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MACROPHAGE CD5L IS A NOVEL TARGET FOR CANCER IMMUNOTHERAPY

ABSTRACT: MACROPHAGE CD5L IS A NOVEL TARGET FOR CANCER IMMUNOTHERAPY

PROVIDER: PRJNA858429 | ENA |

REPOSITORIES: ENA

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MACROPHAGE CD5L IS A NOVEL TARGET FOR CANCER IMMUNOTHERAPY

Project description:Tumor associated macrophages (TAMs) can acquire an immunosuppressive, M2 polarization phenotype, thereby promoting tumor growth and protecting it from chemo or immuno-therapy. Since TAMs are plastic cells, their selective reprogramming presents an attractive therapeutic strategy. CD5L is a macrophage glycoprotein that controls key mechanisms in inflammatory responses and promotes M2 polarization. Here we report that CD5L TAMs expression in lung adenocarcinoma correlates with poor outcome. Additionally, cancer cell CMs induced macrophage M2 polarization and enhanced CD5L expression. We have raised a novel monoclonal antibody (mAb), RImAb, that specifically binds to human and mouse CD5L and blocks its M2 polarizing activity. RImAb administration reduced tumor growth in a mouse subcutaneous syngeneic model of lung cancer and modified the tumor microenvironment, altering intratumoral immune cell population profile, decreasing vascularity, and increasing the inflammatory milieu. The present study reveals a key function for CD5L protein in modulating macrophage activity and its interactions within the TME. Targeting CD5L with a mAb, was able to reduce tumor growth and modulate the TME, thus representing a promising approach to cancer immunotherapy.

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A phosphatase-like nanomaterial promotes autophagy and reprograms macrophage for cancer immunotherapy

Project description:Macrophages are very plastic and play key roles in maintenance of tissue homeostasis. In cancer progression, macrophages also take parts through all the processes, from the initiation, progression, to the final tumor metastasis. Although energy deprivation and autophagy are widely used for cancer therapy, most of these strategies are not meant to target macrophages resulting in undesired effects and unsatisfactory outcomes for cancer immunotherapy. Herein, we developed a lanthanum nickel oxide (LNO) nanozyme that possesses phosphatase-like activity for ATP hydrolysis. Meanwhile, the autophagy of macrophages induced by LNO promotes the polarization of macrophages from M2-like macrophage (M2) to M1-like macrophage (M1) and reduces tumor-associated macrophages in tumor-bearing mice, exhibiting capability of killing tumor-associated macrophage and anti-tumor effect in vivo. Furthermore, pre-coating by myeloid cell membrane on the surface of LNO significantly enhanced antitumor immunity. Our findings demonstrate that phosphatase-like nanozyme, LNO can specifically induce macrophage autophagy that improves therapeutic efficacy and offers valuable strategies for cancer immunotherapy.

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Novel HLA ligands and Tcell epitopes for immunotherapy of lung cancer

Project description:Analysis of gene expression data to evaluate candidate targets for immunotherapy. Analysis of gene expression data to evaluate candidate targets for immunotherapy, We analyse 7 lung cancer samples and 3 reference samples (2x kidney, 1x lung).

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IGSF8 is an Innate Immune Checkpoint and Cancer Immunotherapy Target

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Extracellular matrix educates a tumor macrophage phenotype found in ovarian cancer metastasis

Project description:Recent studies have shown the tumor extracellular matrix (ECM) associates with immunosuppression, and that targeting the ECM can improve immune infiltration and immunotherapy response. A question that remains is whether the ECM is directly educating the immune phenotypes seen in cancer. We identified a tumor-associated macrophage (TAM) population correlated with poor prognosis, interruption of the cancer immunity cycle, and tumor ECM composition. To investigate whether ECM was capable of generating the TAM phenotype seen, we developed a decellularized tissue model that retains the native ECM architecture and composition. Macrophages cultured on decellularized ovarian metastasis shared transcriptional profiles with the TAMs found in human tissues. ECM educated macrophages have a tissue remodeling and immunoregulatory phenotype, inducing altered T cell function. We conclude that the tumor ECM is directly educating this macrophage population found in cancer tissues. Therefore, current and emerging cancer therapies that target the tumor ECM may be tailored to improve macrophage phenotype and their downstream regulation of immunity.

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