Publications by authors named "Fernando P Canale"

Article Synopsis
  • Tumor progression leads to fibrosis, which involves excessive buildup of extracellular matrix and reduces immune cell infiltration, particularly affecting CD8 T cells.
  • Tumor-associated macrophages (TAMs) adapt to the stiff fibrotic environment by promoting collagen production through signaling from transforming growth factor-β.
  • This collagen production by TAMs creates a challenging metabolic environment that limits the effectiveness of CD8 T cells, hindering their ability to mount strong antitumor responses in breast cancer patients.
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Article Synopsis
  • Conventional CD4 T lymphocytes, particularly those expressing CD39, play a critical, yet not fully understood, role in fighting tumors, showing distinct characteristics in cancer environments.
  • In mouse cancer models, these CD39 Tconv cells displayed traits of exhaustion, high cytotoxic potential, and specific protein expressions, differentiating them from their counterparts in lymphoid organs.
  • In breast cancer patients, CD39 Tconv cells were less common in non-tumoral tissues and linked to improved survival rates, highlighting CD39 as a potential biomarker for assessing immune responses in tumors.
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IL-17 immune responses in cancer are controversial, with both tumor-promoting and tumor-repressing effects observed. To clarify the role of IL-17 signaling in cancer progression, we used syngeneic tumor models from different tissue origins. We found that deficiencies in host IL-17RA or IL-17A/F expression had varying effects on the growth of different solid tumors including melanoma, sarcoma, lymphoma, and leukemia.

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Article Synopsis
  • Scientists studied how immune cells stop working well in liver cancer to help create better treatments.
  • They found that certain cells called macrophages make an enzyme that weakens their ability to fight tumors.
  • They also discovered a protein in T cells that can be targeted to improve their effectiveness against cancer when combined with existing therapies.
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The availability of L-arginine in tumours is a key determinant of an efficient anti-tumour T cell response. Consequently, increases of typically low L-arginine concentrations within the tumour may greatly potentiate the anti-tumour responses of immune checkpoint inhibitors, such as programmed death-ligand 1 (PD-L1)-blocking antibodies. However, currently no means are available to locally increase intratumoural L-arginine levels.

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Senescent T cells have been described during aging, chronic infections, and cancer; however, a comprehensive study of the phenotype, function, and transcriptional program of this T cell population in breast cancer (BC) patients is missing. Compared to healthy donors (HDs), BC patients exhibit an accumulation of KLRG-1CD57 CD4 and CD8 T cells in peripheral blood. These T cells infiltrate tumors and tumor-draining lymph nodes.

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While it is now acknowledged that CD4 T cells expressing CD25 and Foxp3 (Treg cells) regulate immune responses and, consequently, influence the pathogenesis of infectious diseases, the regulatory response mediated by Treg cells upon infection by was still poorly characterized. In order to understand the role of Treg cells during infection by this protozoan parasite, we determined in time and space the magnitude of the regulatory response and the phenotypic, functional and transcriptional features of the Treg cell population in infected mice. Contrary to the accumulation of Treg cells reported in most chronic infections in mice and humans, experimental infection was characterized by sustained numbers but decreased relative frequency of Treg cells.

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The ability of CD8 T lymphocytes to eliminate tumors is limited by their ability to engender an immunosuppressive microenvironment. Here we describe a subset of tumor-infiltrating CD8 T cells marked by high expression of the immunosuppressive ATP ecto-nucleotidase CD39. The frequency of CD39CD8 T cells increased with tumor growth but was absent in lymphoid organs.

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