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]