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Infection and Inflammation
Published in Michael Ljungberg, Handbook of Nuclear Medicine and Molecular Imaging for Physicists, 2022
Erik H. J. G. Aarntzen, Andor W. J. M. Glaudemans
In addition to direct recognition and killing by cells of our innate immune system, T- and B-cells can be mobilized when antigen-specific immune responses are required. Viruses, as well as some bacteria, survive and replicate in self-host cells and thereby escape from recognition by innate immune cells. Although macrophages and tissue dendritic cells are mainly phagocytic, they can be activated to express co-stimulatory molecules and major histocompatibility complexes (MHC) containing antigens derived from the infectious microorganism. In response to chemokines like CCL21, these antigen-presenting cells home to draining lymph nodes, bridging innate and adaptive immunity [10, 11].
Basics of Allergy
Published in Pudupakkam K Vedanthan, Harold S Nelson, Shripad N Agashe, PA Mahesh, Rohit Katial, Textbook of Allergy for the Clinician, 2021
Rafeul Alam, Dipa K Sheth, Magdalena M Gorska
In order to increase the probability of antigen encounter, lymphocytes continuously circulate across various tissues. Naïve T and B cells preferentially migrate to lymph nodes due to homing receptors L-selectin and CCR7 (Moser and Loetscher 2001). Their ligands, CCL19 and CCL21 are expressed on High Endothelial Venules (HEV) of lymph nodes.
Immunology
Published in Anthony R. Mundy, John M. Fitzpatrick, David E. Neal, Nicholas J. R. George, The Scientific Basis of Urology, 2010
Anne C. Cunningham, Graeme O’Boyle, John A. Kirby
Aside from their role in leukocyte migration, chemokines are also able to direct some immune effector mechanisms. Some chemokines, particularly those that act to attract polymorphonuclear cells, are able to cause respiratory burst and degranulation, while also influencing the movement of these cells. Chemokines play a role in the activation of lymphocytes by APC, and can influence the polarization of the immune response toward antibody- or cell-based responses. Chemokines are also involved in the metastasis of cancer cells. Cancers are characterized by a distinct metastatic pattern involving the regional lymph nodes, and tissues such as bone marrow, lung, and liver. For example, it has been demonstrated that the chemokine receptor CCR7 is highly expressed in many human cancer cells, malignant tumors, and metastases. Its ligand CCL21 is expressed in organs representing the first destinations of cancer metastasis.
CCL21/CCR7 axis regulates demyelination and vascular cognitive impairment in a mouse model for chronic cerebral hypoperfusion
Published in Neurological Research, 2023
Xuelian Tang, Cunsheng Wei, Rui Zhang, Jie You, Xuemei Chen
CCL21 is a member of the C–C chemokine family, which is associated with cell proliferation, maturation, migration, and inflammation [19]. CCL21 is expressed by lymphoid tissues, endothelial cells, as well as neurons [20,21]. CCL21 is involved in numerous human diseases including rheumatoid arthritis, viral diseases, acute coronary syndrome and cancer metastasis [22–25]. In central nervous system (CNS), the expression of CCL21 is triggered by injury, infectious and hypoperfusion [26]. Data gathered over the recent years show that CCL21, vias its receptor CCR7, plays an important role in Lyme neuroborreliosis, cerebrovascular ischemia, hematopoetic tumors, autoimmune demyelination in the CNS [27]. However, there are no reports on the influence of CCL21 on the WML induced by chronic cerebral hypoperfusion.
Chemokines as the critical factors during bladder cancer progression: an overview
Published in International Reviews of Immunology, 2021
Amir Sadra Zangouei, Amir Abbas Hamidi, Hamid Reza Rahimi, Ehsan Saburi, Majid Mojarrad, Meysam Moghbeli
CCL21 is a chemokine that exerts its function via binding with CCR7. The CCR7 is a GPCR produced by various cells such as naive B and T cells and dendritic cells. CCL21/CCR7 interaction has pivotal roles in immune cells homing, peripheral tolerance, T regulatory cells regulation, and autoimmunity [159]. CCL21 may also play a vital role in mediating the returning of lymphocytes to secondary lymphoid organs and triggering subsequent immune response to foreign antigen, therefore, rendering the rationale for CCL21 based cancer immunotherapy [160]. CCR7 also plays a critical role in lymphocyte and dendritic cell trafficking into and within lymph nodes [161]. A hallmark of DC maturation is the up regulation of functional CCR7 receptors. This receptor is also involved in T cell homing to various secondary lymphoid organs such as lymph nodes and the spleen as well as the trafficking of T cells within the spleen. Furthermore, CCR7 regulate T cell homeostasis in lymph nodes, and may also function in the activation and polarization of T cells [162]. CCR7 up regulation was significantly associated with lymph node involvement and poor survival. Moreover, increased CCR7 expression was correlated with elevated MVD and MLVD which showed CCR7 as an inducer of angiogenesis and lymphangiogenesis. CCR7 activation by CCL21 significantly increased ERK1/2 phosphorylation in UBC cells [78]. The CCL21/CCR7 axis increased T24 cell proliferation and migration. CCL21 also up regulated the MMP2 and MMP9 expressions during cell invasion. Moreover, there was significant reduced apoptosis rate following CCL21 treatment in comparison with control in which CCL21 up regulated and down regulated the BCL2 and BAX, respectively [79].
Clinicopathological and prognostic value of chemokine receptor CCR7 expression in head and neck squamous cell carcinoma: a systematic review and meta-analysis
Published in Expert Review of Anticancer Therapy, 2023
Ibrahim Elmakaty, Basel Elsayed, Mohamed Elmarasi, Omar Kujan, Mohammed Imad Malki
Several previous studies have suggested that CCL19/CCL21-CCR7 plays an important role in lymph node cancer cell invasion of lymph nodes [45]. This axis is notable for its role in attracting immune cells to areas of physiological stress as a hemostasis mechanism [46]. CCL19/CCL21 expression in immune and lymphatic endothelial cells responds to increased CCR7 expression in cancer cells, causing cancer cells to spread to lymph nodes where they reside [45]. Furthermore, this axis interacts with numerous molecules and mediates the activation of numerous pathways. MiR-1275 expression, For example, was up-regulated in SCCHN tissues and advanced metastatic SCCHN cells via chemokine receptor type 7 (CCR7) protein levels [47]. Another study found that NF-B and AP1 transcription factors frequently cooperate, leading to increased CCR7 mRNA expression in metastatic SCCHN cells [37]. CCR7 also promotes HNSCC chemotaxis, invasion, and migration through the RhoA/ROCK-Pyk2 cofilin pathway [33]. Furthermore, CCR7 has been shown to promote PCI-37B cell chemotaxis and migration by upregulating and activating MMP-9 protein to induce actin cytoskeleton reorganization [34]. In metastatic HNSCC, CCR7 regulates cell adhesion and migration via beta1 integrin [48]. Furthermore, MAPK members, specifically ERK1/2 and JNK, play important roles in CCR7-mediated regulation of HNSCC metastasis regulation [49]. Furthermore, epithelial-mesenchymal transition (EMT) is thought to play a role in the pathogenesis of many cancers, and CCL21-CCR7 interaction has been shown to regulate EMT progression and promote the stemness of OSCC by activating the JAK2/STAT3 signaling pathway [50]. It is thought that by sabotaging the CCL19/CCL21-CCR7 axis, these proteins, molecules, and pathways can be potential targets for HNSCC therapy, reducing metastasis, recurrence, and increasing overall survival.