Hence, Treg immunosuppressive role has been described in giloblastoma patients (tumour recurrence and poor prognosis) [392] and in CRC patients [393], inhibiting effector T cells (Table 2). fight off and defeat possible attacks or infections. Nevertheless, sometimes this threat comes from an internal factor. Situations such as the existence of a tumour also cause our immune system (IS) to be put on Adenosine alert. Indeed, the link between immunology and cancer is evident these days, with IS being used as one of the important targets for treating cancer. Our IS is able to eliminate those abnormal or damaged cells found in our body, preventing the uncontrolled proliferation of tumour cells that can lead to cancer. However, in several cases, tumour cells can escape from the IS. It has been observed that immune cells, the extracellular matrix, blood vessels, fat cells and various molecules could support tumour growth and development. Thus, the developing tumour receives structural support, irrigation and energy, among other resources, making its survival and progression possible. All these components that accompany and help the tumour to survive and to grow are called the tumour microenvironment (TME). Given the importance of its presence in the tumour development process, this review will focus on one of the components of the TME: immune cells. Immune cells can support anti-tumour immune response protecting us against tumour cells; nevertheless, they can also behave as pro-tumoural cells, thus promoting tumour progression and survival. In this review, the anti-tumour and pro-tumour immunity of several immune cells will be discussed. In addition, the TME influence on this dual effect will be also analysed. Eosinophils: inhibition of T and NK cell function in human NSCLC Basophils: reduction of CD8+ T cell infiltration both human and murine colon cancer[153]/[97] [384]/[385] [391]/[392,393]CD8+ T cellsTc1: cytotoxic activity and high IFN- production in melanoma individuals br / Tc17:IL-17A production in oesophageal SCC individuals br / Tc22: through by IL-6 induction in human being ovarian malignancy br / T cells: NKp30 cytotoxicity in human being acute myeloid leukemiaTc1: low of IFN-, TNF- and high levels of PD-1, incapacity to control tumor progression in melanoma individuals br / Tc17: angiogenic and immunosuppressive function in human being cancers such as Adenosine Adenosine HNSCC and gastric malignancy br / Tc22: increase of IL-22 related to tumor growth in transplant-associated SSC individuals br / T cells: angiogenesis by IL-17 production in human being gallbladder malignancy[394]/[395] br / [396]/[397,398] br / [394]/[399] br / [400]/[401] Open in a separate windows Abbreviations: EBI1 MUC1: mucin 1; OSCC: oral squamous cell carcinoma; Breg cells: regulatory B cells; Th: T helper; Tfh: T follicular herlper; IFN-: interferon gamma; IL: interleukin; EMT: epithelial-mesenchymal transition; CRC: colorectal malignancy; TLS: tertiary lymphoid constructions; Treg cells: regulatory T cells; PD-1: programmed cell death protein 1; SCC: squamous cell carcinoma; HNSCC: head and neck squamous cell carcinoma; NKp30: natural killer cell protein 30 (quantity refer to its molecular excess weight). B cells produced cytokines and chemokines such as lymphotoxin, (involved in the formation of TLS) [379], CXCL10 [402], CCL4 [403], IFN- (increase via TNF-) [404] and murine ABCD-1 chemokine [405]. A study shed more light on anti-tumour B cell activity, demonstrating that these cells are able to help CD8+ T cells through CD27/CD20 [406]. Additionally, the Malignancy Genome Atlas (TCGA) database reported the positive correlation between high levels of manifestation of B cell and Personal computer signature genes and better results, since their presence in individuals with PDAC, lung adenocarcinoma, HNSCC and melanoma showed an increase in overall survival [407]. B cells are found in smaller proportions.