Regulatory networks induced by live parasites impair both Th1 and Th2 pathways in patent lymphatic filariasis: implications for parasite persistence.
Identifieur interne : 003A76 ( PubMed/Corpus ); précédent : 003A75; suivant : 003A77Regulatory networks induced by live parasites impair both Th1 and Th2 pathways in patent lymphatic filariasis: implications for parasite persistence.
Auteurs : Subash Babu ; Carla P. Blauvelt ; V. Kumaraswami ; Thomas B. NutmanSource :
- Journal of immunology (Baltimore, Md. : 1950) [ 0022-1767 ] ; 2006.
English descriptors
- KwdEn :
- Animals, Antibodies, Blocking (pharmacology), Antigens, CD, Antigens, Differentiation (immunology), Antigens, Differentiation (metabolism), Brugia malayi (growth & development), Brugia malayi (immunology), CTLA-4 Antigen, Cells, Cultured, Cytokines (biosynthesis), Down-Regulation (immunology), Elephantiasis, Filarial (immunology), Elephantiasis, Filarial (parasitology), Forkhead Transcription Factors (biosynthesis), Forkhead Transcription Factors (genetics), GATA3 Transcription Factor (antagonists & inhibitors), Host-Parasite Interactions (immunology), Humans, Immune Tolerance (genetics), Signal Transduction (genetics), Signal Transduction (immunology), Suppressor of Cytokine Signaling Proteins (biosynthesis), Suppressor of Cytokine Signaling Proteins (genetics), T-Box Domain Proteins, Th1 Cells (immunology), Th1 Cells (metabolism), Th1 Cells (parasitology), Th2 Cells (immunology), Th2 Cells (metabolism), Th2 Cells (parasitology), Transcription Factors (antagonists & inhibitors), Transforming Growth Factor beta (biosynthesis), Transforming Growth Factor beta (genetics), Ubiquitin-Protein Ligases (antagonists & inhibitors).
- MESH :
- chemical , antagonists & inhibitors : GATA3 Transcription Factor, Transcription Factors, Ubiquitin-Protein Ligases.
- chemical , biosynthesis : Cytokines, Forkhead Transcription Factors, Suppressor of Cytokine Signaling Proteins, Transforming Growth Factor beta.
- chemical , genetics : Forkhead Transcription Factors, Suppressor of Cytokine Signaling Proteins, Transforming Growth Factor beta.
- chemical , immunology : Antigens, Differentiation.
- chemical , metabolism : Antigens, Differentiation.
- chemical , pharmacology : Antibodies, Blocking.
- genetics : Immune Tolerance, Signal Transduction.
- growth & development : Brugia malayi.
- immunology : Brugia malayi, Down-Regulation, Elephantiasis, Filarial, Host-Parasite Interactions, Signal Transduction, Th1 Cells, Th2 Cells.
- metabolism : Th1 Cells, Th2 Cells.
- parasitology : Elephantiasis, Filarial, Th1 Cells, Th2 Cells.
- Animals, Antigens, CD, CTLA-4 Antigen, Cells, Cultured, Humans, T-Box Domain Proteins.
Abstract
Patent lymphatic filariasis is characterized by a profound down-regulation of immune responses with both parasite Ag-specific tolerance and bystander suppression. Although this down-regulation is confined to the Th1 arm of the immune system in response to parasite Ag, we hypothesized a more generalized suppression in response to live parasites. Indeed, when we examined the cytokine profile of a cohort of filaria-infected (n = 10) and uninfected (n = 10) individuals in response to live infective-stage larvae or microfilariae of Brugia malayi, we found significant impairment of both Th1 and Th2 cytokines characterized by diminished production of IFN-gamma, TNF-alpha, IL-4, IL-5, and IL-10 in infected patients. The molecular basis of this impaired Th1/Th2 response was examined, and we identified three major networks of immunoregulation and tolerance. First, impaired induction of T-bet and GATA-3 mRNA underlies the Th1/Th2 deficiency in infected individuals. Second, regulatory networks, as evidenced by significantly increased expression of Foxp3 (natural regulatory T cell marker) and regulatory effectors such as TGF-beta, CTLA-4, PD-1, ICOS, and indoleamine 2,3-dioxygenase play an important role in immunosuppression. Third, the compromise of effector T cell function is mediated by the enhanced induction of anergy-inducing factors cbl-b, c-cbl (cbl is abbreviation for Casitas B lymphoma), Itch, and Nedd4. Indeed, blocking CTLA-4 or neutralizing TGF-beta restored the ability to mount Th1/Th2 responses to live parasites and reversed the induction of anergy-inducing factors. Hence, we conclude that a profound impairment of live parasite-specific Th1 and Th2 immune responses occurs in lymphatic filariasis that is governed at the transcriptional level by a complex interplay of inhibitory mediators.
