Immunosurveillance

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Guido Kroemer - One of the best experts on this subject based on the ideXlab platform.

  • atp and cancer Immunosurveillance
    The EMBO Journal, 2021
    Co-Authors: Guido Kroemer, Takahiro Yamazaki, Oliver Kepp, Lucillia Bezu, Francesco Di Virgilio, Mark J Smyth, Lorenzo Galluzzi
    Abstract:

    While intracellular adenosine triphosphate (ATP) occupies a key position in the bioenergetic metabolism of all the cellular compartments that form the tumor microenvironment (TME), extracellular ATP operates as a potent signal transducer. The net effects of purinergic signaling on the biology of the TME depend not only on the specific receptors and cell types involved, but also on the activation status of cis- and trans-regulatory circuitries. As an additional layer of complexity, extracellular ATP is rapidly catabolized by ectonucleotidases, culminating in the accumulation of metabolites that mediate distinct biological effects. Here, we discuss the molecular and cellular mechanisms through which ATP and its degradation products influence cancer Immunosurveillance, with a focus on therapeutically targetable circuitries.

  • subversion of calreticulin exposure as a strategy of immune escape
    Cancer Cell, 2021
    Co-Authors: Guido Kroemer, Laurence Zitvogel
    Abstract:

    In this issue, Lin et al. report that, in malignant cells, stanniocalcin-1 (STC1) prevents the cell surface exposure of the "eat me" signal calreticulin, thereby avoiding phagocytosis by antigen-presenting cells. STC1 overexpression joins an arsenal of mechanisms through which tumor cells suppress calreticulin exposure and escape from Immunosurveillance.

  • secreted calreticulin mutants subvert anticancer Immunosurveillance
    OncoImmunology, 2020
    Co-Authors: Peng Liu, Guido Kroemer, Liwei Zhao, Oliver Kepp
    Abstract:

    Mutations of the gene coding for calreticulin (CALR) that cause the loss of the C-terminal KDEL motif abolish its retention in the endoplasmic reticulum and cause CALR to be secreted from cells. Specific CALR mutants bearing a novel C-terminus can precipitate the manifestation of myeloproliferative diseases via the autocrine activation of the thrombopoietin receptor. We recently employed the retention using selective hooks (RUSH) technology to monitor CALR trafficking and demonstrated the secretion of C-terminally truncated variants of CALR in vitro and in vivo. Of note, extracellular CALR inhibited the phagocytosis of dying cancer cells by dendritic cells (DC). Via this mechanism, mutant CALR induced immunosuppression, which decreased the efficacy of immunogenic anticancer chemotherapies and PD-1 blockade.

  • secreted calreticulin mutants subvert anticancer Immunosurveillance
    OncoImmunology, 2020
    Co-Authors: Peng Liu, Guido Kroemer, Liwei Zhao, Oliver Kepp
    Abstract:

    Mutations of the gene coding for calreticulin (CALR) that cause the loss of the C-terminal KDEL motif abolish its retention in the endoplasmic reticulum and cause CALR to be secreted from cells. Sp...

  • leptin producing oncolytic virus makes tumor infiltrating t cells fit not fat
    Immunity, 2019
    Co-Authors: Guido Kroemer, Laurence Zitvogel
    Abstract:

    Effective anticancer Immunosurveillance after oncolytic viral infection is often hindered by the defective metabolic function of tumor-infiltrating lymphocytes (TILs). A recent paper by Rivadeneira et al. demonstrates that intratumoral delivery of leptin by a recombinant oncolytic vaccinia virus can metabolically enhance TIL effector and memory functions through improved mitochondrial oxidative phosphorylation, thereby enhancing therapeutic efficacy.

Laurence Zitvogel - One of the best experts on this subject based on the ideXlab platform.

  • subversion of calreticulin exposure as a strategy of immune escape
    Cancer Cell, 2021
    Co-Authors: Guido Kroemer, Laurence Zitvogel
    Abstract:

    In this issue, Lin et al. report that, in malignant cells, stanniocalcin-1 (STC1) prevents the cell surface exposure of the "eat me" signal calreticulin, thereby avoiding phagocytosis by antigen-presenting cells. STC1 overexpression joins an arsenal of mechanisms through which tumor cells suppress calreticulin exposure and escape from Immunosurveillance.

  • leptin producing oncolytic virus makes tumor infiltrating t cells fit not fat
    Immunity, 2019
    Co-Authors: Guido Kroemer, Laurence Zitvogel
    Abstract:

    Effective anticancer Immunosurveillance after oncolytic viral infection is often hindered by the defective metabolic function of tumor-infiltrating lymphocytes (TILs). A recent paper by Rivadeneira et al. demonstrates that intratumoral delivery of leptin by a recombinant oncolytic vaccinia virus can metabolically enhance TIL effector and memory functions through improved mitochondrial oxidative phosphorylation, thereby enhancing therapeutic efficacy.

