC1 protein controls the expression of genes contributing to T cell function and regulates immune response.
The researchers developed a new class of bifunctional immunotherapeutic agents called Y-traps, which can target and disable multiple immune suppressive molecules. These Y-traps were found to be effective in inhibiting tumor growth and activating antitumor immunity, even against cancers that do not respond to existing immunotherapies.
A new study has found that the immune system uses a specific balance of T cell types to tolerate beneficial bacteria, while triggering inflammation in pathogenic species. The discovery could lead to new treatments for inflammatory bowel diseases like Crohn's and ulcerative colitis.
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The Vilcek Prize in Biomedical Science is awarded to Alexander Rudensky for his work on regulatory T cells and their role in cancer treatment. Two younger immigrants, Polina Anikeeva and Sergiu P. Pasca, receive $50,000 prizes for their promising contributions to biomedical engineering and brain disease research.
A recent study by KAIST medical scientists reveals that regulatory T cells undergo inflammatory changes in patients with viral hepatitis, leading to the secretion of inflammatory cytokines called TNF. This discovery could pave the way for the development of new clinical treatments for severe viral hepatitis.
Researchers at Helmholtz Munich successfully halted an autoimmune reaction in the early stages of islet autoimmunity, a key step in developing potential treatments for type 1 diabetes. The study reveals that inhibiting the miRNA181a/NFAT5 axis can increase Treg formation and reduce immune activation.
Loss of Roquin leads to autoimmune disorders due to imbalance in Treg functions. Inactive Roquin primarily affects regulatory T cells' ability to control T cell activation.
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Daily low doses of interleukin-2 (IL-2) have been found to be safe and beneficial for patients with chronic graft-versus-host disease, including significant improvements in pediatric patients. IL-2 therapy boosts the production of inflammation-damping Treg cells, providing a mechanism for promoting tolerance in patients with chronic GVHD.
Dendritic cells known as cDC2s are crucial for robust T cell induction and antibody production in vaccination. The study found that intradermal injections may be more efficient than traditional methods, expanding the number of people who can be vaccinated during a pandemic.
Two distinct mechanisms have been identified by which Th17 and Th1 lymphocytes breach the blood-brain barrier in multiple sclerosis, targeting neurons and degrading myelin insulation. Understanding these pathways could lead to development of specific therapies to block immune cell entry.
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Researchers have found that oral bacteria can induce an overactive immune response in the gut, leading to inflammatory bowel disease. The study identified a specific bacterium, Klebsiella pneumoniae, as a strong inducer of this response.
Researchers developed a hybrid Th1/17 T cell that combines the strong effector traits of Th1 cells with the durability of Th17 cells, providing a potent and durable anti-tumor response in preclinical models. The hybrid cells maintained their effectiveness even after long-term persistence in the body.
Researchers at Salk Institute identify Lkb1 protein as key regulator of Tregs, which play a crucial role in preventing autoimmunity and suppressing cancer growth. The discovery has significant implications for developing effective treatments for these diseases.
Treg cells suppress immune function, but eliminating them doesn't eliminate their effects. In fact, dying Tregs release metabolites that affect T-cells, making them unhealthy and reducing the cancer-fighting effect of immunotherapy. The study suggests a new approach to limit this function and block the suppressive activity.
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Researchers at UNC Lineberger Comprehensive Cancer Center discovered a complex signaling system that triggers Th17 immune cell development, which plays a role in autoimmune disorders, inflammation, and cancer. This finding could lead to new treatments for related diseases.
A new study by the University of Bonn has identified a way to enhance the impact of killer T cells in fighting cancer. By blocking a protein called IKKβ, researchers were able to increase the effectiveness of killer T cells against tumor cells.
Researchers found that targeting the CTLA-4 molecule at the right time during malaria infection allows mice to quickly clear the disease and develop lasting immunity. The study suggests a new approach for combating malaria, potentially involving immunotherapy drugs or small molecules.
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Researchers found significant differences in bacterial genera between MS patients and healthy controls, with Acinetobacter and Akkermansia being more abundant in patients. Exposure to extracts from these bacteria increased proinflammatory T cell differentiation and inhibited regulatory T cell differentiation.
