STAT2 Mediated Epigenetic and Epitranscriptomic Regulation of CD4 + T Helper Cell Differentiation in Non‐Small Cell Lung Cancer ( NSCLC )
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| Format: | Artículo Open Access |
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Wiley
2026
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| author | Roshni Bibi Melvin George Koustav Sarkar |
| author_facet | Roshni Bibi Melvin George Koustav Sarkar Roshni Bibi Melvin George Koustav Sarkar |
| collection | Wiley Open Access |
| contents | STAT2 Mediated Epigenetic and Epitranscriptomic Regulation of CD4 + T Helper Cell Differentiation in Non‐Small Cell Lung Cancer ( NSCLC ) Roshni Bibi Melvin George Koustav Sarkar Immunology ABSTRACT Non‐small cell lung cancer (NSCLC) is an aggressive malignancy necessitating innovative therapeutic approaches to augment antitumour immunity. Our study examined the function of the STAT2 protein in CD4 + T helper cells, which are essential for the immune response to cancer. We utilised CRISPR/Cas9 to ablate STAT2 in CD4 + T cells from stage I NSCLC patients ( n = 30), assessing its impact on cellular function and diverse epigenetic pathways. Our findings indicate that the depletion of STAT2 markedly enhances the anti‐cancer efficacy of T lymphocytes. Deletion of STAT2 diminished oxidative stress, enhanced the synthesis of advantageous TH1 cytokines. STAT2 depletion reduced DNA methylation and R‐loop formation. T cells deficient in STAT2 showed enhanced efficacy in activating cytotoxic T lymphocytes to eliminate cancer cells. These findings identify STAT2 as a crucial regulator of immune function in the lung cancer microenvironment. Targeted STAT2 inhibition in tumour‐reactive T cells may reinstate anti‐tumour immunity, although systemic inhibition requires further research on targeted intervention strategies. 10.1111/imm.70121 http://onlinelibrary.wiley.com/termsAndConditions#vor |
| doi_str_mv | 10.1111/imm.70121 |
| format | Artículo Open Access |
| id | wiley_oa_10_1111_imm_70121 |
| institution | Wiley Open Access |
| license_str_mv | http://onlinelibrary.wiley.com/termsAndConditions#vor |
| publishDate | 2026 |
| publisher | Wiley |
| record_format | wiley_oa |
| spellingShingle | STAT2 Mediated Epigenetic and Epitranscriptomic Regulation of CD4 + T Helper Cell Differentiation in Non‐Small Cell Lung Cancer ( NSCLC ) Roshni Bibi Melvin George Koustav Sarkar Immunology STAT2 Mediated Epigenetic and Epitranscriptomic Regulation of CD4 + T Helper Cell Differentiation in Non‐Small Cell Lung Cancer ( NSCLC ) Roshni Bibi Melvin George Koustav Sarkar Immunology ABSTRACT Non‐small cell lung cancer (NSCLC) is an aggressive malignancy necessitating innovative therapeutic approaches to augment antitumour immunity. Our study examined the function of the STAT2 protein in CD4 + T helper cells, which are essential for the immune response to cancer. We utilised CRISPR/Cas9 to ablate STAT2 in CD4 + T cells from stage I NSCLC patients ( n = 30), assessing its impact on cellular function and diverse epigenetic pathways. Our findings indicate that the depletion of STAT2 markedly enhances the anti‐cancer efficacy of T lymphocytes. Deletion of STAT2 diminished oxidative stress, enhanced the synthesis of advantageous TH1 cytokines. STAT2 depletion reduced DNA methylation and R‐loop formation. T cells deficient in STAT2 showed enhanced efficacy in activating cytotoxic T lymphocytes to eliminate cancer cells. These findings identify STAT2 as a crucial regulator of immune function in the lung cancer microenvironment. Targeted STAT2 inhibition in tumour‐reactive T cells may reinstate anti‐tumour immunity, although systemic inhibition requires further research on targeted intervention strategies. 10.1111/imm.70121 http://onlinelibrary.wiley.com/termsAndConditions#vor |
| title | STAT2 Mediated Epigenetic and Epitranscriptomic Regulation of CD4 + T Helper Cell Differentiation in Non‐Small Cell Lung Cancer ( NSCLC ) |
| topic | Immunology |
| url | https://onlinelibrary.wiley.com/doi/10.1111/imm.70121 |