Anti-CCR7 monoclonal antibody, clone 4E23 [APC]

Chemokine (C-C motif) ligand 19 (CCL19) is a critical regulator of the induction of T cell activation, immune tolerance, and inflammatory responses during continuous immune surveillance, homeostasis, and development. Migration of CC-chemokine receptor 7 (CCR7)-expressing cells to secondary lymphoid organs is a crucial step in the onset of adaptive immunity, which is initiated by a complex interaction between CCR7 and its cognate ligands. Recent advances in knowledge regarding the response of the CCL19-CCR7 axis to viral infections have elucidated the complex network of interplay among the invading virus, target cells and host immune responses. Viruses use various strategies to evade or delay the cytokine response, gaining additional time to replicate in the host. In this review, we summarize the impacts of CCL19 and CCR7 expression on the regulation of viral pathogenesis with an emphasis on the corresponding signaling pathways and adjuvant mechanisms. We present and discuss the expression, signaling adaptor proteins and effects of CCL19 and CCR7 as these molecules differentially impact different viral infections and viral life cycles in host homeostatic strategies. The underlying mechanisms discussed in this review may assist in the design of novel agents to modulate chemokine activity for viral prevention.

Multiple sclerosis (MS) is a neurodegenerative and immune-mediated disorder that characterizes by demyelination and neuro-inflammation. This study aimed to investigate the effects of pleiotrophin (PTN) on treatment of early injuries of white matter of MS patients. Experimental autoimmune encephalomyelitis (EAE) animal models were established by injecting 200 mu g myelinoligodendrocyte glyeoprotein 33-35 (MOG35-55) and were divided into PTN+MOG group and PBS+MOG group. Meanwhile, normal mice group was assigned as control group (NC group). Immunofluorescence double label was used to examined co-expression of molecules. LV5-PTN and LV3-siPTN were established and transfected into microglia cells. All brain imaging data was acquired with MRI scanner. Quantitative real-time RT-PCR (qRT-PCR) and western blot were used to evaluate mRNA and protein expression, respectively. Lesion sites mainly appeared in NAWM of bilateral occipital lobes in EAE models. PTN treatment significantly enhanced CCr7 and reduced CD206 expression compared to PBS+MOG group (P<0.05). PTN participated in mitogen-activated protein kinase (MAPK) signaling pathway in EAE models. PTN treatment significantly regulated levels of functional cytokines in both M1 and M2 type microglia cells compared to PBS+MOG group (P<0.05). LV5-PTN and LV3-siPTN transfection modulated levels of PTN and MAPK molecule in microglia cells undergoing treatment of M1 or M2 inducer. PTN strengthened M1/M2 transformation by regulating functional cytokines. In conclusion, PTN regulated functional heterogeneity of microglia cells in EAE animal models of MS by activating CCr-7/CD206 molecules and functional cytokines. PTN could be considered as a promising candidate molecule for treating early injuries of white matter of patients with MS.