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Rodrigues Mantuano, N.

Publications and source records attributed to Rodrigues Mantuano, N..

3 recordsLinked to original sources

Longitudinal profiling of tumor-reactive T cells during TIL therapy in metastatic melanoma

Adoptive cell therapy (ACT) with expanded autologous tumor-infiltrating lymphocytes (TILs) can induce durable responses in metastatic melanoma, yet many patients relapse. We profiled tumor-reactive T cell dynamics during TIL therapy using single-cell RNA and TCR sequencing from seven patients to elucidate underlying reasons. We found that tumor-reactive T cells preferentially expanded early during ex vivo TIL culture, transitioning from exhausted to reinvigorated effector states. Particularly, CD8+ exhausted T cells (Tex) and CD4+ follicular helper T cell (Tfh), but not CD4+ Tex, were efficiently reinvigorated. Further, we resolved the heterogeneity of tumor-reactive CD8+ and CD4+ subsets, defining unique signatures for their identification during TIL expansion. In addition, non-responders (NRs) exhibit increased levels of Type 17 T cells in TIL products, suggesting a potential association with resistance to therapy. After transfer, tumor-reactive clones rapidly extravasated and established a stem-like reservoir. However, in NRs, CD4+ regulatory T cells (Tregs) expanded de novo and tumor-reactive CD8+ T cells reacquired exhaustion markers, limiting their functionality. By contrast, responders (Rs) retained a pool of less differentiated, stem-like cells. Collectively, these data provide a comprehensive analysis of T cell fates during TIL-ACT providing the basis for new approaches to enhance therapeutic strategies.

immunology↗

Engagement of sialylated glycans with Siglec receptors on myeloid suppressor cells inhibit anti-cancer immunity via CCL2

Overexpression of sialic acids on glycans, called hypersialylation is a common alteration found in cancer. Hypersialylation can, for example, enhance immune evasion via interaction with sialic acid-binding immunoglobulin-like lectin (Siglec) receptors on tumor-infiltrating immune cells. Here, we tested the role of sialic acid on myeloid-derived suppressor cells (MDSCs) and their interaction with Siglec receptors. We found that MDSCs derived from the blood of lung cancer patients and tumor-bearing mice strongly express inhibitory Siglec receptors. In murine cancer models of emergency myelopoiesis, Siglec-E knockout on myeloid cells resulted in prolonged survival and increased infiltration of activated T cells. Targeting suppressive myeloid cells by blocking Siglec receptors or desialylation led to strong reduction of their suppressive potential. We further identified CCL2 as mediator involved in T cell suppression upon interaction of sialoglycans and Siglec receptors on MDSCs. Our results provide mechanistic insights how sialylated glycans inhibit anti-cancer immunity by facilitating CCL2 expression. O_FIG O_LINKSMALLFIG WIDTH=142 HEIGHT=200 SRC="FIGDIR/small/547025v1_ufig1.gif" ALT="Figure 1"> View larger version (42K): org.highwire.dtl.DTLVardef@e7664forg.highwire.dtl.DTLVardef@1edd220org.highwire.dtl.DTLVardef@7e630dorg.highwire.dtl.DTLVardef@198ff40_HPS_FORMAT_FIGEXP M_FIG C_FIG

immunology↗

Hyperglycemia enhances cancer immune evasion by inducing alternative macrophage polarization through increased O-GlcNAcylation

Diabetes mellitus (DM) significantly increases the risk for cancer and cancer progression. Hyperglycemia is the defining characteristic of DM and tightly correlates with a poor prognosis in cancer patients. The hexosamine biosynthetic pathway (HBP) is emerging as a pivotal cascade linking high glucose, tumor progression and impaired immune function. Here we show that enhanced glucose flow through the HBP drives cancer progression and immune evasion by increasing O-GlcNAcylation in tumor-associated macrophages (TAMs). Increased O-GlcNAc skewed macrophage polarization to a M2-like phenotype. HBP or O-GlcNAcylation inhibition reprogrammed TAMs to an anti-tumoral phenotype. Finally, we found an upregulation of M2 markers on TAMs in DM2 patients with colorectal cancer compared to non-diabetic normoglycemic patients. Our results provide evidence for a new and targetable mechanism of cancer immune evasion in patients with hyperglycemia, advocating for strict control of hyperglycemia in cancer patients.\n\nSignificanceHyperglycemia increases O-GlcNAc levels in TAMs, programing them to a pro-tumorigenic phenotype (M2-like), contributing to cancer progression. Inhibition of O-GlcNAcylation could therefore be used to reprogram intratumoral macrophages to an anti-tumoral phenotype.

cancer biology↗