Immunopathogenesis of lymphatic filarial disease.
Identifieur interne : 002019 ( PubMed/Checkpoint ); précédent : 002018; suivant : 002020Immunopathogenesis of lymphatic filarial disease.
Auteurs : Subash Babu [Inde] ; Thomas B. NutmanSource :
- Seminars in immunopathology [ 1863-2300 ] ; 2012.
Descripteurs français
- KwdFr :
- MESH :
- diagnostic : Filariose lymphatique.
- immunologie : Filariose lymphatique.
- étiologie : Lymphoedème.
- Animaux, Filariose lymphatique, Humains, Immunité acquise, Immunité innée.
English descriptors
- KwdEn :
- MESH :
- complications : Elephantiasis, Filarial.
- diagnosis : Elephantiasis, Filarial.
- etiology : Lymphedema.
- immunology : Elephantiasis, Filarial.
- Adaptive Immunity, Animals, Humans, Immunity, Innate.
Abstract
Although two thirds of the 120 million people infected with lymph-dwelling filarial parasites have subclinical infections, ~40 million have lymphedema and/or other pathologic manifestations including hydroceles (and other forms of urogenital disease), episodic adenolymphangitis, tropical pulmonary eosinophilia, lymphedema, and (in its most severe form) elephantiasis. Adult filarial worms reside in the lymphatics and lymph nodes and induce changes that result in dilatation of lymphatics and thickening of the lymphatic vessel walls. Progressive lymphatic damage and pathology results from the summation of the effect of tissue alterations induced by both living and nonliving adult parasites, the host inflammatory response to the parasites and their secreted antigens, the host inflammatory response to the endosymbiont Wolbachia, and those seen as a consequence of secondary bacterial or fungal infections. Inflammatory damage induced by filarial parasites appears to be multifactorial, with endogenous parasite products, Wolbachia, and host immunity all playing important roles. This review will initially examine the prototypical immune responses engendered by the parasite and delineate the regulatory mechanisms elicited to prevent immune-mediated pathology. This will be followed by a discussion of the proposed mechanisms underlying pathogenesis, with the central theme being that pathogenesis is a two-step process-the first initiated by the parasite and host innate immune system and the second propagated mainly by the host's adaptive immune system and by other factors (including secondary infections).
DOI: 10.1007/s00281-012-0346-4
PubMed: 23053393
Affiliations:
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pubmed:23053393Le document en format XML
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Nutman</name></author></analytic><series><title level="j">Seminars in immunopathology</title><idno type="eISSN">1863-2300</idno><imprint><date when="2012" type="published">2012</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adaptive Immunity</term><term>Animals</term><term>Elephantiasis, Filarial (complications)</term><term>Elephantiasis, Filarial (diagnosis)</term><term>Elephantiasis, Filarial (immunology)</term><term>Humans</term><term>Immunity, Innate</term><term>Lymphedema (etiology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Filariose lymphatique ()</term><term>Filariose lymphatique (diagnostic)</term><term>Filariose lymphatique (immunologie)</term><term>Humains</term><term>Immunité acquise</term><term>Immunité innée</term><term>Lymphoedème (étiologie)</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Elephantiasis, Filarial</term></keywords><keywords scheme="MESH" qualifier="diagnosis" xml:lang="en"><term>Elephantiasis, Filarial</term></keywords><keywords scheme="MESH" qualifier="diagnostic" xml:lang="fr"><term>Filariose lymphatique</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Lymphedema</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Filariose lymphatique</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Elephantiasis, Filarial</term></keywords><keywords scheme="MESH" qualifier="étiologie" xml:lang="fr"><term>Lymphoedème</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adaptive Immunity</term><term>Animals</term><term>Humans</term><term>Immunity, Innate</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Filariose lymphatique</term><term>Humains</term><term>Immunité acquise</term><term>Immunité innée</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Although two thirds of the 120 million people infected with lymph-dwelling filarial parasites have subclinical infections, ~40 million have lymphedema and/or other pathologic manifestations including hydroceles (and other forms of urogenital disease), episodic adenolymphangitis, tropical pulmonary eosinophilia, lymphedema, and (in its most severe form) elephantiasis. Adult filarial worms reside in the lymphatics and lymph nodes and induce changes that result in dilatation of lymphatics and thickening of the lymphatic vessel walls. Progressive lymphatic damage and pathology results