scholarly journals LncRNA NEAT1 Interacted With DNMT1 to Regulate Malignant Phenotype of Cancer Cell and Cytotoxic T Cell Infiltration via Epigenetic Inhibition of p53, cGAS, and STING in Lung Cancer

2020 ◽  
Vol 11 ◽  
Author(s):  
Fang Ma ◽  
Yi-Yu Lei ◽  
Meng-Ge Ding ◽  
Li-Hua Luo ◽  
Yang-Chun Xie ◽  
...  
Keyword(s):  
Lung Cancer ◽  
T Cell ◽  
Cancer Cell ◽  
Cell Infiltration ◽  
Cytotoxic T Cell ◽  
Malignant Phenotype ◽  
T Cell Infiltration ◽  
Lncrna Neat1

scholarly journals Modelling the interplay between the CD4$$^{+}$$/CD8$$^{+}$$ T-cell ratio and the expression of MHC-I in tumours

2021 ◽  
Vol 83 (1) ◽  
Author(s):  
Christian John Hurry ◽  
Alexander Mozeika ◽  
Alessia Annibale
Keyword(s):  
Immune Response ◽  
T Cell ◽  
Critical Level ◽  
Cell Infiltration ◽  
Cytotoxic T Cell ◽  
Mhc I ◽  
Cell Ratio ◽  
T Cell Infiltration ◽  
Immunological Mechanisms ◽  
Tcr Repertoire

AbstractDescribing the anti-tumour immune response as a series of cellular kinetic reactions from known immunological mechanisms, we create a mathematical model that shows the CD4$$^{+}$$ + /CD8$$^{+}$$ + T-cell ratio, T-cell infiltration and the expression of MHC-I to be interacting factors in tumour elimination. Methods from dynamical systems theory and non-equilibrium statistical mechanics are used to model the T-cell dependent anti-tumour immune response. Our model predicts a critical level of MHC-I expression which determines whether or not the tumour escapes the immune response. This critical level of MHC-I depends on the helper/cytotoxic T-cell ratio. However, our model also suggests that the immune system is robust against small changes in this ratio. We also find that T-cell infiltration and the specificity of the intra-tumour TCR repertoire will affect the critical MHC-I expression. Our work suggests that the functional form of the time evolution of MHC-I expression may explain the qualitative behaviour of tumour growth seen in patients.

Vaccination against galectin-1 promotes cytotoxic T-cell infiltration in melanoma and reduces tumor burden

2022 ◽  
Author(s):  
Julia Femel ◽  
Luuk van Hooren ◽  
Melanie Herre ◽  
Jessica Cedervall ◽  
Falk Saupe ◽  
...  
Keyword(s):  
T Cell ◽  
Tumor Burden ◽  
Cell Infiltration ◽  
Cytotoxic T Cell ◽  
T Cell Infiltration

P1602MICROVASCULAR INFLAMMATION WITHOUT DSA OR C4D: AN ORPHAN CATEGORY IN BANFF CLASSIFICATION WITH INTENSE CAPILLARITIS AND CYTOTOXIC T-CELL INFILTRATION

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Anna Buxeda ◽  
Laura Llinàs ◽  
Javier Gimeno ◽  
Carlos Arias Cabrales ◽  
Carla Burballa Tarrega ◽  
...  
Keyword(s):  
Kidney Transplantation ◽  
T Cell ◽  
Nk Cells ◽  
Lymphocyte Subsets ◽  
Normal Group ◽  
Cell Infiltration ◽  
Cytotoxic T Cell ◽  
Antibody Mediated Rejection ◽  
T Cell Infiltration ◽  
Peritubular Capillaries

Abstract Background and Aims Antibody-mediated rejection (ABMR) associated with donor-specific HLA antibodies (DSA) is the leading cause of late allograft failure after kidney transplantation. Microvascular inflammation (MVI) without detectable circulating DSA or C4d + cannot be classified as ABMR according to Banff-2017. The involvement of intragraft lymphocyte subsets in the development of humoral damage in kidney transplantation (KT) is relevant. We aimed to analyze lymphocyte subset distribution in kidney transplant biopsies (KTBx) with ABMR compared with MVI and with normal KTBx. Method KTBx with ABMR, MVI (g+ptc≥2, without DSA) or normal findings were included. DSA were identified with Luminex single antigen assays. Intragraft lymphocyte subsets’ characterization was performed by immunohistochemistry: T-lymphocytes (CD3, CD4, CD8, Foxp3), B-lymphocytes / plasmatic cells (CD20, CD138), NK cells (CD56), macrophages / monocytes (CD68), cytotoxic cells (TIA1) and activated cells (PD1) were evaluated. Results We analyzed 34 KTBx: 21 ABMR, 5 MVI and 8 KTBx with normal findings. KT with ABMR and MVI had more proteinuria at the time of the biopsy compared with the normal group (575 mg/24h and 964 mg/24h vs 147 mg/24h, p=0.002 and p=0.005 respectively). DSA were more frequently detected in patients with ABMR (95.2% vs 0% and 37.5%, p<0.001 and p=0.003 respectively). KTBx with ABMR and MVI had increased cytotoxic T-cell infiltration apparently corresponding to NK cells in peritubular capillaries (ptc) compared to normal group. Moreover, both groups showed a greater number of macrophages and monocytes in glomeruli. KT with MVI but not with ABMR had a significantly increased activated cell infiltration (PD1+) in ptc compared to the normal group, and showed an increased cytotoxic T-cell infiltration in glomeruli compared to ABMR and normal groups. Conclusion ABMR and MVI have an increased infiltration of NK cells with cytotoxic activity in ptc that differs from the normal group. However, KT with MVI show greater infiltration of activated cells in ptc and cytotoxic T-cell in glomeruli compared to ABMR suggesting the possibility of different activation pathways.

