Abstract
CCR7, collaborated with its ligands CCL19 and CCL21, controls extensive migratory events in the immune system. CCR7-bearing dendritic cells can swarm into T-cell zones in lymph nodes, initiating the antigen presentation and T-cell response. Abnormal expression of CCR7 in dendritic cells will cause a series of inflammatory diseases due to the chaotic dendritic cell trafficking. In this review, we take an in-depth look at the structural–functional domains of CCR7 and CCR7-bearing dendritic cell trajectory to lymph nodes. Then, we summarize the regulatory network of CCR7, including transcriptional regulation, translational and posttranslational regulation, internalization, desensitization, and recycling. Furthermore, the potential strategies of targeting the CCR7 network to regulate dendritic cell migration and to deal with inflammatory diseases are integrated, which not only emphasizes the possibility of CCR7 to be a potential target of immunotherapy but also has an implication on the homing of dendritic cells to benefit inflammatory diseases.
Highlights
Dendritic cells (DCs) are the center of both innate and acquired immunity, embodied in their role in the recognition of internal and external antigens and immunomodulators (Banchereau and Steinman, 1998; Minton, 2017)
DCs can successfully swarm into T-cell zones of draining lymph nodes (dLNs) via the chemokine receptor 7 (CCR7)-CCL19/CCL21 axis. How do they get into the lymph nodes and how do they locate to the T-cell zones correctly? we present the main processes of CCR7-mediated migration and localization of DCs in dLNs, along with the subsequent contact and activation of T cells (Figure 2)
According to a recent study, mature DCs (mDCs) possess distinct intracellular pools of CCR7 derived from the plasma membrane or the secretory pathway of newly synthesized receptors, and they always resided at the trans-Golgi network (TGN)
Summary
Dendritic cells (DCs) are the center of both innate and acquired immunity, embodied in their role in the recognition of internal and external antigens and immunomodulators (Banchereau and Steinman, 1998; Minton, 2017). We present the main processes of CCR7-mediated migration and localization of DCs in dLNs, along with the subsequent contact and activation of T cells (Figure 2).
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