scholarly journals Neuropathogenic SIVsmmFGb Genetic Diversity and Selection-Induced Tissue-Specific Compartmentalization During Chronic Infection and Temporal Evolution of Viral Genes in Lymphoid Tissues and Regions of the Central Nervous System

2010 ◽  
Vol 26 (6) ◽  
pp. 663-679 ◽  
Author(s):  
Aaron B. Reeve ◽  
Nicholas C. Pearce ◽  
Kalpana Patel ◽  
Katherine V. Augustus ◽  
Francis J. Novembre
Keyword(s):  
Genetic Diversity ◽  
Central Nervous System ◽  
Nervous System ◽  
Chronic Infection ◽  
Temporal Evolution ◽  
Lymphoid Tissues ◽  
Tissue Specific ◽  
Viral Genes ◽  
The Central Nervous System

scholarly journals Reduced Genetic Diversity in Lymphoid and Central Nervous System Tissues and Selection-Induced Tissue-Specific Compartmentalization of Neuropathogenic SIVsmmFGb during Acute Infection

2009 ◽  
Vol 25 (6) ◽  
pp. 583-601 ◽  
Author(s):  
Aaron B. Reeve ◽  
Kalpana Patel ◽  
Nicholas C. Pearce ◽  
Katherine V. Augustus ◽  
Heber G. Domingues ◽  
...  
Keyword(s):  
Genetic Diversity ◽  
Central Nervous System ◽  
Nervous System ◽  
Acute Infection ◽  
Tissue Specific

Detection of feline immunodeficiency proviral sequences in lymphoid tissues and the central nervous system by in situ gene amplification

1998 ◽  
Vol 73 (1) ◽  
pp. 109-119 ◽  
Author(s):  
Sabina Macchi ◽  
Fabrizio Maggi ◽  
Concetta Di Iorio ◽  
Alessandro Poli ◽  
Mauro Bendinelli ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Gene Amplification ◽  
Lymphoid Tissues ◽  
The Central Nervous System

scholarly journals The gateway reflex: breaking through the blood barriers

2021 ◽  
Author(s):  
Kaoru Murakami ◽  
Yuki Tanaka ◽  
Masaaki Murakami
Keyword(s):  
Central Nervous System ◽  
T Cells ◽  
Endothelial Cells ◽  
Nervous System ◽  
Neural Circuits ◽  
Inflammatory Diseases ◽  
Special Focus ◽  
Tissue Specific ◽  
The Central Nervous System ◽  
Pass Through

Abstract We have been studying inflammatory diseases, with a special focus on IL-6, and discovered two concepts related to inflammation development. One is the gateway reflex, which is induced by the activation of specific neural circuits followed by establishing gateways for autoreactive CD4+ T cells to pass through blood barriers toward the central nervous system (CNS) and retina during tissue-specific inflammatory diseases. We found that the formation of these gateways is dependent on the IL-6 amplifier, which is machinery for enhanced NF-κB activation in endothelial cells at specific sites. We have found five gateway reflexes in total. Here, we introduce the gateway reflex and the IL-6 amplifier.

scholarly journals Simian Immunodeficiency Virus Replicates to High Levels in Naturally Infected African Green Monkeys without Inducing Immunologic or Neurologic Disease

2001 ◽  
Vol 75 (5) ◽  
pp. 2262-2275 ◽  
Author(s):  
Suzanne R. Broussard ◽  
Silvija I. Staprans ◽  
Robert White ◽  
Evelyn M. Whitehead ◽  
Mark B. Feinberg ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Cell Lines ◽  
Peripheral Blood ◽  
Brain Parenchyma ◽  
Natural Host ◽  
Lymphoid Tissues ◽  
Immunodeficiency Virus ◽  
The Central Nervous System ◽  
Green Monkeys

ABSTRACT African green monkeys can maintain long-term persistent infection with simian immunodeficiency viruses (SIVagm) without developing AIDS and thus provide an important model for understanding mechanisms of natural host resistance to disease. This study assessed the levels and anatomic distribution of SIVagm in healthy, naturally infected monkeys. Quantitative competitive reverse transcriptase PCR assays developed to measure SIVagm from two African green monkey subspecies demonstrated high levels of SIV RNA in plasma (>6 × 106 RNA copies/ml) in sabaeus and vervet monkeys. Infectious virus was readily recovered from plasma and peripheral blood mononuclear cells and shown to be highly cytopathic in human cell lines and macrophages. SIVagm DNA levels were highest in the gastrointestinal tract, suggesting that the gut is a major site for SIVagm replication in vivo. Appreciable levels of virus were also found within the brain parenchyma and the cerebrospinal fluid (CSF), with lower levels detected in peripheral blood cells and lymph nodes. Virus isolates from the CSF and brain parenchyma readily infected macrophages in culture, whereas lymph node isolates were more restricted to growth in human T-cell lines. Comparison of env V2-C4 sequences showed extensive amino acid diversity between SIVagm recovered from the central nervous system and that recovered from lymphoid tissues. Homology between brain and CSF viruses, macrophage tropism, and active replication suggest compartmentalization in the central nervous system without associated neuropathology in naturally infected monkeys. These studies provide evidence that the nonpathogenic nature of SIVagm in the natural host can be attributed neither to more effective host control over viral replication nor to differences in the tissue and cell tropism from those for human immunodeficiency virus type 1-infected humans or SIV-infected macaques.