Researchers found that pentoxifylline boosts the effectiveness of immune-checkpoint inhibitors in mice with melanoma, increasing the cure rate to around 40 percent. Disabling regulatory T cells could lead to improved cancer treatment outcomes.
Researchers discovered ILCregs, a regulatory subpopulation of innate lymphoid cells, that suppress intestinal inflammation by secreting IL-10 and TGF-β1. This unique population has a distinct genetic identity from other immune cells and may hold potential for treating chronic inflammatory diseases.
Researchers found that loss of liver kinase B1 (LKB1) in regulatory T cells disrupts cell metabolism and function, leading to functional exhaustion. This may contribute to allergic reactions and autoimmune disorders like asthma, multiple sclerosis, and lupus.
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A new study reveals that regulatory T cells can either suppress or reactivate latent cytomegalovirus in different mouse tissues, such as the spleen and salivary gland. Depletion of these immune cells reduced viral load in the spleen but increased it in the salivary gland.
Researchers have pinpointed a specific subset of immune cells, known as TH2 subset or type 2 "helper" T cells, which are central to allergies. The identified cells, dubbed TH2A, were found to produce multiple inflammatory signaling molecules and unique gene expression patterns that drive allergic responses.
Researchers identified a group of regulatory T cells linked to inflammation in JIA, which can be used as a diagnostic marker and predict treatment responsiveness. The team also found that patients' DNA features affect treatment outcomes, enabling personalized medicine for improved care.
Researchers from McGill University Health Centre cracked the code to understanding regulatory T cell function, a key component of our immune system. The study's findings have significant implications for treating autoimmune diseases such as arthritis and Crohn's disease.
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Targeting a subset of immune cells called regulatory T cells could be an effective approach to treating cancers. By blocking or deleting a surface protein called neuropilin-1, researchers found that tumor growth was dramatically reduced in mice, suggesting this could lead to more effective immunotherapy treatments.
Research reveals that cellular stress enhances Th17 cell activation, increasing the risk of autoimmune diseases such as arthritis and multiple sclerosis. Inhibiting cellular stress may hold promise for reducing disease symptoms by preserving other T cell responses.
A new study presents data from an FDA-approved clinical trial testing the generic vaccine BCG to reverse advanced type 1 diabetes. The findings suggest that BCG may induce a permanent increase in expression of genes that restore beneficial regulatory T cells (Tregs) preventing autoimmune attacks on the body's own tissue.
Okinawa Institute of Science and Technology researchers identified JunB as a key target to selectively disable toxic T Helper 17 cells, reducing the risk of auto-immune diseases. By inhibiting JunB, these cells can still accumulate in the gut and respond to infections without turning rogue.
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Researchers at UCSF have discovered that regulatory T cells trigger stem cells to promote healthy hair growth. The study suggests that defects in Tregs could be responsible for alopecia areata and potentially play a role in other forms of baldness.
Researchers at Brigham and Women's Hospital have developed an antibody that can precisely target regulatory T cells, unleashing the immune system to kill cancer cells. The antibody decreased tumor growth in models of melanoma, glioblastoma, and colorectal carcinoma.
Researchers at MUSC found that using FDA-approved small molecules can improve the potency and function of T cells in adoptive T cell therapy, making them more effective against melanoma. The treatment reduces regulatory T cells in the tumor microenvironment and enhances antitumor activity.
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A research team has identified a key molecular target that regulates antibody production in both helper and regulatory T cells, which may lead to the development of new treatments for autoimmune diseases like lupus and rheumatoid arthritis.
A study led by Georgia State University found that cytokine IL-36γ promotes the development of pro-inflammatory T helper cells and inhibits regulatory T cells in humans. This discovery could lead to new therapeutic approaches for inflammatory bowel disease, particularly ulcerative colitis.
Researchers at MUSC found that Th17 cells can be expanded outside the body without losing effectiveness, providing a promising alternative to classic T cells used in adoptive immunotherapy. This breakthrough enables longer window periods for obtaining effective T cells via expansion outside the body.
Researchers at UF Health have found a way to expand and preserve certain cord-blood cells, known as Tregs, which modulate the immune system and prevent autoimmune diseases like Type 1 diabetes. This discovery has important implications for patients with the disease and could potentially be used as a treatment or preventive measure.
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