Dendritic cells (DCs) are efficient antigen-presenting cells (APCs) and potent activators of naïve T cells. Therefore, they act as a connective ring between innate and adaptive immunity. DC subsets are heterogeneous in their ontogeny and functions. They have proven to potentially take up and process tumor-associated antigens (TAAs). In this regard, researchers have developed strategies such as genetically engineered or TAA-pulsed DC vaccines; these manipulated DCs have shown significant outcomes in clinical and preclinical models. Here, we review DC classification and address how DCs are skewed into an immunosuppressive phenotype in cancer patients. Additionally, we present the advancements in DCs as a platform for cancer immunotherapy, emphasizing the technologies used for in vivo targeting of endogenous DCs, ex vivo generated vaccines from peripheral blood monocytes, and induced pluripotent stem cell-derived DCs (iPSC-DCs) to boost antitumoral immunity.

Macrophages (Mfs) play an essential role in maintaining body homeostasis. They perform dual functions produced by different subtypes. Mfs not only fight against pathogens and foreign bodies such as bacteria or cancer cells but also participate in healing and repairing damaged tissue since they maintain both proinflammatory and anti-inflammatory effects sequentially. Tumors possess the ability to polarize Mfs from proinflammatory M1 subtype to anti-inflammatory M2-like Mfs called tumor-associated macrophages, which, in turn, help the tumors to acquire cancer hallmarks. Consequently, this polarization allows tumors to grow and spread. In this light, Mfs have been a subject of intense study, and researchers have developed protocols to derive different Mfs subtypes either as a new state-of-the-art therapeutic approach or to understand the crosstalk between cancer and Mfs. In this review, we present the use of primary Mfs in adoptive immunotherapy for cancer, illustrate the reciprocating interplay between cancer and Mfs, and the resulting structural and functional change on both cell types. Furthermore, we summarize the recent cutting-edge approaches of using Mfs in cancer immunotherapy.

Background Tuberculosis (TB) remains a major global public health problem and the leading cause of mortality by a single infectious agent. TB is a chronic infectious disease that is primarily caused by Mycobacterium tuberculosis (Mtb). Macrophage (Mφ) are the main hosts of Mtb, the interaction between Mtb and Mφ plays an important role in the pathogenesis of TB.Summary The macrophages used in the current study are mostly derived from tumor cell lines or peripheral blood mononuclear cells (PBMC), but the application of such cells still have many problems needed to be sloved, such as the loss of function due to changes in genetic structure and the difficulty in cell acquisition. Human induced pluripotent stem cells (hiPS) represent an innovative source for the standardized in vitro generation of Mφ, and show novel promise in exploring disease pathogenesis, particularly TB. Current studies have revealed that autophagy plays a central role in the interaction between Mtb and Mφ, but the molecular mechanism involoved remains unclear and the exact role of hiPS-derived macrophages (hiPS-Mφ) in regulating autophagy induced by Mtb also remains unclear. To investigate the similarities and differences in hiPS-Mφ and THP-1-Mφ in anti-tuberculosis immunity, this study successfully obtained macrophages derived from hiPS and THP-1, then explored the mechanism behind Bacillus Calmette-Guerin (BCG)-induced autophagy through transcriptome sequencing analysis, qPCR, Western Blot Analysis and cell submicroscopic structure observation etc.. Our findings revealed that BCG infection of hiPS-Mφ and THP-1-Mφ would promote autophagy by regulating the expression of autophagy-related genes, which also indicated that the BCG-induced autophagy in hiPS-Mφ and THP-1-Mφ may be associated with PI3K/AKT/mTOR signaling pathway. However, there are some differences in the mechanism by which BCG infects macrophages from different sources and induces autophagy. Considering the above findings, we have provided novel insights into the role of macrophages along with autophagy in the anti-tuberculosis immune mechanism and the possibility of establishing an in vitro hiPS-Mφ-TB disease model.