  • contribution of annexin a1 to anticancer Immunosurveillance
    OncoImmunology, 2019
    Co-Authors: Laurence Zitvogel, Erika Vacchelli, Elisa Elena Baracco, Gautier Stoll, Peter Van Endert, Guido Kroemer
    Abstract:

    Mouse cancers lacking the expression of annexin A1 (ANXA1) fail to respond to immunogenic chemotherapies. This has been initially explained by the requirement of extracellular ANXA1 (which is released from dying cancer cells) to engage formyl peptide receptor-1 (FPR1) on dendritic cells (DC) for the establishment of corpse/DC synapses. Here, we show that ANXA1-deficent cancer cells exhibit a defect in the exposure of calreticulin (CALR), which is an important "eat-me" signal, facilitating the phagocytic uptake of dead-cell antigens by DC. Of note, intratumoral injection of recombinant CALR protein was able to restore the therapeutic response of ANXA1-deficient cancers to anthracycline-based chemotherapy. Carcinomas developing in patients tend to downregulate ANXA1 expression as compared to their normal tissues of origin. ANXA1-low breast, colorectal, lung and kidney cancers are scarcely infiltrated by DC and cytotoxic T lymphocytes, supporting the idea that ANXA1 deficiency facilitates immune escape. We propose that such ANXA1-low cancers might be particularly suitable to local immunotherapy with CALR protein.

  • failure of Immunosurveillance accelerates aging
    OncoImmunology, 2019
    Co-Authors: Maria Perezlanzon, Laurence Zitvogel, Guido Kroemer
    Abstract:

    Immunosurveillance is generally conceived as a mechanism through which the immune system detects and eliminates (pre-)malignant cells, thus reducing the risk of developing cancer. A recent paper by Ovadya et al. demonstrates that knockout of the gene coding for perforin-1 causes accelerated accumulation of senescent cells in multiple mouse organs, thereby speeding up the aging process. These results suggest that Immunosurveillance plays a much broader role in maintaining organismal health than it had been suspected.

  • unchaining nk cell mediated anticancer Immunosurveillance
    Nature Immunology, 2016
    Co-Authors: Laurence Zitvogel, Guido Kroemer
    Abstract:

    In natural killer (NK) cells, CIS restrains a signaling pathway elicited by interleukin 15 (IL-15) that leads to activation of the kinase JAK1. Removal of CIS from NK cells increases their capacity to reduce the metastatic dissemination of breast cancer and melanoma in mice.

Robert D. Schreiber - One of the best experts on this subject based on the ideXlab platform.

  • interferons immunity and cancer immunoediting
    Nature Reviews Immunology, 2006
    Co-Authors: Gavin P Dunn, Catherine M Koebel, Robert D. Schreiber
    Abstract:

    A clear picture of the dynamic relationship between the host immune system and cancer is emerging as the cells and molecules that participate in naturally occurring antitumour immune responses are being identified. The interferons (IFNs) - that is, the type I IFNs (IFNalpha and IFNbeta) and type II IFN (IFNgamma) - have emerged as central coordinators of tumour-immune-system interactions. Indeed, the decade-old finding that IFNgamma has a pivotal role in promoting antitumour responses became the focus for a renewed interest in the largely abandoned concept of cancer Immunosurveillance. More recently, type I IFNs have been found to have distinct functions in this process. In this Review, we discuss the roles of the IFNs, not only in cancer Immunosurveillance but also in the broader process of cancer immunoediting.

  • The immunobiology of cancer Immunosurveillance and immunoediting
    Immunity, 2004
    Co-Authors: Gavin P Dunn, Lloyd J. Old, Robert D. Schreiber
    Abstract:

    The last fifteen years have seen a reemergence of interest in cancer Immunosurveillance and a broadening of this concept into one termed cancer immunoediting. The latter, supported by strong experimental data derived from murine tumor models and provocative correlative data obtained by studying human cancer, holds that the immune system not only protects the host against development of primary nonviral cancers but also sculpts tumor immunogenicity. Cancer immunoediting is a process consisting of three phases: elimination (i.e., cancer Immunosurveillance), equilibrium, and escape. Herein, we summarize the data supporting the existence of each of the three cancer immunoediting phases. The full understanding of the immunobiology of cancer Immunosurveillance and immunoediting will hopefully stimulate development of more effective immunotherapeutic approaches to control and/or eliminate human cancers.

