[3, 8] TAMs generally fail to express pro-inflammatory cytokines for T helper type 1 (Th1) responses but are excellent producers of immunosuppressive cytokines for Th2 responses.[4] As TAMs generally exhibit low antigen-presenting and co-stimulating capacity, they ordinarily fail to activate T-cell-mediated adaptive immunity.[4, 7] Therefore, unlike M1 macrophages, which are highly microbicidal and tumoricidal, the M2-like TAMs are immunosuppressive

and facilitate tumour progression.[4, 7] Experimental and epidemiological studies demonstrated that TAMs play an important selleck products role in tumour growth, angiogenesis, metastasis, matrix remodelling and immune evasion in various human and animal tumours.[5, 7-10] Recently, TAMs are ‘accused’ for their

chemo-resistance and radio-protective effects in mouse tumour models, because an increased density of TAMs is associated with poor efficacy in chemotherapy,[11, 12] and radiotherapy-induced macrophage aggregation is paralleled by decreased radiocurability.[13-15] Clinical studies also revealed connections between the state of TAMs and poor outcomes of human tumours. The density, activation and histological location of TAMs can be used to predict patients’ survival time in different types of cancer.[16-20] For instance, an increased number of TAMs was selleck chemical correlated with a shortened progress-free survival in classical Hodgkin lymphoma.[16] Besides, Kurahara et al.[18] observed that a larger number of M2-polarized TAMs correlated with increased CHIR-99021 solubility dmso density of lymphatic vessels, high incidence of lymph node metastasis and a poor prognosis in patients with pancreatic cancer. Therefore, TAMs are now considered as a promising target for tumour therapy, and reduction of their tumour-promoting activities has become a hot study area.[21] Generally, the approaches to targeting TAMs are by following

two routes: decreasing the quantity of TAMs in tumour tissue or shifting TAMs from tumour-promoting to tumoricidal status. Although the clinical application of a TAM-targeted approach is still far from clear, a number of experimental studies have collectively shown the effect of this approach on faster tumour rejection and better therapeutic outcome,[22-26] which sheds inspirational light on further clinical studies. In this review, we will discuss current TAM-targeted strategies for anti-tumour therapy. Since the functions of TAMs largely depend on their accumulation and activation in tumour tissues, TAM-targeted anti-tumour approaches are principally based on: (i) inhibiting macrophage recruitment; (ii) suppressing TAM survival; (iii) enhancing M1 tumoricidal activity of TAMs; and (iv) blocking M2 tumour-promoting activity of TAMs. These strategies are summarized in Fig. 1. Some tumour-released and stroma-released cytokines and chemokines facilitate the recruitment of macrophages to tumour tissues.