| Vol. 12.40 – 23 October, 2020 |
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| The authors showed that depletion of transforming growth factor-β receptor 2 (TGFβR2) in CD4+ T cells, but not CD8+ T cells, halts cancer progression as a result of tissue healing and remodeling of the blood vasculature, causing cancer cell hypoxia and death in distant avascular regions. [Nature] |
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| PUBLICATIONSRanked by the impact factor of the journal |
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| Following the finding that transforming growth factor-β (TGF-β) suppresses T helper 2 (TH2)-cell-mediated cancer immunity, scientists showed that blocking TGF-β signaling in CD4+ T cells remodels the tumor microenvironment and restrains cancer progression. [Nature] |
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| Through an interaction-dependent labeling approach, intratumoral TSA-reactive CD4+, CD8+ T cells, and TSA-suppressive CD4+ T cells could be detected and separated from bystander T cells based on their cell-surface enzymatic fucosyl-biotinylation. [Cell] |
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| The assessment included incidence of biopsy confirmed acute rejection, assessment of natural regulatory T cell infusion related adverse effects, and signs of over immunosuppression. [British Medical Journal] |
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| The mechanisms by which regulatory T (Treg) cells differentially control allergic and autoimmune responses remain unclear. Researchers showed that Treg cells in food allergy had decreased expression of transforming growth factor beta 1 (TGF-β1) because of interleukin-4- and signal transducer and activator of transciription-6-dependent inhibition of Tgfb1 transcription. [Immunity] |
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| Scientists report a potent synergy between selective SIRPα blockade and immune checkpoint blockade in increasing memory T cell responses and reverting exclusion in syngeneic and orthotopic tumor models. [Journal of Clinical Investigation] |
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| Investigators demonstrated that envelope glycoproteins (Env)-induced oxidative stress was responsible for their death by apoptosis. Moreover, they report that peroxisomes, organelles involved in the control of oxidative stress, are targeted by Env-mediated autophagy. [Autophagy] |
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| Researchers report that certain ligands could be obscured by the glycosaminoglycans and glycoproteins that coat pathogenic as well as malignant phagocytic targets. [Current Biology] |
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| The single deletion of tumor necrosis factor receptor (TNFR) 1 induced subclinical colonic epithelial dysfunction and mucosal immune abnormalities, including accumulation of neutrophils and depletion of B cells. [Cell Reports] |
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| Scientists demonstrated that apoptosis induced by JQ1 was solely attributed to the pro-apoptotic protein Bim. Conversely, cell-cycle regulation by JQ1 was associated with multiple Myc-associated gene targets. [Cell Reports] |
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| Investigators report that ubiquitin-specific protease 19 acted as an anti-inflammatory switch that inhibited inflammatory responses and promoted M2-like macrophage polarization. [Cellular & Molecular Immunology] |
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| Scientists compare and contrast the T cell tolerance checkpoints and discuss their specific roles, with the aim of providing an integrated view of T cell peripheral tolerance and fate regulation. [Nature Reviews Immunology] |
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| The authors summarize what they have learned about GPCRs that transduce anti-inflammatory signals, their structures and signaling pathways and the prospect of targeting these receptors for novel anti-inflammatory therapies. [Acta Pharmacologica Sinica] |
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| ASLAN Pharmaceuticals announced that it plans to develop ASLAN003, its next generation inhibitor of dihydroorotate dehydrogenase, in autoimmune conditions, such as multiple sclerosis. [ASLAN Pharmaceuticals] |
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| January 18 – January 20, 2021 Virtual |
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| Houston Methodist Research Institute – Houston, Texas, United States |
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| H. Lee Moffitt Cancer Center & Research Institute – Tampa, Florida, United States |
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| Stockholm University – Stockholm, Sweden |
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| Terasaki Research Institute – Los Angeles, California, United States |
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| University of California, Davis – Sacramento, California, United States |
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