Ziv Y, Ron N, Butovsky O, Landa G, Sudai E, Greenberg N, Cohen H, Kipnis J, Schwartz MImmune cells contribute to the maintenance of neurogenesis and spatial learning abilities in adulthood. Nat Neurosci 9:268-275
Department of Neurobiology, Weizmann Institute of Science, 76100 Rehovot, Israel.Nature Neuroscience (Impact Factor: 16.1). 03/2006; 9(2):268-75. DOI: 10.1038/nn1629
Neurogenesis is known to take place in the adult brain. This work identifies T lymphocytes and microglia as being important to the maintenance of hippocampal neurogenesis and spatial learning abilities in adulthood. Hippocampal neurogenesis induced by an enriched environment was associated with the recruitment of T cells and the activation of microglia. In immune-deficient mice, hippocampal neurogenesis was markedly impaired and could not be enhanced by environmental enrichment, but was restored and boosted by T cells recognizing a specific CNS antigen. CNS-specific T cells were also found to be required for spatial learning and memory and for the expression of brain-derived neurotrophic factor in the dentate gyrus, implying that a common immune-associated mechanism underlies different aspects of hippocampal plasticity and cell renewal in the adult brain.
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- "Recently, schizophrenia has increasingly been associated with progressive neurodegeneration, and one of the predominant underlying mechanisms appears to be immuno-inflammatory processes (Durrenberger et al. 2014; Pasternak et al. 2012; Pérez-Neri et al. 2006). Further to this, animal studies have established beneficial roles of T cells in cognition and behaviour ; for example, T cell replenishment restored cognitive impairment caused by systemic immune deficiency (Brynskikh et al. 2008; Kipnis et al. 2004; Wolf et al. 2009; Ziv et al. 2006). Herein, the relevance of T cells in schizophrenia, more specifically the implications of T cells in the etiology, course and treatment have been highlighted. "
ABSTRACT: Schizophrenia is a severe and highly complex neurodevelopmental disorder with an unknown etiopathology. Recently, immunopathogenesis has emerged as one of the most compelling etiological models of schizophrenia. Over the past few years considerable research has been devoted to the role of innate immune responses in schizophrenia. The findings of such studies have helped to conceptualize schizophrenia as a chronic low-grade inflammatory disorder. Although the contribution of adaptive immune responses has also been emphasized, however, the precise role of T cells in the underlying neurobiological pathways of schizophrenia is yet to be ascertained comprehensively. T cells have the ability to infiltrate brain and mediate neuro-immune cross-talk. Conversely, the central nervous system and the neurotransmitters are capable of regulating the immune system. Neurotransmitter like dopamine, implicated widely in schizophrenia risk and progression can modulate the proliferation, trafficking and functions of T cells. Within brain, T cells activate microglia, induce production of pro-inflammatory cytokines as well as reactive oxygen species and subsequently lead to neuroinflammation. Importantly, such processes contribute to neuronal injury/death and are gradually being implicated as mediators of neuroprogressive changes in schizophrenia. Antipsychotic drugs, commonly used to treat schizophrenia are also known to affect adaptive immune system; interfere with the differentiation and functions of T cells. This understanding suggests a pivotal role of T cells in the etiology, course and treatment of schizophrenia and forms the basis of this review.
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- "In particular, very little is known about the changes induced by EE in microglia. One potential mechanism behind the pro-neurogenic actions of EE is that EE triggers an increased surveillance of the hippocampal tissue by T cells, which somehow drive microglia to increase their expression of IGF-1, ultimately resulting in an increased number of newborn neurons in adult rats (Ziv et al. 2006 ). Whether this interaction between T cells and microglia in EE involves any type of antigen presentation is still unknown, even though EE induced microglia to express the major histocompatibility complex class II (MHC-II). "
ABSTRACT: An emerging view in Neuroscience is that cognitive functions such as learning and memory engage all the various cell types making-up the brain, including surveillant microglia, the resident immune cells. These complex functions prominently depend on the structural remodeling of neuronal circuits, rooted in the formation, strengthening, and elimination of synaptic structures, but also on the continuous integration of newborn neurons into the mature circuitry. In this chapter, we will focus our attention on the emerging roles of microglia in adult neurogenesis within its two consensus regions, the hippocampus and the olfactory bulb. We will discuss the underlying cellular and molecular mechanisms based on evidence from both inflammatory and non-inflammatory conditions. Doing so, we will also examine their implications for learning and memory, and the effects of environmental enrichment, running paradigms, normal aging, and neurodegenerative diseases on microglia, adult neurogenesis, and the behavioural outcome. Lastly, we will summarize the key points that emerge from our current understanding of these new roles of microglia in adult neurogenesis, learning and memory, and the most promising directions to pursue in this recent field of investigation.
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- "/gbe/evu212 Advance Access publication September 19, 2014 terms identified by K a are included in a curated collection of neural/immune-related GO terms (Geifman et al. 2010). The nervous and immune systems (both innate and adaptive) are known to interact with each other; the nervous system modulates the function of the immune system, which in turn influences the nervous system (Sternberg 2006; Ziv et al. 2006; Ransohoff and Brown 2012; Wraith and Nicholson 2012). This strong connection between the fast-evolving genes and the neural/immune systems was also observed in our parallel analysis on the placental–marsupial "
ABSTRACT: Cephalochordates, the sister group of tunicates plus vertebrates, have been called "living fossils" due to their resemblance to fossil chordates from Cambrian strata. The genome of the cephalochordate Branchiostoma floridae shares remarkable synteny with vertebrates and is free from whole-genome duplication. We performed RNA sequencing from larvae and adults of Asymmetron lucayanum, a cephalochordate distantly related to B. floridae. Comparisons of about 430 orthologous gene groups among both cephalochordates and 10 vertebrates using an echinoderm, a hemichordate, and a mollusk as outgroups showed that cephalochor-dates are evolving more slowly than the slowest evolving vertebrate known (the elephant shark), with A. lucayanum evolving even more slowly than B. floridae. Against this background of slow evolution, some genes, notably several involved in innate immunity, stand out as evolving relatively quickly. This may be due to the lack of an adaptive immune system and the relatively high levels of bacteria in the inshore waters cephalochordates inhabit. Molecular dating analysis including several time constraints revealed a divergence time of ~120 Ma for A. lucayanum and B. floridae. The divisions between cephalochordates and vertebrates, and that between chordates and the hemichordate plus echinoderm clade likely occurred before the Cambrian.
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