Development and Function of Myeloid Subsets (Advances in Immunology)

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Andreas Schlitzer andreas. Dendritic cell development Dendritic cells DCs have been progressively recognized as a separate hematopoietic lineage of myeloid cells, alongside granulocytes, macrophages, and monocytes. Early imprinting of conventional dendritic cell identity With the advent of single-cell transcriptomics and sophisticated genomic barcode-tracing strategies, it has become clear that the long-curated model of a stepwise hematopoietic development process is an oversimplification of myeloid hematopoiesis.

Tissue factors influencing dendritic cell subset identity Within peripheral tissues, several cues have been identified to contribute to the tissue-specific regulation and development of cDCs. Table 1. Characteristics of human and mouse dendritic cells. Inflammatory dendritic cells New evidence suggests that tumors can convert TIDCs into immunosuppressive regulatory cells.

F recommended References 1. Nat Immunol. J Immunol. Cancer Immunol Res. Lee PN: Correspondence re: E. Fontham et al. Cancer epidemiol. Cancer Epidemiol Biomarkers Prev. PubMed Abstract Nat Rev Immunol. Semin Immunopathol. J Exp Med. Yi T, Cyster JG: EBI2-mediated bridging channel positioning supports splenic dendritic cell homeostasis and particulate antigen capture. Nat Commun.

Sci Immunol. Lutz MB, Schuler G: Immature, semi-mature and fully mature dendritic cells: which signals induce tolerance or immunity? Trends Immunol. Immunol Lett. Curr Opin Biotechnol. Am J Pathol. Immunol Cell Biol. J Leukoc Biol. Front Immunol. Cancer Res. Swiecki M, Colonna M: The multifaceted biology of plasmacytoid dendritic cells. Clin Cancer Res. Cell Rep. J Clin Invest. Annu Rev Immunol.

Int J Dermatol. J Neuroimmunol. Curr Opin Immunol. J Exp Clin Cancer Res. Hum Immunol. Cancer Immunol Immunother. Nat Med. Int Immunopharmacol. PLoS One.

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Int J Cancer. Anticancer Res. Hirano T: Interleukin 6 and its receptor: ten years later. Int Rev Immunol. Immunopharmacol Immunotoxicol. Comments on this article Comments 0. Article Versions 1 version 1. This is an open access article distributed under the terms of the Creative Commons Attribution Licence , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Manager RIS Sente. Track an article to receive email alerts on any updates to this article.

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You registered with F via Facebook, so we cannot reset your password. Global reach, higher impact. Journal of Genomics - Submit manuscript now Int J Biol Sci ; 7 5 Brian F. Zamarron, WanJun Chen. Traditional wisdom holds that intact immune responses, such as immune surveillance or immunoediting, are required for preventing and inhibiting tumor development; but recent evidence has also indicated that unresolved immune responses, such as chronic inflammation, can promote the growth and progression of cancer. These immune cells and the cellular factors produced from them, including both immunosuppressive and inflammatory cytokines, play dual roles in promoting or discouraging cancer development, and their ultimate role in cancer progression may rely heavily on the tumor microenvironment and the events leading to initial propagation of carcinogenesis.

Cancer cell development and survival is a multifactor process, involving genetic mutation of normal cells as well as physiological changes within both cancer cells and also the body's defense mechanisms 1 , 2. Cellular changes, such as gain of function mutations of oncogenes and loss of function mutations in tumor suppressor genes, can lead to relative cellular immortality, proliferation, and carcinogenesis.

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In addition to cellular changes, the body's normal defense mechanisms can play a key role in encouraging or combating carcinogenesis and tumor spread. Of particular importance is the immune response to cancer cell development and progression, as well as the potential role the immune response might play in initial tumor formation. In this regard, compelling evidence has been documented, both in animal tumor models and in human cancers, that chronic inflammation plays a decisive role in the development of certain cancers such as hepatocellular carcinoma HCC and colon cancer.