PubMed: 16493086
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pubmed:16493086Le document en format XML
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Although this down-regulation is confined to the Th1 arm of the immune system in response to parasite Ag, we hypothesized a more generalized suppression in response to live parasites. Indeed, when we examined the cytokine profile of a cohort of filaria-infected (n = 10) and uninfected (n = 10) individuals in response to live infective-stage larvae or microfilariae of Brugia malayi, we found significant impairment of both Th1 and Th2 cytokines characterized by diminished production of IFN-gamma, TNF-alpha, IL-4, IL-5, and IL-10 in infected patients. The molecular basis of this impaired Th1/Th2 response was examined, and we identified three major networks of immunoregulation and tolerance. First, impaired induction of T-bet and GATA-3 mRNA underlies the Th1/Th2 deficiency in infected individuals. Second, regulatory networks, as evidenced by significantly increased expression of Foxp3 (natural regulatory T cell marker) and regulatory effectors such as TGF-beta, CTLA-4, PD-1, ICOS, and indoleamine 2,3-dioxygenase play an important role in immunosuppression. Third, the compromise of effector T cell function is mediated by the enhanced induction of anergy-inducing factors cbl-b, c-cbl (cbl is abbreviation for Casitas B lymphoma), Itch, and Nedd4. Indeed, blocking CTLA-4 or neutralizing TGF-beta restored the ability to mount Th1/Th2 responses to live parasites and reversed the induction of anergy-inducing factors. Hence, we conclude that a profound impairment of live parasite-specific Th1 and Th2 immune responses occurs in lymphatic filariasis that is governed at the transcriptional level by a complex interplay of inhibitory mediators.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">16493086</PMID><DateCreated><Year>2006</Year><Month>02</Month><Day>22</Day></DateCreated><DateCompleted><Year>2006</Year><Month>04</Month><Day>28</Day></DateCompleted><DateRevised><Year>2016</Year><Month>11</Month><Day>24</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0022-1767</ISSN><JournalIssue CitedMedium="Print"><Volume>176</Volume><Issue>5</Issue><PubDate><Year>2006</Year><Month>Mar</Month><Day>01</Day></PubDate></JournalIssue><Title>Journal of immunology (Baltimore, Md. : 1950)</Title><ISOAbbreviation>J. Immunol.</ISOAbbreviation></Journal><ArticleTitle>Regulatory networks induced by live parasites impair both Th1 and Th2 pathways in patent lymphatic filariasis: implications for parasite persistence.</ArticleTitle><Pagination><MedlinePgn>3248-56</MedlinePgn></Pagination><Abstract><AbstractText>Patent lymphatic filariasis is characterized by a profound down-regulation of immune responses with both parasite Ag-specific tolerance and bystander suppression. Although this down-regulation is confined to the Th1 arm of the immune system in response to parasite Ag, we hypothesized a more generalized suppression in response to live parasites. Indeed, when we examined the cytokine profile of a cohort of filaria-infected (n = 10) and uninfected (n = 10) individuals in response to live infective-stage larvae or microfilariae of Brugia malayi, we found significant impairment of both Th1 and Th2 cytokines characterized by diminished production of IFN-gamma, TNF-alpha, IL-4, IL-5, and IL-10 in infected patients. The molecular basis of this impaired Th1/Th2 response was examined, and we identified three major networks of immunoregulation and tolerance. First, impaired induction of T-bet and GATA-3 mRNA underlies the Th1/Th2 deficiency in infected individuals. Second, regulatory networks, as evidenced by significantly increased expression of Foxp3 (natural regulatory T cell marker) and regulatory effectors such as TGF-beta, CTLA-4, PD-1, ICOS, and indoleamine 2,3-dioxygenase play an important role in immunosuppression. Third, the compromise of effector T cell function is mediated by the enhanced induction of anergy-inducing factors cbl-b, c-cbl (cbl is abbreviation for Casitas B lymphoma), Itch, and Nedd4. Indeed, blocking CTLA-4 or neutralizing TGF-beta restored the ability to mount Th1/Th2 responses to live parasites and reversed the induction of anergy-inducing factors. Hence, we conclude that a profound impairment of live parasite-specific Th1 and Th2 immune responses occurs in lymphatic filariasis that is governed at the transcriptional level by a complex interplay of inhibitory mediators.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Babu</LastName><ForeName>Subash</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA. sbabu@niaid.nih.gov</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Blauvelt</LastName><ForeName>Carla P</ForeName><Initials>CP</Initials></Author><Author ValidYN="Y"><LastName>Kumaraswami</LastName><ForeName>V</ForeName><Initials>V</Initials></Author><Author ValidYN="Y"><LastName>Nutman</LastName><ForeName>Thomas B</ForeName><Initials>TB</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><Agency>Intramural NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D003160">Comparative Study</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052060">Research Support, N.I.H., Intramural</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Immunol</MedlineTA><NlmUniqueID>2985117R</NlmUniqueID><ISSNLinking>0022-1767</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D019138">Antibodies, Blocking</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015703">Antigens, CD</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000943">Antigens, Differentiation</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D060908">CTLA-4 Antigen</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C556706">CTLA4 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016207">Cytokines</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C418974">FOXP3 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051858">Forkhead Transcription Factors</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D050990">GATA3 Transcription Factor</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D050826">Suppressor of Cytokine Signaling Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D020825">T-Box Domain Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C406820">T-box transcription factor TBX21</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D014157">Transcription Factors</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016212">Transforming Growth Factor beta</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.3.2.27</RegistryNumber><NameOfSubstance UI="D044767">Ubiquitin-Protein Ligases</NameOfSubstance></Chemical></ChemicalList><CitationSubset>AIM</CitationSubset><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D019138" MajorTopicYN="N">Antibodies, Blocking</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015703" 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MajorTopicYN="N">Down-Regulation</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004605" MajorTopicYN="N">Elephantiasis, Filarial</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName><QualifierName UI="Q000469" MajorTopicYN="Y">parasitology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051858" MajorTopicYN="N">Forkhead Transcription Factors</DescriptorName><QualifierName UI="Q000096" MajorTopicYN="N">biosynthesis</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D050990" MajorTopicYN="N">GATA3 Transcription Factor</DescriptorName><QualifierName UI="Q000037" MajorTopicYN="N">antagonists & inhibitors</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006790" MajorTopicYN="N">Host-Parasite Interactions</DescriptorName><QualifierName UI="Q000276" 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