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• W2766860384 endingPage "808" @default.
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• W2766860384 abstract "Cancer immunotherapy is a rapidly evolving field. Despite promising results, long-lasting response rates remain around 20–40%. The immune cell landscape in tumors is heterogeneous across patients and can influence prognosis and outcome of immunotherapy. It is important to investigate mechanisms that underlie migration of immune cells into the TME. Drugs are being tested in preclinical models and clinical trials that can manipulate the immune cell landscape within the TME. These can be used as monotherapy, but more likely in combination with other therapies. Tumors can be divided into ‘hot’ (T cell inflamed) or ‘cold’ (T cell noninflamed) according to the presence of immune cells. In this review, we discuss variables that influence T cell migration into the tumor microenvironment. Chemokines can attract T cells to the tumor site and tumor intrinsic pathways can influence the composition of local chemokines. Tumor-induced vasculature can hamper T cell migration. Other immune cells and tumor-derived molecules can block T cell proliferation and survival. It is important to better understand these mechanisms in order to target them therapeutically. Enhancing T cell infiltration may increase response rates to immunotherapy and increase survival. Tumors can be divided into ‘hot’ (T cell inflamed) or ‘cold’ (T cell noninflamed) according to the presence of immune cells. In this review, we discuss variables that influence T cell migration into the tumor microenvironment. Chemokines can attract T cells to the tumor site and tumor intrinsic pathways can influence the composition of local chemokines. Tumor-induced vasculature can hamper T cell migration. Other immune cells and tumor-derived molecules can block T cell proliferation and survival. It is important to better understand these mechanisms in order to target them therapeutically. Enhancing T cell infiltration may increase response rates to immunotherapy and increase survival. small protein molecules that attract (immune) cells expressing the binding receptors. CCL and CXCL distinguish different chemokines based on the cysteine residue. In CCL the two cysteines are adjacent whereas in the CXCL they are separated by an amino acid. effector cells of the adaptive immune system and are able to eliminate target cells upon stimulation. CTLs are characterized by expression of the CD8 receptor next to the CD3 molecule. the main type of APCs in the body. DCs take up antigen and present it to T cells in order to initiate an adaptive immune response. group of polymorphonuclear immune cells: neutrophils, eosinophils, and basophils. specialized form of blood vessels that facilitate leukocyte migration to lymph nodes. HEV can also form in the TME. collective term for therapies that enhance the body’s own immune system/immune response to fight cancer. The most well-known therapies are antibody-based immunotherapies, and are the checkpoint inhibitors targeting CTLA-4 (ipilimumab) and PD-1 (pembrolizumab and nivolumab). Examples of cell-based immunotherapies are DC vaccination, adoptive T cell transfer, and chimeric antigen receptor T cell therapy. immune cells important in innate immunity (phagocytosis), which also play a role in adaptive immunity by recruitment of other immune cells that can also act as APCs. immune cells from the myeloid lineage present in tumors that can suppress the antitumor effects of T cells. a subset of T cells that facilitates different processes in immune reactions. T-helper cells are mainly characterized by the expression of the CD4 receptor next to the CD3 molecule. can downregulate or inhibit the T cell-mediated immune response. It is beneficial in preventing autoimmunity but can facilitate immune evasion in cancer. form adjacent to sites of inflammation and have all the features of lymph nodes, to facilitate a local adaptive immune response. defines the non-neoplastic cellular environment of a tumor, including blood vessels, immune cells, fibroblasts, extracellular matrix, cytokines, chemokines, and other active compounds. cytokine that induces angiogenesis." @default.
• W2766860384 created "2017-11-10" @default.
• W2766860384 creator A5012962911 @default.
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• W2766860384 date "2017-11-01" @default.
• W2766860384 modified "2023-10-14" @default.
• W2766860384 title "Migrating into the Tumor: a Roadmap for T Cells" @default.
• W2766860384 cites W1019458012 @default.
• W2766860384 cites W1498931318 @default.
• W2766860384 cites W1763337374 @default.
• W2766860384 cites W1865785905 @default.
