Immunology of lymphatic filariasis
Identifieur interne : 002A01 ( Main/Exploration ); précédent : 002A00; suivant : 002A02Immunology of lymphatic filariasis
Auteurs : Subash Babu ; Thomas B. Nutman [États-Unis]Source :
- Parasite immunology [ 0141-9838 ] ; 2014.
Descripteurs français
- KwdFr :
- Animaux, Brugia (immunologie), Filariose lymphatique (immunologie), Filariose lymphatique (parasitologie), Humains, Immunité cellulaire, Interleukine-10 (génétique), Interleukine-10 (métabolisme), Lymphocytes T CD4+ (métabolisme), Lymphocytes T CD4+ (physiologie), Modèles animaux de maladie humaine, Wuchereria bancrofti (immunologie).
- MESH :
- génétique : Interleukine-10.
- immunologie : Brugia, Filariose lymphatique, Wuchereria bancrofti.
- métabolisme : Interleukine-10, Lymphocytes T CD4+.
- parasitologie : Filariose lymphatique.
- physiologie : Lymphocytes T CD4+.
- Animaux, Humains, Immunité cellulaire, Modèles animaux de maladie humaine.
English descriptors
- KwdEn :
- Animals, Brugia (immunology), CD4-Positive T-Lymphocytes (metabolism), CD4-Positive T-Lymphocytes (physiology), Disease Models, Animal, Elephantiasis, Filarial (immunology), Elephantiasis, Filarial (parasitology), Humans, Immunity, Cellular, Interleukin-10 (genetics), Interleukin-10 (metabolism), Wuchereria bancrofti (immunology).
- MESH :
- chemical , genetics : Interleukin-10.
- immunology : Brugia, Elephantiasis, Filarial, Wuchereria bancrofti.
- metabolism : CD4-Positive T-Lymphocytes, Interleukin-10.
- parasitology : Elephantiasis, Filarial.
- physiology : CD4-Positive T-Lymphocytes.
- Animals, Disease Models, Animal, Humans, Immunity, Cellular.
Abstract
The immune responses to filarial parasites encompass a complex network of innate and adaptive cells whose interaction with the parasite underlies a spectrum of clinical manifestations. The predominant immunological feature of lymphatic filariasis is an antigen - specific Th2 response and an expansion of IL-10 producing CD4+ T cells that is accompanied by a muted Th1 response. This antigen specific T cell hypo-responsiveness appears to be crucial for the maintenance of the sustained, long-standing infection often with high parasite densities. While the correlates of protective immunity to lymphatic filariasis are still incompletely understood, primarily due to the lack of suitable animal models to study susceptibility, it is clear that T cells and to a certain extent B cells are required for protective immunity. Host immune responses, especially CD4+ T cell responses clearly play a role in mediating pathological manifestations of LF, including lymphedema, hydrocele and elephantiasis. The main underlying defect in the development of clinical pathology appears to be a failure to induce T cell hypo-responsiveness in the face of antigenic stimulation. Finally, another intriguing feature of filarial infections is their propensity to induce bystander effects on a variety of immune responses, including responses to vaccinations, allergens and to other infectious agents. The complexity of the immune response to filarial infection therefore provides an important gateway to understanding the regulation of immune responses to chronic infections, in general.
Url:
DOI: 10.1111/pim.12081
PubMed: 24134686
PubMed Central: 3990654
Affiliations:
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Le document en format XML
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Nutman</name><affiliation wicri:level="2"><nlm:aff id="A2">Helminth Immunology Section Laboratory of Parasitic Diseases National Institute of Allergy and Infectious Diseases Bethesda, MD 20892-0425</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Maryland</region></placeName><wicri:cityArea>Helminth Immunology Section Laboratory of Parasitic Diseases National Institute of Allergy and Infectious Diseases Bethesda</wicri:cityArea></affiliation></author></analytic><series><title level="j">Parasite immunology</title><idno type="ISSN">0141-9838</idno><idno type="eISSN">1365-3024</idno><imprint><date when="2014">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Brugia (immunology)</term><term>CD4-Positive T-Lymphocytes (metabolism)</term><term>CD4-Positive T-Lymphocytes (physiology)</term><term>Disease Models, Animal</term><term>Elephantiasis, Filarial (immunology)</term><term>Elephantiasis, Filarial (parasitology)</term><term>Humans</term><term>Immunity, Cellular</term><term>Interleukin-10 (genetics)</term><term>Interleukin-10 (metabolism)</term><term>Wuchereria bancrofti (immunology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Brugia (immunologie)</term><term>Filariose lymphatique (immunologie)</term><term>Filariose lymphatique (parasitologie)</term><term>Humains</term><term>Immunité cellulaire</term><term>Interleukine-10 (génétique)</term><term>Interleukine-10 (métabolisme)</term><term>Lymphocytes T CD4+ (métabolisme)</term><term>Lymphocytes T CD4+ (physiologie)</term><term>Modèles animaux de maladie humaine</term><term>Wuchereria bancrofti (immunologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Interleukin-10</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Interleukine-10</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Brugia</term><term>Filariose lymphatique</term><term>Wuchereria bancrofti</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Brugia</term><term>Elephantiasis, Filarial</term><term>Wuchereria bancrofti</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>CD4-Positive T-Lymphocytes</term><term>Interleukin-10</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Interleukine-10</term><term>Lymphocytes T CD4+</term></keywords><keywords scheme="MESH" qualifier="parasitologie" xml:lang="fr"><term>Filariose lymphatique</term></keywords><keywords scheme="MESH" qualifier="parasitology" xml:lang="en"><term>Elephantiasis, Filarial</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Lymphocytes T CD4+</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>CD4-Positive T-Lymphocytes</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Humans</term><term>Immunity, Cellular</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Humains</term><term>Immunité cellulaire</term><term>Modèles animaux de maladie humaine</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p id="P1">The immune responses to filarial parasites encompass a complex network of innate and adaptive cells whose interaction with the parasite underlies a spectrum of clinical manifestations. The predominant immunological feature of lymphatic filariasis is an antigen - specific Th2 response and an expansion of IL-10 producing CD4<sup>+</sup> T cells that is accompanied by a muted Th1 response. This antigen specific T cell hypo-responsiveness appears to be crucial for the maintenance of the sustained, long-standing infection often with high parasite densities. While the correlates of protective immunity to lymphatic filariasis are still incompletely understood, primarily due to the lack of suitable animal models to study susceptibility, it is clear that T cells and to a certain extent B cells are required for protective immunity. Host immune responses, especially CD4<sup>+</sup> T cell responses clearly play a role in mediating pathological manifestations of LF, including lymphedema, hydrocele and elephantiasis. The main underlying defect in the development of clinical pathology appears to be a failure to induce T cell hypo-responsiveness in the face of antigenic stimulation. Finally, another intriguing feature of filarial infections is their propensity to induce bystander effects on a variety of immune responses, including responses to vaccinations, allergens and to other infectious agents. The complexity of the immune response to filarial infection therefore provides an important gateway to understanding the regulation of immune responses to chronic infections, in general.</p></div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Maryland</li></region></list><tree><noCountry><name sortKey="Babu, Subash" sort="Babu, Subash" uniqKey="Babu S" first="Subash" last="Babu">Subash Babu</name></noCountry><country name="États-Unis"><region name="Maryland"><name sortKey="Nutman, Thomas B" sort="Nutman, Thomas B" uniqKey="Nutman T" first="Thomas B." last="Nutman">Thomas B. Nutman</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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