We are analyzing https://link.springer.com/article/10.1007/s00262-019-02374-0.

Title:
CD4+ T cells indirectly kill tumor cells via induction of cytotoxic macrophages in mouse models | Cancer Immunology, Immunotherapy
Description:
It is well recognized that CD4+ T cells may play an important role in immunosurveillance and immunotherapy against cancer. However, the details of how these cells recognize and eliminate the tumor cells remain incompletely understood. For the past 25 years, we have focused on how CD4+ T cells reject multiple myeloma cells in a murine model (MOPC315). In our experimental system, the secreted tumor-specific antigen is taken up by tumor-infiltrating macrophages that process it and present a neoepitope [a V region-derived idiotypic (Id) peptide] on MHC class II molecules to Th1 cells. Stimulated Th1 cells produce IFNγ, which activates macrophages in a manner that elicits an M1-like, tumoricidal phenotype. Through an inducible nitric oxide synthetase (iNOS)-dependent mechanism, the M1 macrophages secrete nitric oxide (NO) that diffuses into neighboring tumor cells. Inside the tumor cells, NO-derived reactive nitrogen species, including peroxynitrite, causes nitrosylation of proteins and triggers apoptosis by the intrinsic apoptotic pathway. This mode of indirect tumor recognition by CD4+ T cells operates independently of MHC class II expression on cancer cells. However, secretion of the tumor-specific antigen, and uptake and MHCII presentation on macrophages, is required for rejection. Similar mechanisms can also be observed in a B-lymphoma model and in the unrelated B16 melanoma model. Our findings reveal a novel mechanism by which CD4+ T cells kill tumor cells indirectly via induction of intratumoral cytotoxic macrophages. The data suggest that induction of M1 polarization of tumor-infiltrating macrophages, by CD4+ T cells or through other means, could serve as an immunotherapeutic strategy.
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Keywords {🔍}

cells, pubmed, article, google, scholar, cas, bogen, cancer, tumor, central, immunol, cell, haabeth, macrophages, tumorspecific, class, fauskanger, myeloma, tveita, antigen, cytotoxic, mhc, melanoma, eur, httpsdoiorgeji, hofgaard, corthay, research, immunology, immunotherapy, bjarne, immunosurveillance, access, med, vivo, idiotypespecific, eradicate, privacy, cookies, content, kill, induction, role, model, nitric, oxide, lauritzsen, weiss, dembic, lundin,

Topics {✒️}

indirect cd4 + t-cell-mediated elimination major histocompatibility complex-restricted month download article/chapter t-cell-mediated rejection fas ligand–fas interaction b-cell lymphoma resulting myelomas activate tumor-specific secreted tumor-specific antigen cell receptor-bearing thymocytes class ii molecules full article pdf article cancer immunology naive tumor-specific cd4 b-lymphoma cells process b-cell tumors antitumor immune respons naive idiotype-specific cd4 + cells eradicate melanoma antigen-negative cells lauritzsen gf mhc-restricted th1 b-cell lymphoma privacy choices/manage cookies lorvik kb related subjects influenza vaccine research indirect tumor recognition b-cell cancer tveita aa weak positive selection cells cd4-positive tumor-specific antigen anti-tumour activity european economic area single cell level neighboring tumor cells eradicating tumor cells tumor-specific cd4 + b-lymphoma model tumour-derived antigen tumour-specific cd4 tumor escape mechanism tumor-reactive cd4 + melanosome membrane protein central role norwegian cancer society metastatic melanoma tumor-specific lyt-1 + 2 van den broek article bogen

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         headline:CD4+ T cells indirectly kill tumor cells via induction of cytotoxic macrophages in mouse models
         description:It is well recognized that CD4+ T cells may play an important role in immunosurveillance and immunotherapy against cancer. However, the details of how these cells recognize and eliminate the tumor cells remain incompletely understood. For the past 25 years, we have focused on how CD4+ T cells reject multiple myeloma cells in a murine model (MOPC315). In our experimental system, the secreted tumor-specific antigen is taken up by tumor-infiltrating macrophages that process it and present a neoepitope [a V region-derived idiotypic (Id) peptide] on MHC class II molecules to Th1 cells. Stimulated Th1 cells produce IFNγ, which activates macrophages in a manner that elicits an M1-like, tumoricidal phenotype. Through an inducible nitric oxide synthetase (iNOS)-dependent mechanism, the M1 macrophages secrete nitric oxide (NO) that diffuses into neighboring tumor cells. Inside the tumor cells, NO-derived reactive nitrogen species, including peroxynitrite, causes nitrosylation of proteins and triggers apoptosis by the intrinsic apoptotic pathway. This mode of indirect tumor recognition by CD4+ T cells operates independently of MHC class II expression on cancer cells. However, secretion of the tumor-specific antigen, and uptake and MHCII presentation on macrophages, is required for rejection. Similar mechanisms can also be observed in a B-lymphoma model and in the unrelated B16 melanoma model. Our findings reveal a novel mechanism by which CD4+ T cells kill tumor cells indirectly via induction of intratumoral cytotoxic macrophages. The data suggest that induction of M1 polarization of tumor-infiltrating macrophages, by CD4+ T cells or through other means, could serve as an immunotherapeutic strategy.
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      headline:CD4+ T cells indirectly kill tumor cells via induction of cytotoxic macrophages in mouse models
      description:It is well recognized that CD4+ T cells may play an important role in immunosurveillance and immunotherapy against cancer. However, the details of how these cells recognize and eliminate the tumor cells remain incompletely understood. For the past 25 years, we have focused on how CD4+ T cells reject multiple myeloma cells in a murine model (MOPC315). In our experimental system, the secreted tumor-specific antigen is taken up by tumor-infiltrating macrophages that process it and present a neoepitope [a V region-derived idiotypic (Id) peptide] on MHC class II molecules to Th1 cells. Stimulated Th1 cells produce IFNγ, which activates macrophages in a manner that elicits an M1-like, tumoricidal phenotype. Through an inducible nitric oxide synthetase (iNOS)-dependent mechanism, the M1 macrophages secrete nitric oxide (NO) that diffuses into neighboring tumor cells. Inside the tumor cells, NO-derived reactive nitrogen species, including peroxynitrite, causes nitrosylation of proteins and triggers apoptosis by the intrinsic apoptotic pathway. This mode of indirect tumor recognition by CD4+ T cells operates independently of MHC class II expression on cancer cells. However, secretion of the tumor-specific antigen, and uptake and MHCII presentation on macrophages, is required for rejection. Similar mechanisms can also be observed in a B-lymphoma model and in the unrelated B16 melanoma model. Our findings reveal a novel mechanism by which CD4+ T cells kill tumor cells indirectly via induction of intratumoral cytotoxic macrophages. The data suggest that induction of M1 polarization of tumor-infiltrating macrophages, by CD4+ T cells or through other means, could serve as an immunotherapeutic strategy.
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