However, cells of the immune system can also inhibit tumor growth and progression through the recognition and rejection of malignant cells, a process referred to as immunosurveillance or immunoediting 3 , 4. In this respect, immunodeficiency can predispose an individual to the development of both spontaneous and virally induced cancers, and established tumors often generate immunosuppressive microenvironments that can block productive antitumor immunity.

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However, the cellular and molecular mechanisms that positively and negatively regulate the function and phenotype of TAM remain largely unknown. Elucidation of these mechanisms would have a significant impact on understanding the pathogenesis of inflammation-associated cancers, and could aid progress in the development of more effective cancer therapies. This review will explore the dual-roles played by key T lymphocyte subsets in cancer development and progression, as well as discussing the potential link between TAM cells and T lymphocytes as they relate to tumor formation, growth and survival.

A causal association between viral infection and tumor development has been well established and supported in animal studies as well as epidemiological studies. For example, the risk of developing HCC appears to be intimately linked to the duration of Hepatitis B and C viral infection-induced inflammatory processes 1 , 5 - 7. Normally, inflammation serves to protect a defined region of infected or damaged tissue by recruiting cells necessary to resolve the insult while also isolating the area to prevent the spread of infection and, once resolved, normal tissue function is typically restored.

However, inflammation sometimes fails to subside and this unresolved inflammation can promote tumor cell growth, survival and angiogenesis 1. Intriguingly, evidence continues to accumulate indicating that unresolved chronic inflammation plays a critical role in the initiation, promotion, malignant conversion, and metastasis of several human cancers 1. Additionally, inflammation associated with the hepatitis B and C viruses is the primary cause of liver cancer. Infection with the bacterium Helicobacter pylori plays a central role in the development of most cancers of the stomach 8.

Beyond infections, many autoimmune diseases are associated with an increased risk of lymphoma, and inappropriate immune responses to commensal flora in ulcerative colitis are strongly linked to colon cancer 1 , 8 - Evidence now links inflammation to tumor development in both genetic tumor syndromes and in the context of chronic carcinogen exposure.

Administration of non-steroidal anti-inflammatory drugs NSAIDs in randomized studies have shown reduced incidence of colon cancer in patients with familial adenomatous polyposis and, perhaps more remarkably, reduces the incidence of lung cancer in smokers 10 - TAM are a heterogeneous cell population according to oxygen availability hypoxia vs. In early stage tumor development Type 1 macrophages M1 may infiltrate, activated in response to inflammatory mediators, and release pro-inflammatory cytokines and chemokines, such as CXCL19 and CXCL10, in order to attract and encourage Th1, Th17 and NK cell development and differentiation.

In contrast, in more advanced tumors or in hypoxic regions of the tumor microenvironment TAM polarize to a more type 2 macrophage M2 related cell, releasing factors to encourage Th2 differentiation and recruitment Myeloid-derived suppressive cells represent a heterogeneous population of immature myeloid cells not already committed into macrophages, dendritic cells or granulocytes.

These cells are found within both human and mouse tumors. Whereas MDSC would normally differentiate after migration, the cytokines and cellular factors found within the tumor microenvironment prevent differentiation and instead encourage expansion and activation of the immature myeloid cell population 19 , and may result in the suppression of tumor immunity through a variety of mechanisms. IL-6 is a key cytokine amongst these cellular factors, encouraging cancer cell proliferation while also inhibiting their apoptosis through activation of signal transducer and activator of transcription 3 Stat3 1 , IL-6 has also been shown to play an important role in carcinogen-driven liver cancer development 7 , Additionally, IL-6 acts as an angiogenic factor, and has been implicated in many of the same processes as TNF.

TNF plays an indispensible role in the hepatic procarcinogen diethylnitrosamine-induced experimental hepatocellular carcinoma, as ablation of TNF receptor I in mice almost completely abolished obesity-enhanced HCC development 7. Spontaneous lymphocytic infiltrates can be consistently observed in a variety of human cancers, and in some cases these infiltrating lymphocytes correlate with a favorable prognosis 3. Anti-tumor specific effector immune cells develop within the draining lymph nodes, but have also been found to proliferate within the tumor microenvironment despite potential immunosuppressive factors 26 , however the extent to which these cells are able to contribute to anti-cancer immunity is unclear; particularly with respect to the immunosuppressive conditions present within the tumor.