scholarly journals Therapeutic Induction of Tertiary Lymphoid Structures in Cancer Through Stromal Remodeling

2021 ◽  
Vol 12 ◽  
Author(s):  
Anna Johansson-Percival ◽  
Ruth Ganss
Keyword(s):  
T Cell ◽  
Tumor Microenvironment ◽  
Cancer Immunotherapy ◽  
Tumor Rejection ◽  
Cell Infiltration ◽  
Cytotoxic T Cell ◽  
T Cell Infiltration ◽  
Anti Cancer ◽  
Tertiary Lymphoid Structures ◽  
Lymphoid Structures

Improving the effectiveness of anti-cancer immunotherapy remains a major clinical challenge. Cytotoxic T cell infiltration is crucial for immune-mediated tumor rejection, however, the suppressive tumor microenvironment impedes their recruitment, activation, maturation and function. Nevertheless, solid tumors can harbor specialized lymph node vasculature and immune cell clusters that are organized into tertiary lymphoid structures (TLS). These TLS support naïve T cell infiltration and intratumoral priming. In many human cancers, their presence is a positive prognostic factor, and importantly, predictive for responsiveness to immune checkpoint blockade. Thus, therapeutic induction of TLS is an attractive concept to boost anti-cancer immunotherapy. However, our understanding of how cancer-associated TLS could be initiated is rudimentary. Exciting new reagents which induce TLS in preclinical cancer models provide mechanistic insights into the exquisite stromal orchestration of TLS formation, a process often associated with a more functional or “normalized” tumor vasculature and fueled by LIGHT/LTα/LTβ, TNFα and CC/CXC chemokine signaling. These emerging insights provide innovative opportunities to induce and shape TLS in the tumor microenvironment to improve immunotherapies.

scholarly journals Identification and Analyses of Extra-Cranial and Cranial Rhabdoid Tumor Molecular Subgroups Reveal Tumors with Cytotoxic T Cell Infiltration

Cell Reports ◽  
2019 ◽  
Vol 29 (8) ◽  
pp. 2338-2354.e7 ◽  
Author(s):  
Hye-Jung E. Chun ◽  
Pascal D. Johann ◽  
Katy Milne ◽  
Marc Zapatka ◽  
Annette Buellesbach ◽  
...  
Keyword(s):  
T Cell ◽  
Rhabdoid Tumor ◽  
Cell Infiltration ◽  
Cytotoxic T Cell ◽  
Molecular Subgroups ◽  
T Cell Infiltration

scholarly journals Identification of Biomarkers Related to CD8+ T Cell Infiltration With Gene Co-expression Network in Lung Squamous Cell Carcinoma

2021 ◽  
Vol 9 ◽  
Author(s):  
Min Tang ◽  
Yukun Li ◽  
Xianyu Luo ◽  
Jiao Xiao ◽  
Juan Wang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Squamous Cell Carcinoma ◽  
T Cell ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Lung Squamous Cell Carcinoma ◽  
Cell Infiltration ◽  
Hub Genes ◽  
T Cell Infiltration ◽  
Potential Biomarker

Lung squamous cell carcinoma (LSCC) is one of the most common types of lung cancer in adults worldwide. With the development of modern medicine, cancer treatment that harnesses the power of the immune system might be particularly effective for treating LSCC. In this research, LSCC expression data, which quantify the cellular composition of immune cells, were analyzed by weighted gene coexpression network analysis (WGCNA) and a deconvolution algorithm based on the Gene Expression Omnibus (GEO) database, and the results indicated a close relationship between LSCC and CD8+ T cells. Six hub genes (SYT3, METTL8, HSPB3, GFM1, ERLIN2, and CLCN2) were verified by gene–gene network and protein–protein interaction (PPI) network analyses. We found that the six hub genes were increased in cancer tissues and were closely correlated with cancer development and progression. After immune correlation analysis, METTL8 was selected as a prognostic biomarker. Finally, we found that the METTL8 levels were increased in multiple lung cancer cell lines and LSCC tissues. METTL8 inhibition could clearly induce G1 cell cycle arrest and suppress proliferation. Therefore, METTL8, which is related to CD8+ T cell infiltration, might be identified as a potential biomarker and gene therapy target in LSCC.

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