• W2766860384 cites W1889335134 @default.
• W2766860384 cites W1892403101 @default.
• W2766860384 cites W1908442436 @default.
• W2766860384 cites W1921451985 @default.
• W2766860384 cites W1944707476 @default.
• W2766860384 cites W1963773088 @default.
• W2766860384 cites W1973759139 @default.
• W2766860384 cites W1983517349 @default.
• W2766860384 cites W1989792740 @default.
• W2766860384 cites W1990779902 @default.
• W2766860384 cites W1991013609 @default.
• W2766860384 cites W1992364481 @default.
• W2766860384 cites W2006202974 @default.
• W2766860384 cites W2011238385 @default.
• W2766860384 cites W2018444159 @default.
• W2766860384 cites W2034586064 @default.
• W2766860384 cites W2037801848 @default.
• W2766860384 cites W2038914273 @default.
• W2766860384 cites W2038974826 @default.
• W2766860384 cites W2039123767 @default.
• W2766860384 cites W2044315378 @default.
• W2766860384 cites W2046182607 @default.
• W2766860384 cites W2046560134 @default.
• W2766860384 cites W2049491375 @default.
• W2766860384 cites W2055746114 @default.
• W2766860384 cites W2060672294 @default.
• W2766860384 cites W2067931754 @default.
• W2766860384 cites W2068868975 @default.
• W2766860384 cites W2075094265 @default.
• W2766860384 cites W2075497099 @default.
• W2766860384 cites W2078917646 @default.
• W2766860384 cites W2080202443 @default.
• W2766860384 cites W2086834665 @default.
• W2766860384 cites W2089202428 @default.
• W2766860384 cites W2092772483 @default.
• W2766860384 cites W2098578630 @default.
• W2766860384 cites W2101583195 @default.
• W2766860384 cites W2103021272 @default.
• W2766860384 cites W2104065243 @default.
• W2766860384 cites W2108972938 @default.
• W2766860384 cites W2113906692 @default.
• W2766860384 cites W2116158418 @default.
• W2766860384 cites W2121391430 @default.
• W2766860384 cites W2121820529 @default.
• W2766860384 cites W2123363005 @default.
• W2766860384 cites W2126481441 @default.
• W2766860384 cites W2126932404 @default.
• W2766860384 cites W2130351739 @default.
• W2766860384 cites W2136731993 @default.
• W2766860384 cites W2136859769 @default.
• W2766860384 cites W2138113004 @default.
• W2766860384 cites W2138880254 @default.
• W2766860384 cites W2139141669 @default.
• W2766860384 cites W2142644858 @default.
• W2766860384 cites W2154667937 @default.
• W2766860384 cites W2160245658 @default.
• W2766860384 cites W2161558877 @default.
• W2766860384 cites W2162222767 @default.
• W2766860384 cites W2167259432 @default.
• W2766860384 cites W2176126538 @default.
• W2766860384 cites W2185780593 @default.
• W2766860384 cites W2251635988 @default.
• W2766860384 cites W2255455167 @default.
• W2766860384 cites W2277674451 @default.
• W2766860384 cites W2294356527 @default.
• W2766860384 cites W2294927533 @default.
• W2766860384 cites W2298299219 @default.
• W2766860384 cites W2308639964 @default.
• W2766860384 cites W2314878272 @default.
• W2766860384 cites W2322919275 @default.
• W2766860384 cites W2335922116 @default.
• W2766860384 cites W2338576144 @default.
• W2766860384 cites W2346108121 @default.
• W2766860384 cites W2349584574 @default.
• W2766860384 cites W2401056916 @default.
• W2766860384 cites W2410618438 @default.
• W2766860384 cites W2463432841 @default.
• W2766860384 cites W2474950788 @default.
• W2766860384 cites W2510964254 @default.
• W2766860384 cites W2511951051 @default.
• W2766860384 cites W2512913584 @default.
• W2766860384 cites W2513439890 @default.
• W2766860384 cites W2514202874 @default.
• W2766860384 cites W2528861955 @default.

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