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Significance Regulatory T cells (Tregs) inhibit autoimmune responses and are essential for immune homeostasis. By contrast, in settings of cancerous inflammation, Tregs represent a strong protumorigenic immune cell population via the incapacitation of various tumoricidal immune cells. By using multiple gene-deficient mouse systems, we show that IL-27 specifically induces ectonucleotidase CD39 expression on tumor-infiltrating Tregs in a STAT1-dependent manner. Protumorigenic activity of Tregs is

The incidence of atherosclerosis is higher among patients with several autoimmune diseases such as psoriasis, rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). It is well documented that innate immune cells including macrophages and dendritic cells sense lipid species such as saturated fatty acids and oxidized low-density lipoprotein and produce pro-inflammatory cytokines and chemokines. However, whether a hyperlipidemic environment also impacts autoimmune T cell responses has be

Abstract By comparing imatinib-sensitive and -resistant chronic myeloid leukemia (CML) cell models, we investigated the molecular mechanisms by which tetrahydrobenzimidazole derivative TMQ0153 triggered caspase-dependent apoptosis at low concentrations accompanied by loss of mitochondrial membrane potential (MMP) and increase of cytosolic free Ca 2+ levels. Interestingly, at higher concentrations, TMQ0153 induced necroptotic cell death with accumulation of ROS, both preventable by N -acetyl-L-cy

We report the rapid detection of SARS-CoV-2 in infected patients (mid-turbinate swabs and exhaled breath aerosol samples) in concentrations as low as 60 copies/mL of the virus in seconds by electrical transduction of the SARS-CoV-2 S1 spike protein antigen via SARS-CoV-2 S1 spike protein antibodies immobilized on bilayer quasi-freestanding epitaxial graphene without gate or signal amplification. The sensor demonstrates the spike protein antigen detection in a concentration as low as 1 ag/mL. The

Dendritic cells play an essential role in bridging innate and adaptive immunity by recognizing cellular stress including pathogen- and damage-associated molecular patterns and by shaping the types of antigen-specific T cell immunity. Although lidocaine is widely used in clinical settings that trigger cellular stress, it remains unclear whether such treatment impacts the activation of innate immune cells and subsequent differentiation of T cells. Here we showed that lidocaine inhibited the produc

Merkel cell carcinoma is a skin cancer often driven by Merkel cell polyomavirus (MCPyV) with high rates of response to anti-PD-1 therapy despite low mutational burden. MCPyV-specific CD8 T cells are implicated in anti-PD-1-associated immune responses and provide a means to directly study tumor-specific T cell responses to treatment. Using mass cytometry and combinatorial tetramer staining, we find that baseline frequencies of blood MCPyV-specific cells correlated with response and survival. Freq

Cardiovascular disease such as atherosclerosis is caused by imbalanced lipid metabolism and represents a leading cause of death worldwide. Epidemiological studies show that patients with systemic autoimmune diseases exhibit a higher incidence of atherosclerosis. Conversely, hyperlipidemia has been known to accelerate the incidence of autoimmune diseases in humans and in animal models. However, there is a considerable gap in our understanding of how atherosclerosis impacts the development of the

<h3>Background</h3> Merkel cell carcinoma (MCC) is an aggressive skin cancer often associated with clonal integration of Merkel cell polyomavirus (MCPyV) and expression of T antigen oncoproteins in 80% of cases with the remainder of cases caused by UV mutations.^1,2 PD-1 blockade is effective in treating both etiologies of MCC patients, however, only ~60% of patients respond.³ MCPyV-specific T cells are implicated in immunotherapeutic responses⁴, yet further quali

MCC bulk TCR seq data (fastq) from sorted CD8 T cell populations (from PBMC) and tumor. CD39neg: CD39– CD8 T cells CD39pos: CD39+CLA–CD103– CD8 T cells CLA: CD39+CLA+ CD8 T cells CD103: CD39+CLA–CD103+ CD8 T cells

MCC bulk TCR seq data (fastq) from sorted CD8 T cell populations (from PBMC) and tumor. CD39neg: CD39– CD8 T cells CD39pos: CD39+CLA–CD103– CD8 T cells CLA: CD39+CLA+ CD8 T cells CD103: CD39+CLA–CD103+ CD8 T cells

Abstract Immunotherapeutic strategies for disinhibiting T cell responses have revolutionized lung cancer treatment. However, the identification of tumor-reactive T cells and the acquisition of adequate tissue for molecular and immune profiling remains a challenge that hinders our ability to adequately characterize the mechanisms of immunotherapy response versus resistance. To address this gap, we are investigating the use of bronchoalveolar lavage (BAL) as an alternative to blood or tumor biopsy