The recombination-activating gene 1 of Pleurodeles waltl (urodele amphibian) is transcribed in lymphoid tissues and in the central nervous system

2001 ◽  
Vol 52 (3-4) ◽  
pp. 264-275 ◽  
Author(s):  
Jean-Pol Frippiat ◽  
Christophe Frippiat ◽  
Pascaline Kremarik ◽  
Armelle Ropars ◽  
Christian Dournon
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Lymphoid Tissues ◽  
Recombination Activating Gene ◽  
The Central Nervous System ◽  
Pleurodeles Waltl

scholarly journals Tissue-restricted control of established central nervous system autoimmunity by TNF receptor 2–expressing Treg cells

2021 ◽  
Vol 118 (13) ◽  
pp. e2014043118
Author(s):  
Emilie Ronin ◽  
Charlotte Pouchy ◽  
Maryam Khosravi ◽  
Morgane Hilaire ◽  
Sylvie Grégoire ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Disease Onset ◽  
Treg Cells ◽  
Lymphoid Tissues ◽  
Target Tissue ◽  
Tnf Receptor ◽  
Autoimmune Encephalomyelitis ◽  
The Central Nervous System

CD4+Foxp3+ regulatory T (Treg) cells are central modulators of autoimmune diseases. However, the timing and location of Treg cell–mediated suppression of tissue-specific autoimmunity remain undefined. Here, we addressed these questions by investigating the role of tumor necrosis factor (TNF) receptor 2 (TNFR2) signaling in Treg cells during experimental autoimmune encephalomyelitis (EAE), a model of multiple sclerosis. We found that TNFR2-expressing Treg cells were critical to suppress EAE at peak disease in the central nervous system but had no impact on T cell priming in lymphoid tissues at disease onset. Mechanistically, TNFR2 signaling maintained functional Treg cells with sustained expression of CTLA-4 and Blimp-1, allowing active suppression of pathogenic T cells in the inflamed central nervous system. This late effect of Treg cells was further confirmed by treating mice with TNF and TNFR2 agonists and antagonists. Our findings show that endogenous Treg cells specifically suppress an autoimmune disease by acting in the target tissue during overt inflammation. Moreover, they bring a mechanistic insight to some of the adverse effects of anti-TNF therapy in patients.

scholarly journals Genome-wide analysis identifies significant contribution of brain-expressed genes in chronic, but not acute, back pain

2020 ◽  
Author(s):  
Andrey V Bortsov ◽  
Marc Parisien ◽  
Samar Khoury ◽  
Dmitri V Zaykin ◽  
Amy E Martinsen ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Back Pain ◽  
Chronic Back Pain ◽  
Genetic Contribution ◽  
Tissue Specific ◽  
Genome Wide Analysis ◽  
Genome Wide ◽  
Acute Back Pain ◽  
The Central Nervous System

Back pain is the leading cause of disability worldwide. Although most cases of back pain are acute, 20% of people with acute back pain go on to experience chronic back pain symptoms. It is unclear if acute and chronic pain states have similar or distinct underlying genetic mechanisms. Here we performed a genome-wide analysis for acute and chronic back pain in 375,158 individuals and found a significant genetic contribution to chronic, but not to acute, back pain. Using the UK Biobank cohort for discovery and the HUNT cohort for replication, we identified 7 loci for chronic back pain, of which 3 are novel. Pathway analyses, tissue-specific heritability enrichment analyses, epigenetic characterization, and tissue-specific transcriptome mapping in mouse pain models suggest a substantial genetic contribution to chronic, but not acute, back pain from the loci predominantly expressed in the central nervous system. Our findings show that chronic back pain is more heritable than acute back pain and is driven mostly by genes expressed in the central nervous system.

scholarly journals CalpA, a Drosophila calpain homolog specifically expressed in a small set of nerve, midgut, and blood cells.

1995 ◽  
Vol 15 (2) ◽  
pp. 824-834 ◽  
Author(s):  
U Theopold ◽  
M Pintér ◽  
S Daffre ◽  
Y Tryselius ◽  
P Friedrich ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Blood Cells ◽  
Signal Pathways ◽  
Cdna Clones ◽  
Hydrophobic Region ◽  
Tissue Specific ◽  
Calcium Dependent ◽  
The Central Nervous System ◽  
Additional Segment

Calpains are calcium-dependent proteases believed to participate in calcium-regulated signal pathways in cells. Ubiquitous calpains as well as tissue-specific calpains have been found in vertebrates. We isolated cDNA clones for a highly tissue-specific calpain gene from Drosophila melanogaster, CalpA, at 56C-D on the second chromosome. The expression of the CalpA gene product was monitored by using a specific antiserum directed against the product expressed by one cDNA clone. The encoded protein is found in a few neurons in the central nervous system, in scattered endocrine cells in the midgut, and in blood cells. In the blood cell line mbn-2, calpain is associated with a granular component in the cytoplasm. The expression of this protein is more restricted than that of the corresponding transcripts, which are widely distributed in the central nervous system, digestive tract, and other tissues. The sequence of CalpA is closely related to that of vertebrate calpains, but an additional segment is inserted in the calmodulin-like carboxy-terminal domain. This insert contains a hydrophobic region that may be involved in membrane attachment of the enzyme. Differential splicing also gives rise to a minor transcript that lacks the calmodulin-like domain.

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