Casual association between immune cells and colorectal cancer: A Mendelian Randomization Study
##plugins.themes.bootstrap3.article.sidebar##
##plugins.themes.bootstrap3.article.main##
Abstract
Abstract
Colorectal cancer (CRC) is a multifactorial disease influenced by genetic, environmental, and immunological factors. This study employs Mendelian randomization (MR) to investigate the causal associations between immune cell types and the risk of developing colorectal cancer. Utilizing large-scale genomic data, we identified genetic variants associated with various immune cell populations, including T cells, B cells, and macrophages. By leveraging these variants as instrumental variables, we assessed their impact on CRC risk through two-sample MR analysis.
Our examination identified a total of 29 immune cells linked to colorectal cancer (CRC). The risk of CRC was correlated with CCR2 on monocytes (OR = 0.9384, 95% CI = 0.8890– 0.9905, p = 0.0212), Basophil Absolute Count (OR = 1.0466, 95% CI = 1.0027–1.0925, p = 0.0370), CD64 on CD14+ CD16+ monocytes (OR = 0.7853, 95% CI = 0.6616– 0.9321, p = 0.0057), Naive CD4+ T cell Absolute Count (OR = 0.8826, 95% CI = 0.7961– 0.9786, p=0.0177), Immature Myeloid-Derived Suppressor Cells %CD33dim HLA DR- CD66b- (OR = 0.9204, 95% CI = 0.8516– 0.9948, p = 0.0366), CD33dim HLA DR+ CD11b- %CD33dim HLA DR+ (OR = 0.9504, 95% CI = 0.9072– 0.9956, p = 0.0319), and CD33dim HLA DR+ CD11b+ %CD33dim HLA DR+ (OR = 1.0509, 95% CI = 1.0021– 1.1021, p = 0.0403). Notably, while the absolute count of basophils, and CD33dim HLA DR+ CD11b+ %CD33dim HLA DR+ served as a risk factor, CCR2 on monocytes, CD64 on CD14+ CD16+ monocytes, Naive CD4+ T cell Absolute Count, Immature Myeloid-Derived Suppressor Cells %CD33dim HLA DR- CD66b-, and CD33dim HLA DR+ CD11b- %CD33dim HLA DR+ acted as protective factors. These results underline the importance of immune modulation in colorectal carcinogenesis and offer insights into potential therapeutic targets for prevention and treatment. Further research is warranted to elucidate the underlying mechanisms by which immune cells influence CRC development.