Immune cells promote metastasis, a major cause of cancer death. Tumor-infiltrating immune cells, including myeloid cells like macrophages, support metastasis by suppressing immune responses that would otherwise eliminate cancer cells. These cells facilitate tumor cell invasion, intravasation, and survival in circulation, as well as their arrest, extravasation, and persistent growth at metastatic sites. Tumor cells evade immune surveillance by recruiting immune suppressive cells, such as regulatory T cells (Tregs), myeloid-derived suppressor cells (MDSCs), and tumor-associated macrophages (TAMs). These cells suppress CD8+ T cells and NK cells, which are critical for immune surveillance. Tumor cells also create pre-metastatic niches by recruiting myeloid cells and other immune cells to distant sites, enhancing metastatic efficiency. Myeloid cells, such as TAMs, promote tumor cell egress by increasing vascular leakiness and facilitating intravasation. They also support tumor cell survival by protecting them from immune attack and providing a supportive environment. Macrophages, neutrophils, and platelets contribute to metastasis by promoting extravasation, survival, and growth of metastatic foci. Therapeutic strategies targeting these immune cells, such as inhibiting PD1/CTLA4, blocking Treg and MDSC function, or targeting CSF-1R or CCL2/CCR2 pathways, show promise in reducing metastasis. These approaches aim to enhance antitumor immunity by blocking immunosuppressive cells and promoting immune responses against cancer. Understanding the mechanisms of immune cell recruitment and function in metastasis is crucial for developing effective therapies.Immune cells promote metastasis, a major cause of cancer death. Tumor-infiltrating immune cells, including myeloid cells like macrophages, support metastasis by suppressing immune responses that would otherwise eliminate cancer cells. These cells facilitate tumor cell invasion, intravasation, and survival in circulation, as well as their arrest, extravasation, and persistent growth at metastatic sites. Tumor cells evade immune surveillance by recruiting immune suppressive cells, such as regulatory T cells (Tregs), myeloid-derived suppressor cells (MDSCs), and tumor-associated macrophages (TAMs). These cells suppress CD8+ T cells and NK cells, which are critical for immune surveillance. Tumor cells also create pre-metastatic niches by recruiting myeloid cells and other immune cells to distant sites, enhancing metastatic efficiency. Myeloid cells, such as TAMs, promote tumor cell egress by increasing vascular leakiness and facilitating intravasation. They also support tumor cell survival by protecting them from immune attack and providing a supportive environment. Macrophages, neutrophils, and platelets contribute to metastasis by promoting extravasation, survival, and growth of metastatic foci. Therapeutic strategies targeting these immune cells, such as inhibiting PD1/CTLA4, blocking Treg and MDSC function, or targeting CSF-1R or CCL2/CCR2 pathways, show promise in reducing metastasis. These approaches aim to enhance antitumor immunity by blocking immunosuppressive cells and promoting immune responses against cancer. Understanding the mechanisms of immune cell recruitment and function in metastasis is crucial for developing effective therapies.