Cytokine · 2025
The role of cytokines in immune cell-mediated multiple myeloma and the identification of therapeutic targets.
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Wang Chao, Cai Yi, Jie Jie
Аннотация
INTRODUCTION: Multiple Myeloma (MM) disrupts immune function and causes multisystem damage. Despite treatment advances, the pathogenesis of relapse and resistance remain unclear. This study assesses the causal relationships between immune cell subtypes and MM using Mendelian randomization (MR), explores the mediating role of cytokines, and identifies potential therapeutic targets.
METHODS: We employed a two-step MR approach to analyze mediating effects. Sensitivity analyses and Bayesian Weighted Mendelian Randomization (BWMR) were utilized to ensure the accuracy of results and to mitigate pleiotropy and heterogeneity. Additionally, Summary-data-based MR (SMR) was used to identify potential drug targets.
RESULTS: The findings indicate causal effects of 20 immune cell subtypes and three cytokines on MM. SLAM mediated 9.16 % of the effect of CD4+ cells on MM. SMR analysis identified CD4+ and naive CD4+ cells as potential therapeutic targets for MM.
CONCLUSIONS: Through two-step MR and SMR analysis, this study reveals the mediating role of SLAM in the impact of CD4+ immune cells on MM and identifies two immune cell drug targets. Inhibiting the KIT gene may enhance the antitumor function of CD4+ T cells, offering new insights and potential strategies for immunotherapy of MM. These findings provide a theoretical basis for understanding the pathophysiology of MM and for developing novel immune-targeted therapies.
METHODS: We employed a two-step MR approach to analyze mediating effects. Sensitivity analyses and Bayesian Weighted Mendelian Randomization (BWMR) were utilized to ensure the accuracy of results and to mitigate pleiotropy and heterogeneity. Additionally, Summary-data-based MR (SMR) was used to identify potential drug targets.
RESULTS: The findings indicate causal effects of 20 immune cell subtypes and three cytokines on MM. SLAM mediated 9.16 % of the effect of CD4+ cells on MM. SMR analysis identified CD4+ and naive CD4+ cells as potential therapeutic targets for MM.
CONCLUSIONS: Through two-step MR and SMR analysis, this study reveals the mediating role of SLAM in the impact of CD4+ immune cells on MM and identifies two immune cell drug targets. Inhibiting the KIT gene may enhance the antitumor function of CD4+ T cells, offering new insights and potential strategies for immunotherapy of MM. These findings provide a theoretical basis for understanding the pathophysiology of MM and for developing novel immune-targeted therapies.