Journal of Vaccine Research 2024, Vol.14, No.5, 255-268 http://medscipublisher.com/index.php/jvr 261 Figure 2 HER2-specific T cells persisted in patients with a PR or SD (Adopted from Disis et al., 2023) Image caption: A, Kaplan–Meier curves of the OS inmonths from enrollment for responding patients (PRþSD, n ¼9) in blue and nonresponders (PD, n ¼ 8) in black. B, Sum of stimulating HER2 peptide (p776, 927, and p1166) specific T-cell responses (y axis) in pre vaccine, preinfusion (postvaccine), and 1, 3, and 5 months post T-cell infusion for responders (blue, n ¼ 9) versus nonresponders (black, n ¼ 8) during the treatment. Each dot represents mean (SE) at the time point in the group. NS, not significant, P<0.05, P<0.01 (Adopted from Disis et al., 2023) 5 Immune Escape Mechanisms in Breast Cancer 5.1 Tumor immune evasion Breast cancer cells have developed sophisticated mechanisms to evade the immune system, which significantly hampers the efficacy of immunotherapies. One primary method of immune evasion is the downregulation of antigen presentation. Tumor cells often reduce the expression of major histocompatibility complex (MHC) molecules, which are crucial for presenting tumor antigens to T cells. This downregulation prevents the immune system from recognizing and attacking the tumor cells effectively. Additionally, breast cancer cells can secrete immunosuppressive cytokines such as TGF-β and IL-10, which inhibit the activation and proliferation of effector T cells and promote the development of regulatory T cells (Tregs) that suppress immune responses (Knudson et al., 2018). Another significant mechanism is the upregulation of immune checkpoint molecules like PD-L1, which binds to
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