Table 1: List of immune components within the prostate cancer microenvironment and their roles in influencing tumor progression and treatment response.
Immune Component |
Description |
Role in Prostate Cancer |
References |
Tumor-Infiltrating Lymphocytes (TILs) |
T cells that infiltrate the tumor microenvironment, including CD8+ cytotoxic T cells and CD4+ helper T cells. |
CD8+ T cells recognize and kill cancer cells, associated with a better prognosis. CD4+ T cells can promote or suppress anti-tumor responses depending on their subset (e.g., Th1, Th2). |
[5,6] |
Regulatory T Cells (Tregs) |
A subset of CD4+ T cells that suppress immune responses and maintain tolerance. |
Tregs often accumulate in the TME and inhibit anti-tumor immunity through cytokine secretion (e.g., IL-10, TGF-β) and direct suppression of CTLs. |
[19,20] |
Dendritic Cells (DCs) |
Professional antigen-presenting cells that process and present antigens to T cells. |
DCs are crucial for initiating T-cell responses. In prostate cancer, their function can be impaired by the TME, reducing effective T cell activation. |
[21,22] |
Macrophages |
Versatile immune cells can adopt different functional states, including M1 (pro-inflammatory) and M2 (anti-inflammatory). |
M2 macrophages in prostate cancer support tumor progression by secreting cytokines and growth factors that enhance angiogenesis and tissue repair while suppressing anti-tumor immunity. |
[23,24] |
Tumor-Associated Macrophages (TAMs) |
Macrophages found within the tumor microenvironment, often exhibit an M2-like phenotype. |
TAMs promote tumor growth, metastasis, and angiogenesis while inhibiting anti-tumor immunity. Targeting TAMs is a potential therapeutic approach. |
[25,26] |
Cytokines and Chemokines |
Signaling molecules that regulate immune responses and influence tumor behavior. |
Pro-inflammatory cytokines (e.g., TNF-α, IFN-γ) can initiate anti-tumor responses, whereas anti-inflammatory cytokines (e.g., IL-10, TGF-β) contribute to immune suppression. Chemokines attract immune cells, influencing their recruitment to the tumor site. |
[27,28] |