from the summation of the effect of tissue alterations induced by both living and nonliving adult parasites, the host inflammatory response to the parasites and their secreted antigens, the host inflammatory response to the endosymbiont Wolbachia, and those seen as a consequence of secondary bacterial or fungal infections. Inflammatory damage induced by filarial parasites appears to be multifactorial, with endogenous parasite products, Wolbachia, and host immunity all playing important roles. This review will initially examine the prototypical immune responses engendered by the parasite and delineate the regulatory mechanisms elicited to prevent immune-mediated pathology. This will be followed by a discussion of the proposed mechanisms underlying pathogenesis, with the central theme being that pathogenesis is a two-step process-the first initiated by the parasite and host innate immune system and the second propagated mainly by the host's adaptive immune system and by other factors (including secondary infections).</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">23053393</PMID><DateCreated><Year>2012</Year><Month>11</Month><Day>15</Day></DateCreated><DateCompleted><Year>2013</Year><Month>04</Month><Day>12</Day></DateCompleted><DateRevised><Year>2017</Year><Month>02</Month><Day>20</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1863-2300</ISSN><JournalIssue CitedMedium="Internet"><Volume>34</Volume><Issue>6</Issue><PubDate><Year>2012</Year><Month>Nov</Month></PubDate></JournalIssue><Title>Seminars in immunopathology</Title><ISOAbbreviation>Semin Immunopathol</ISOAbbreviation></Journal><ArticleTitle>Immunopathogenesis of lymphatic filarial disease.</ArticleTitle><Pagination><MedlinePgn>847-61</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1007/s00281-012-0346-4</ELocationID><Abstract><AbstractText>Although two thirds of the 120 million people infected with lymph-dwelling filarial parasites have subclinical infections, ~40 million have lymphedema and/or other pathologic manifestations including hydroceles (and other forms of urogenital disease), episodic adenolymphangitis, tropical pulmonary eosinophilia, lymphedema, and (in its most severe form) elephantiasis. Adult filarial worms reside in the lymphatics and lymph nodes and induce changes that result in dilatation of lymphatics and thickening of the lymphatic vessel walls. Progressive lymphatic damage and pathology results from the summation of the effect of tissue alterations induced by both living and nonliving adult parasites, the host inflammatory response to the parasites and their secreted antigens, the host inflammatory response to the endosymbiont Wolbachia, and those seen as a consequence of secondary bacterial or fungal infections. Inflammatory damage induced by filarial parasites appears to be multifactorial, with endogenous parasite products, Wolbachia, and host immunity all playing important roles. This review will initially examine the prototypical immune responses engendered by the parasite and delineate the regulatory mechanisms elicited to prevent immune-mediated pathology. This will be followed by a discussion of the proposed mechanisms underlying pathogenesis, with the central theme being that pathogenesis is a two-step process-the first initiated by the parasite and host innate immune system and the second propagated mainly by the host's adaptive immune system and by other factors (including secondary infections).</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Babu</LastName><ForeName>Subash</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>NIRT ICER, Chennai, India. sbabu@mail.nih.gov</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nutman</LastName><ForeName>Thomas B</ForeName><Initials>TB</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>Z99 AI999999</GrantID><Agency>Intramural NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052060">Research Support, N.I.H., Intramural</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2012</Year><Month>10</Month><Day>03</Day></ArticleDate></Article><MedlineJournalInfo><Country>Germany</Country><MedlineTA>Semin Immunopathol</MedlineTA><NlmUniqueID>101308769</NlmUniqueID><ISSNLinking>1863-2297</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>PLoS Negl Trop Dis. 2009;3(4):e420</RefSource><PMID Version="1">19381284</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Am J Trop Med Hyg. 1995 Dec;53(6):633-8</RefSource><PMID Version="1">8561266</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Immunol. 2003 Feb 15;170(4):1930-8</RefSource><PMID 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Nutman</name></noCountry><country name="Inde"><noRegion><name sortKey="Babu, Subash" sort="Babu, Subash" uniqKey="Babu S" first="Subash" last="Babu">Subash Babu</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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