Immunopathogenic mechanisms in tourette syndrome: A critical review
Identifieur interne : 002261 ( Main/Exploration ); précédent : 002260; suivant : 002262Immunopathogenic mechanisms in tourette syndrome: A critical review
Auteurs : Davide Martino [Italie] ; Russell C. Dale [Australie] ; Donald L. Gilbert [États-Unis] ; Gavin Giovannoni [Royaume-Uni] ; James F. Leckman [États-Unis]Source :
- Movement Disorders [ 0885-3185 ] ; 2009-07-15.
English descriptors
- KwdEn :
- Autoantibodies (metabolism), Environment, Gene Expression Regulation (immunology), Humans, Immune System (cytology), Immune System (pathology), Immune System (physiopathology), Models, Immunological, Stress, Psychological (immunology), Tourette Syndrome (genetics), Tourette Syndrome (immunology), Tourette Syndrome (pathology), antineuronal antibodies, autoimmunity, group A beta haemolytic Streptococcus; tic, tourette syndrome.
- MESH :
- chemical , metabolism : Autoantibodies.
- cytology : Immune System.
- genetics : Tourette Syndrome.
- immunology : Gene Expression Regulation, Stress, Psychological, Tourette Syndrome.
- pathology : Immune System, Tourette Syndrome.
- physiopathology : Immune System.
- Environment, Humans, Models, Immunological.
Abstract
Tourette syndrome (TS) has a multifactorial etiology, in which genetic, environmental, immunological and hormonal factors interact to establish vulnerability. This review: (i) summarizes research exploring the exposure of TS patients to immune‐activating environmental factors, and (ii) focuses on recent findings supporting a role of the innate and adaptive immune systems in the pathogenesis of TS and related disorders. A higher exposure prior to disease onset to group A β‐haemolytic streptococcal (GABHS) infections in children with tics and obsessive‐compulsive (OC) symptoms has been documented, although their influence upon the course of disease remains uncertain. Increased activation of immune responses in TS is suggested by changes in gene expression profiles of peripheral immune cells, relative frequency of lymphocyte subpopulations, and synthesis of immune effector molecules. Increased activity of cell‐mediated mechanisms is suggested by the increased expression of genes controlling natural killer and cytotoxic T cells, increased plasma levels of some pro‐inflammatory cytokines which correlate with disease severity, and increased synthesis of antineuronal antibodies. Important methodological differences might account for some inconsistency among results of studies addressing autoantibodies in TS. Finally, a general predisposition to autoimmune responses in TS patients is indicated by the reduced frequency of regulatory T cells, which induce tolerance towards self‐antigens. Although the pathogenic role of immune activation in TS has not been definitively proven, a pathophysiological model is proposed to explain the possible effect of immunity upon dopamine transmission regulation and the generation of tics. © 2009 Movement Disorder Society
Url:
- https://api.istex.fr/document/8B4C2D81D77CFBA70C20BDB32995A60E440E4368/fulltext/pdf
- http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3972005
DOI: 10.1002/mds.22504
Affiliations:
- Australie, Italie, Royaume-Uni, États-Unis
- Angleterre, Connecticut, Grand Londres, Ohio
- Londres, Sydney
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Le document en format XML
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Leckman</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Departments of Psychiatry, Pediatrics and Psychology, Child Study Center, Yale University School of Medicine, New Haven, Connecticut</wicri:regionArea><placeName><region type="state">Connecticut</region></placeName></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="sub">Official Journal of the Movement Disorder Society</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2009-07-15">2009-07-15</date><biblScope unit="vol">24</biblScope><biblScope unit="issue">9</biblScope><biblScope unit="page" from="1267">1267</biblScope><biblScope unit="page" to="1279">1279</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">8B4C2D81D77CFBA70C20BDB32995A60E440E4368</idno><idno type="DOI">10.1002/mds.22504</idno><idno type="ArticleID">MDS22504</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Autoantibodies (metabolism)</term><term>Environment</term><term>Gene Expression Regulation (immunology)</term><term>Humans</term><term>Immune System (cytology)</term><term>Immune System (pathology)</term><term>Immune System (physiopathology)</term><term>Models, Immunological</term><term>Stress, Psychological (immunology)</term><term>Tourette Syndrome (genetics)</term><term>Tourette Syndrome (immunology)</term><term>Tourette Syndrome (pathology)</term><term>antineuronal antibodies</term><term>autoimmunity</term><term>group A beta haemolytic Streptococcus; tic</term><term>tourette syndrome</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Autoantibodies</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Immune System</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Tourette Syndrome</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Gene Expression Regulation</term><term>Stress, Psychological</term><term>Tourette Syndrome</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Immune System</term><term>Tourette Syndrome</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Immune System</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Environment</term><term>Humans</term><term>Models, Immunological</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Tourette syndrome (TS) has a multifactorial etiology, in which genetic, environmental, immunological and hormonal factors interact to establish vulnerability. This review: (i) summarizes research exploring the exposure of TS patients to immune‐activating environmental factors, and (ii) focuses on recent findings supporting a role of the innate and adaptive immune systems in the pathogenesis of TS and related disorders. A higher exposure prior to disease onset to group A β‐haemolytic streptococcal (GABHS) infections in children with tics and obsessive‐compulsive (OC) symptoms has been documented, although their influence upon the course of disease remains uncertain. Increased activation of immune responses in TS is suggested by changes in gene expression profiles of peripheral immune cells, relative frequency of lymphocyte subpopulations, and synthesis of immune effector molecules. Increased activity of cell‐mediated mechanisms is suggested by the increased expression of genes controlling natural killer and cytotoxic T cells, increased plasma levels of some pro‐inflammatory cytokines which correlate with disease severity, and increased synthesis of antineuronal antibodies. Important methodological differences might account for some inconsistency among results of studies addressing autoantibodies in TS. Finally, a general predisposition to autoimmune responses in TS patients is indicated by the reduced frequency of regulatory T cells, which induce tolerance towards self‐antigens. Although the pathogenic role of immune activation in TS has not been definitively proven, a pathophysiological model is proposed to explain the possible effect of immunity upon dopamine transmission regulation and the generation of tics. © 2009 Movement Disorder Society</div></front></TEI><affiliations><list><country><li>Australie</li><li>Italie</li><li>Royaume-Uni</li><li>États-Unis</li></country><region><li>Angleterre</li><li>Connecticut</li><li>Grand Londres</li><li>Ohio</li></region><settlement><li>Londres</li><li>Sydney</li></settlement></list><tree><country name="Italie"><noRegion><name sortKey="Martino, Davide" sort="Martino, Davide" uniqKey="Martino D" first="Davide" last="Martino">Davide Martino</name></noRegion></country><country name="Australie"><noRegion><name sortKey="Dale, Russell C" sort="Dale, Russell C" uniqKey="Dale R" first="Russell C." last="Dale">Russell C. Dale</name></noRegion></country><country name="États-Unis"><region name="Ohio"><name sortKey="Gilbert, Donald L" sort="Gilbert, Donald L" uniqKey="Gilbert D" first="Donald L." last="Gilbert">Donald L. Gilbert</name></region><name sortKey="Leckman, James F" sort="Leckman, James F" uniqKey="Leckman J" first="James F." last="Leckman">James F. Leckman</name></country><country name="Royaume-Uni"><region name="Angleterre"><name sortKey="Giovannoni, Gavin" sort="Giovannoni, Gavin" uniqKey="Giovannoni G" first="Gavin" last="Giovannoni">Gavin Giovannoni</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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