DOI: 10.57760/sciencedb.28406
title: Immune Escape through NKG2A Upregulation in Tuberculosis
title: Immune Escape through NKG2A Upregulation in Tuberculosis

description: Research BackgroundThe mechanisms of immune escape in tuberculosis that hinder an effective immune response and lead to immune cell depletion remain unresolved. Blocking NKG2A, an inhibitory receptor, has been shown to activate and enhance the function of cytotoxic lymphocytes, which has proven effective in tumor immunotherapy and may offer new insights for the immunotherapy of tuberculosis.Data ContentThis dataset integrates single-cell data on tuberculosis (TB) infection along with clinical cohort and flow cytometry analyses. It covers multi-dimensional data collected from June 2022 to March 2025, including but not limited to:Single-cell Data: Demonstrates the significant upregulation of KLRC1-encoded NKG2A in T and NK cells from patients with active TB, reflecting cellular function states such as cell activation, toxic granule secretion, and metabolic activity.Clinical Cohort Data: Detailed records of patients' clinical characteristics, treatment processes, and outcomes, providing a clinical context for understanding the role of NKG2A in the progression of TB.Flow Cytometry Analysis Data: Visually presents changes in the expression of key molecules (such as MPEG1, granzyme A, iNOS, TRAIL, granzyme B, and CD107a) in T cells and NK cells after NKG2A blockade, as well as the reactivation of the Ras-p38/AKT signaling pathway in NK cells, revealing the precise regulation of NKG2A blockade on cellular function and signal transduction.Research SignificanceThese data are significant for deepening the understanding of the mechanisms of immune escape in tuberculosis and provide valuable resources for exploring NKG2A blockade as a potential therapeutic strategy to restore the host's antimicrobial response. By analyzing this dataset, researchers can further explore the application potential of NKG2A blockade in tuberculosis immunotherapy, laying the foundation for the development of more effective treatment methods for tuberculosis.
description: Research BackgroundThe mechanisms of immune escape in tuberculosis that hinder an effective immune response and lead to immune cell depletion remain unresolved. Blocking NKG2A, an inhibitory receptor, has been shown to activate and enhance the function of cytotoxic lymphocytes, which has proven effective in tumor immunotherapy and may offer new insights for the immunotherapy of tuberculosis.Data ContentThis dataset integrates single-cell data on tuberculosis (TB) infection along with clinical cohort and flow cytometry analyses. It covers multi-dimensional data collected from June 2022 to March 2025, including but not limited to:Single-cell Data: Demonstrates the significant upregulation of KLRC1-encoded NKG2A in T and NK cells from patients with active TB, reflecting cellular function states such as cell activation, toxic granule secretion, and metabolic activity.Clinical Cohort Data: Detailed records of patients' clinical characteristics, treatment processes, and outcomes, providing a clinical context for understanding the role of NKG2A in the progression of TB.Flow Cytometry Analysis Data: Visually presents changes in the expression of key molecules (such as MPEG1, granzyme A, iNOS, TRAIL, granzyme B, and CD107a) in T cells and NK cells after NKG2A blockade, as well as the reactivation of the Ras-p38/AKT signaling pathway in NK cells, revealing the precise regulation of NKG2A blockade on cellular function and signal transduction.Research SignificanceThese data are significant for deepening the understanding of the mechanisms of immune escape in tuberculosis and provide valuable resources for exploring NKG2A blockade as a potential therapeutic strategy to restore the host's antimicrobial response. By analyzing this dataset, researchers can further explore the application potential of NKG2A blockade in tuberculosis immunotherapy, laying the foundation for the development of more effective treatment methods for tuberculosis.