A critical function of these cells is to suppress the activation of effector immune cells that are specific for self-antigens, limiting autoimmunity and inflammation under physiologically normal conditions. Studies of murine tumors indicate that Tregs inhibit the immune response to tumors, and depletion of these cells promotes rejection of several murine tumor cell lines including melanoma, fibrosarcoma, leukemia and myeloma. The role of Tregs in carcinogenesis and metastasis in humans is just beginning to emerge.

The role of Tregs in the development of liver carcinomas, however, remains largely unknown. However, the experimental evidence supporting this notion awaits further investigation. Th17 cells are involved in several autoimmune diseases and chronic inflammatory syndromes. In addition, IL is a key factor for maintaining and expanding Th17 inflammatory cell populations In addition, a study of murine tumor formation, using the B16 melanoma cell line, found that IL signaling was critical for tumor development, with direct effects on tumor and stromal cells inducing IL-6 production which then led to activation of Stat3 Thus, the combined cellular products from both Th17 and myeloid cells infiltrating the tumor, and the interaction between these cell types, may play a critical role in the balance of anti- and pro-tumor immune responses within the HCC microenvironment.

IL may play a similarly complex role in the development and survival of cancer cells. Despite this, however, IL can also activate STAT3 and may thereby help to promote tumor development, playing a part in cell proliferation and survival 24 , The role of IL in cancer development being either primarily anti-tumor, preventing inflammation and tumor angiogenesis, or primarily pro-tumor, encouraging cell survival and suppressing effector T cells, may depend upon the conditions of initial carcinogenesis as well as the presence of other cells such as Tregs.

Accumulated evidence has indicated that chronic and unresolved inflammation may play a critical role in the initiation, development, growth, and metastasis of cancer. The net outcome of the battle between the anti-tumor and the tumor promoting immune cells and their associated cytokines within the tumor environment will determine the ultimate fate of the affected tumors. Thus, understanding the interactions and mutual regulation of these complex immune networks within the tumor environment, rather than the role of individual components, is much more likely to guide us towards developing effective and specific cancer therapeutics.

Further research into better understanding this balance at all stages of carcinogenesis is essential for the development of effective cancer therapies that target or utilize immunological mechanisms. Once a tumor is established, however, Tregs and their produced cytokines may instead play a role in promoting tumor survival by inhibiting cancer cell destruction. It is reasonable to assume that effector immune T cells could infiltrate into tumors and counter the growth and progression of cancer cells. However, to what extent Tregs may influence the effector T cell population within the tumor microenvironment remains unclear.

The net outcome of these complex regulations determines whether or not tumor cells grow, recur, and intrude, and thereby have an impact on the eventual survival of patients with cancer. While Treg cells and their cytokines likely serve to promote cancer cell growth and survival in established tumors, these same immunosuppressive properties also prevent autoimmunity and early stage cancer development.


Th17 cells may play a key role in providing a constant proinflammatory environment within established tumors while also influencing cell fate decisions and activation. A proposed model outlining how this cycle of inflammation may perpetuate and lead to cancer development and survival can be found in Figure 1. A proposed model of chronic inflammation progressing to tumor formation.

A chronic insult such as autoimmunity or infection leads to a steady inflamed tissue state. However, these combined suppressive signals may not be sufficient to overcome the self-perpetuating cycle of activation established between Th17 cells and TAM.

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The net effect of these cellular interactions within the tumor microenvironment is to limit anti-tumor immunity from Th1 and CD8 T cells while continuing to encourage chronic inflammation, angiogenesis, and overall cancer cell survival and proliferation. Once initially established, Th17 cells may then create a chronic environment of inflammatory factors that further activates TAM and self-propagates, encouraging angiogenesis and cancer cell survival through STAT3 activation and anti-apoptotic protein production.