CD157 and Brain Immune System in (Patho)physiological Conditions: Focus on Brain Plasticity

Abstract

Ectoenzyme and receptor BST-1/CD157 has been considered as a key molecule involved in the regulation of functional activity of cells in various tissues and organs. It is commonly accepted that CD157 catalyzes NAD+ hydrolysis and acts as a component of integrin adhesion receptor complex. Such properties are important for the regulatory role of CD157 in neuronal and glial cells: in addition to recently discovered role in the regulation of emotions, motor functions, and social behavior, CD157 might serve as an important component of innate immune reactions in the central nervous system. Activation of innate immune system in the brain occurs in response to infectious agents as well as in brain injury and neurodegeneration. As an example, in microglial cells, association of CD157 with CD11b/CD18 complex drives reactive gliosis and neuroinflammation evident in brain ischemia, chronic neurodegeneration, and aging. There are various non-substrate ligands of CD157 belonging to the family of extracellular matrix proteins (fibronectin, collagen I, finbrinogen, and laminin) whose activity is required for controlling cell adhesion and migration. Therefore, CD157 could control structural and functional integrity of the blood-brain barrier and barriergenesis. On the other hand, contribution of CD157 to the regulation of brain development is rather possible since in the embryonic brain, CD157 expression is very high, whereas in the adult brain, CD157 is expressed on neural stem cells and, presumably, is involved in the neurogenesis. Besides, CD157 could mediate astrocytes’ action on neural stem and progenitor cells within neurogenic niches. In this review we will summarize how CD157 may affect brain plasticity acting as a molecule at the crossroad of neurogenesis, cerebral angiogenesis, and immune regulation.

Fibroblast-Conditioned Media Enhance the Yield of Microglia Isolated from Mixed Glial Cultures

“…IL-1, IL-6 and TNF-α), VEGF and diverse fibroblast growth factors (FGFs) (Murase et al 1992 ; Costa et al 2015 ; Jeong et al 2016a ; Russo et al 2021 ). Collagen I and decorin were reported whose activity is required for controlling cell adhesion and migration (Lopatina et al 2020 ). Some pro-inflammatory cytokines are able to upregulate microglial proliferation (Ganter et al 1992 ).…”

CCR7+ CD4 T Cell Immunosurveillance Disrupted in Chronic SIV-Induced Neuroinflammation in Rhesus Brain

“…Specifically, we saw decreased expression of ETC genes, NDUFB7, NDUFB11, and COX4I1, along with a decrease in inositol polyphosphate phosphatase 4A (INPP4A), a suppressor of glutamate excitotoxicity in the CNS linked to neurodegeneration in the striatum (69). We identified an increase in BST1, a risk factor for neurodegenerative diseases, particularly PD (70–75). Additionally, there was an increase in Dot1L, which regulates receptor-interacting protein kinase 1 (RIPK1) and triggers apoptotic death during cerebral ischemia injury.…”

Paracrine ADP Ribosyl Cyclase-Mediated Regulation of Biological Processes

“…The paracrine cell systems described in this review underline the specific functions of the two major ecto-ADPRCs, type II CD38 and CD157, which produce and supply cADPR to neighboring cells. Related to this point, more advanced information on the comparative properties of the two ectoenzymes is needed, beyond the substantially higher cADPR-producing activity of CD38, especially possible differences in their regulation in different cell types and tissues [ 77 , 78 ], including yet undetermined mechanisms of gene expression. Limited but promising examples concern the distinct roles and mechanisms of CD38 and CD157 in (i) inducing an immunosuppressive TME in solid tumors [ 96 ], (ii) showing different substrate properties in the brain that are apparently associated with specific psychiatric symptoms and psychological disorders [ 111 ].…”

“…Research on this topic is in progress, and specifically, the impact of either enzyme defect on cADPR/Ca 2+ /oxytocin needs to be clarified [ 77 ]. Additionally, the possible occurrence of paracrine cADPR-mediated interactions involving the two ectoenzymes CD38 and CD157 and oxytocin/oxytocin receptors is still unknown [ 78 ], although it is suggested by the distinct types of cells expressing either ecto-ADPRC and cells synthesizing oxytocin/oxytocin receptors.…”