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Immune gene expression pathways refer to the collective transcriptional networks that regulate the development, activation, and effector functions of the immune system (Ayers et al., 2017). These pathways encompass a wide array of signaling cascades, including the JAK-STAT, NF-κB, and Toll-like receptor (TLR) pathways, which coordinate the expression of cytokines, chemokines, and cell surface receptors (Cristescu et al., 2018). While not a single therapeutic target, these pathways serve as a critical framework for understanding the immune microenvironment and are frequently used as multi-gene biomarkers to predict clinical outcomes. For instance, high expression of T-cell-related genes is often associated with better responses to immunotherapy in various cancers (Ott et al., 2019). Conversely, chronic overactivation of these pathways is a hallmark of autoimmune and inflammatory disorders. Drugs targeting specific components of these pathways, such as monoclonal antibodies or small molecule inhibitors, aim to modulate the overall immune gene expression profile to achieve therapeutic benefit (Ribas & Wolchok, 2018).
Modulation of immune-related transcriptional programs through checkpoint inhibition, cytokine neutralization, or intracellular signaling blockade (e.g., JAK-STAT inhibition).
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