  • Cancer immunoediting: from Immunosurveillance to tumor escape
    Nature Immunology, 2002
    Co-Authors: Gavin P Dunn, Lloyd J. Old, Hiroaki Ikeda, Allen T Bruce, Robert D. Schreiber
    Abstract:

    The concept that the immune system can recognize and destroy nascent transformed cells was originally embodied in the cancer Immunosurveillance hypothesis of Burnet and Thomas. This hypothesis was abandoned shortly afterwards because of the absence of strong experimental evidence supporting the concept. New data, however, clearly show the existence of cancer Immunosurveillance and also indicate that it may function as a component of a more general process of cancer immunoediting. This process is responsible for both eliminating tumors and sculpting the immunogenic phenotypes of tumors that eventually form in immunocompetent hosts. In this review, we will summarize the historical and experimental basis of cancer immunoediting and discuss its dual roles in promoting host protection against cancer and facilitating tumor escape from immune destruction.

  • cancer immunoediting from immuno surveillance to tumor escape
    2002
    Co-Authors: Gavin P Dunn, Lloyd J. Old, Hiroaki Ikeda, Allen T Bruce, Robert D. Schreiber
    Abstract:

    The concept that the immune system can recognize and destroy nascent transformed cells was originally embodied in the cancer Immunosurveillance hypothesis of Burnet and Thomas. This hypothesis was abandoned shortly afterwards because of the absence of strong experimental evidence supporting the concept. New data, however, clearly show the existence of cancer Immunosurveillance and also indicate that it may function as a component of a more general process of cancer immunoediting. This process is responsible for both eliminating tumors and sculpting the immunogenic phenotypes of tumors that eventually form in immunocompetent hosts. In this review, we will summarize the historical and experimental basis of cancer immunoediting and discuss its dual roles in promoting host protection against cancer and facilitating tumor escape from immune destruction.

Heather D Hickman - One of the best experts on this subject based on the ideXlab platform.

  • influenza a virus negative strand rna is translated for cd8 t cell Immunosurveillance
    Journal of Immunology, 2018
    Co-Authors: Heather D Hickman, Jacqueline W Mays, James S Gibbs, Ivan Kosik, Javier G Magadan, Kazuyo Takeda, Suman R Das, Glennys V Reynoso, Barbara F Ngudiankama, Jiajie Wei
    Abstract:

    Probing the limits of CD8+ T cell Immunosurveillance, we inserted the SIINFEKL peptide into influenza A virus (IAV)-negative strand gene segments. Although IAV genomic RNA is considered noncoding, there is a conserved, relatively long open reading frame present in segment 8, encoding a potential protein termed NEG8. The biosynthesis of NEG8 from IAV has yet to be demonstrated. Although we failed to detect NEG8 protein expression in IAV-infected mouse cells, cell surface Kb-SIINFEKL complexes are generated when SIINFEKL is genetically appended to the predicted C terminus of NEG8, as shown by activation of OT-I T cells in vitro and in vivo. Moreover, recombinant IAV encoding of SIINFEKL embedded in the negative strand of the neuraminidase-stalk coding sequence also activates OT-I T cells in mice. Together, our findings demonstrate both the translation of sequences on the negative strand of a single-stranded RNA virus and its relevance in antiviral Immunosurveillance.

  • influenza a virus negative strand rna is translated for cd8 t cell Immunosurveillance
    bioRxiv, 2018
    Co-Authors: Heather D Hickman, Jacqueline W Mays, James S Gibbs, Ivan Kosik, Javier G Magadan, Kazuyo Takeda, Suman R Das, Glennys V Reynoso, Barbara F Ngudiankama, Jiajie Wei
    Abstract:

    To probe the limits of CD8+ T cell Immunosurveillance, we inserted the model peptide SIINFEKL into influenza A virus (IAV) negative strand gene segments. Although IAV genomic RNA is widely considered as non-coding, there is a conserved, relatively long open reading frame present in the genomic strand of segment eight, encoding a potential protein termed NEG8. The biosynthesis of NEG8 from IAV has yet to be demonstrated. While we failed to detect NEG8 protein expression in IAV infected cells, cell surface Kb-SIINFEKL complexes are generated when SIINFEKL is genetically appended to the predicted COOH-terminus of NEG8, as shown by activation of OT-I T cells in vitro and in vivo. Moreover, recombinant IAV encoding SIINFEKL embedded in the negative strand of the NA-stalk coding sequence also activates OT-I T cells in vivo. Together, our findings demonstrate both the translation of sequences on the negative strand of a single stranded RNA virus and its relevance anti-viral Immunosurveillance.

