Immune Cell Migration in Health and Disease

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Three different sites for presentation of tumour associated antigens have been described: Tumour draining lymph node (TDLN), Tertiary lymphoid structures (TLS) and Tissue resident memory T cells. A population of memory precursor cells are believed to differentiate into CD103+ tissue resident memory T cells. These cells reside in the tumour and can recognize tumour antigens followed by killing the target tumour cell. In addition, tertiary lymphoid structures (TLS) also present a potential site for T cell priming. TLSs are organised cell aggregates formed within or at tumour margins in response to local inflammation and numerous cell-cell interactions occurring within the TME. Since these contain various immune cell types, TLSs can activate local immune response against the tumour, however the mechanism for T-cell priming within the TLSs is unknown.
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45 citations
Cancer associated EMT program activation alters cancer cell secretome by inducing the expression of neutrophil recruiting mediators. Three machineries, namely exocytic trafficking, secretory autophagy, and extracellular vesicles are proposed to enhance the release of neutrophil recruiting mediators from cancer cells. The secreted mediators promote EMT using a feed forward mechanism and initiate a chronic cycle of inflammation that supports cancer cell dissemination. TFs, transcription factors; RE, recycling endosome.
Mini Review
10 September 2021
The Recruitment of Neutrophils to the Tumor Microenvironment Is Regulated by Multiple Mediators
Shuvasree SenGupta
1 more and 
Carole A. Parent

Neutrophils sense and migrate towards chemotactic factors released at sites of infection/inflammation and contain the affected area using a variety of effector mechanisms. Aside from these established immune defense functions, neutrophils are emerging as one of the key tumor-infiltrating immune cells that influence cancer progression and metastasis. Neutrophil recruitment to the tumor microenvironment (TME) is mediated by multiple mediators including cytokines, chemokines, lipids, and growth factors that are secreted from cancer cells and cancer-associated stromal cells. However, the molecular mechanisms that underlie the expression and secretion of the different mediators from cancer cells and how neutrophils integrate these signals to reach and invade tumors remain unclear. Here, we discuss the possible role of the epithelial to mesenchymal transition (EMT) program, which is a well-established promoter of malignant potential in cancer, in regulating the expression and secretion of these key mediators. We also summarize and review our current understanding of the machineries that potentially control the secretion of the mediators from cancer cells, including the exocytic trafficking pathways, secretory autophagy, and extracellular vesicle-mediated secretion. We further reflect on possible mechanisms by which different mediators collaborate by integrating their signaling network, and particularly focus on TGF-β, a cytokine that is highly expressed in invasive tumors, and CXCR2 ligands, which are crucial neutrophil recruiting chemokines. Finally, we highlight gaps in the field and the need to expand current knowledge of the secretory machineries and cross-talks among mediators to develop novel neutrophil targeting strategies as effective therapeutic options in the treatment of cancer.

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56 citations
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32 citations
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