  • intravital mucosal imaging of cd8 resident memory t cells shows tissue autonomous recall responses that amplify secondary memory
    Nature Immunology, 2018
    Co-Authors: Lalit K Beura, Jason S Mitchell, Emily A Thompson, Jason M Schenkel, Javed Mohammed, Sathi Wijeyesinghe, Raissa Fonseca, Brandon J Burbach, Heather D Hickman, Vaiva Vezys
    Abstract:

    CD8+ T cell Immunosurveillance dynamics influence the outcome of intracellular infections and cancer. Here we used two-photon intravital microscopy to visualize the responses of CD8+ resident memory T cells (TRM cells) within the reproductive tracts of live female mice. We found that mucosal TRM cells were highly motile, but paused and underwent in situ division after local antigen challenge. TRM cell reactivation triggered the recruitment of recirculating memory T cells that underwent antigen-independent TRM cell differentiation in situ. However, the proliferation of pre-existing TRM cells dominated the local mucosal recall response and contributed most substantially to the boosted secondary TRM cell population. We observed similar results in skin. Thus, TRM cells can autonomously regulate the expansion of local Immunosurveillance independently of central memory or proliferation in lymphoid tissue.

  • intravital mucosal imaging of cd8 resident memory t cells shows tissue autonomous recall responses that amplify secondary memory
    Nature Immunology, 2018
    Co-Authors: Lalit K Beura, Jason S Mitchell, Emily A Thompson, Jason M Schenkel, Javed Mohammed, Sathi Wijeyesinghe, Raissa Fonseca, Brandon J Burbach, Heather D Hickman, Vaiva Vezys
    Abstract:

    CD8+ T cell Immunosurveillance dynamics influence the outcome of intracellular infections and cancer. Here we used two-photon intravital microscopy to visualize the responses of CD8+ resident memory T cells (TRM cells) within the reproductive tracts of live female mice. We found that mucosal TRM cells were highly motile, but paused and underwent in situ division after local antigen challenge. TRM cell reactivation triggered the recruitment of recirculating memory T cells that underwent antigen-independent TRM cell differentiation in situ. However, the proliferation of pre-existing TRM cells dominated the local mucosal recall response and contributed most substantially to the boosted secondary TRM cell population. We observed similar results in skin. Thus, TRM cells can autonomously regulate the expansion of local Immunosurveillance independently of central memory or proliferation in lymphoid tissue. Masopust and colleagues show that mucosal tissue-resident memory T cells proliferate in situ in response to local antigen and dominate the local recall response.

Vaiva Vezys - One of the best experts on this subject based on the ideXlab platform.

  • intravital mucosal imaging of cd8 resident memory t cells shows tissue autonomous recall responses that amplify secondary memory
    Nature Immunology, 2018
    Co-Authors: Lalit K Beura, Jason S Mitchell, Emily A Thompson, Jason M Schenkel, Javed Mohammed, Sathi Wijeyesinghe, Raissa Fonseca, Brandon J Burbach, Heather D Hickman, Vaiva Vezys
    Abstract:

    CD8+ T cell Immunosurveillance dynamics influence the outcome of intracellular infections and cancer. Here we used two-photon intravital microscopy to visualize the responses of CD8+ resident memory T cells (TRM cells) within the reproductive tracts of live female mice. We found that mucosal TRM cells were highly motile, but paused and underwent in situ division after local antigen challenge. TRM cell reactivation triggered the recruitment of recirculating memory T cells that underwent antigen-independent TRM cell differentiation in situ. However, the proliferation of pre-existing TRM cells dominated the local mucosal recall response and contributed most substantially to the boosted secondary TRM cell population. We observed similar results in skin. Thus, TRM cells can autonomously regulate the expansion of local Immunosurveillance independently of central memory or proliferation in lymphoid tissue.

  • intravital mucosal imaging of cd8 resident memory t cells shows tissue autonomous recall responses that amplify secondary memory
    Nature Immunology, 2018
    Co-Authors: Lalit K Beura, Jason S Mitchell, Emily A Thompson, Jason M Schenkel, Javed Mohammed, Sathi Wijeyesinghe, Raissa Fonseca, Brandon J Burbach, Heather D Hickman, Vaiva Vezys
    Abstract:

    CD8+ T cell Immunosurveillance dynamics influence the outcome of intracellular infections and cancer. Here we used two-photon intravital microscopy to visualize the responses of CD8+ resident memory T cells (TRM cells) within the reproductive tracts of live female mice. We found that mucosal TRM cells were highly motile, but paused and underwent in situ division after local antigen challenge. TRM cell reactivation triggered the recruitment of recirculating memory T cells that underwent antigen-independent TRM cell differentiation in situ. However, the proliferation of pre-existing TRM cells dominated the local mucosal recall response and contributed most substantially to the boosted secondary TRM cell population. We observed similar results in skin. Thus, TRM cells can autonomously regulate the expansion of local Immunosurveillance independently of central memory or proliferation in lymphoid tissue. Masopust and colleagues show that mucosal tissue-resident memory T cells proliferate in situ in response to local antigen and dominate the local recall response.