Regulatory T-cell neutralization in mice during filariasis helps in parasite clearance by enhancing T helper type 17-mediated pro-inflammatory response.
Identifieur interne : 000B63 ( PubMed/Corpus ); précédent : 000B62; suivant : 000B64Regulatory T-cell neutralization in mice during filariasis helps in parasite clearance by enhancing T helper type 17-mediated pro-inflammatory response.
Auteurs : Manisha Pathak ; Pankaj Sharma ; Aditi Sharma ; Meenakshi Verma ; Mrigank Srivastava ; Shailja Misra-BhattacharyaSource :
- Immunology [ 1365-2567 ] ; 2016.
English descriptors
- KwdEn :
- Animals, Antibodies, Neutralizing (pharmacology), Antigens, CD40 (immunology), Antigens, CD40 (metabolism), Bacterial Outer Membrane Proteins (immunology), Cells, Cultured, Dendritic Cells (drug effects), Dendritic Cells (immunology), Dendritic Cells (parasitology), Disease Models, Animal, Elephantiasis, Filarial (drug therapy), Elephantiasis, Filarial (immunology), Elephantiasis, Filarial (metabolism), Elephantiasis, Filarial (parasitology), Eosinophils (drug effects), Eosinophils (immunology), Eosinophils (parasitology), Glucocorticoid-Induced TNFR-Related Protein (antagonists & inhibitors), Glucocorticoid-Induced TNFR-Related Protein (immunology), Glucocorticoid-Induced TNFR-Related Protein (metabolism), Host-Parasite Interactions, Immunization, Inflammation Mediators (immunology), Inflammation Mediators (metabolism), Interferon-gamma (immunology), Interferon-gamma (metabolism), Interleukin-10 (immunology), Interleukin-10 (metabolism), Interleukin-2 Receptor alpha Subunit (antagonists & inhibitors), Interleukin-2 Receptor alpha Subunit (immunology), Interleukin-2 Receptor alpha Subunit (metabolism), Macrophage Activation (drug effects), Mice, Inbred BALB C, T-Lymphocytes, Regulatory (drug effects), T-Lymphocytes, Regulatory (immunology), T-Lymphocytes, Regulatory (metabolism), T-Lymphocytes, Regulatory (parasitology), Th17 Cells (drug effects), Th17 Cells (immunology), Th17 Cells (metabolism), Th17 Cells (parasitology), Time Factors.
- MESH :
- chemical , antagonists & inhibitors : Glucocorticoid-Induced TNFR-Related Protein, Interleukin-2 Receptor alpha Subunit.
- chemical , immunology : Antigens, CD40, Bacterial Outer Membrane Proteins, Glucocorticoid-Induced TNFR-Related Protein, Inflammation Mediators, Interferon-gamma, Interleukin-10, Interleukin-2 Receptor alpha Subunit.
- chemical , metabolism : Antigens, CD40, Glucocorticoid-Induced TNFR-Related Protein, Inflammation Mediators, Interferon-gamma, Interleukin-10, Interleukin-2 Receptor alpha Subunit.
- chemical , pharmacology : Antibodies, Neutralizing.
- drug effects : Dendritic Cells, Eosinophils, Macrophage Activation, T-Lymphocytes, Regulatory, Th17 Cells.
- drug therapy : Elephantiasis, Filarial.
- immunology : Dendritic Cells, Elephantiasis, Filarial, Eosinophils, T-Lymphocytes, Regulatory, Th17 Cells.
- metabolism : Elephantiasis, Filarial, T-Lymphocytes, Regulatory, Th17 Cells.
- parasitology : Dendritic Cells, Elephantiasis, Filarial, Eosinophils, T-Lymphocytes, Regulatory, Th17 Cells.
- Animals, Cells, Cultured, Disease Models, Animal, Host-Parasite Interactions, Immunization, Mice, Inbred BALB C, Time Factors.
Abstract
Lymphatic filariasis leads to profound impairment of parasite-specific T helper type 1 (Th1) and Th2 immune responses and significantly increases the expression of regulatory networks and regulatory effectors like transforming growth factor-β, CD25, cytotoxic T-lymphocyte antigen 4, glucocorticoid-induced tumour necrosis factor receptor (GITR) and regulatory T (Treg) cells, which together play an important role in immunosuppression. While Treg cells suppress the activity of effector cells, monocyte dysfunction, characterized by an alternatively activated immunoregulatory phenotype, is one hypothesis that explains the lack of an antigen-specific T-cell response in infected individuals. In the present study, we administered neutralizing antibodies against the Treg cell-associated markers CD25 and GITR and observed its effects on filaria-induced immunosuppression. Our results show that administration of anti-CD25 and anti-GITR in infected animals not only arrested the accumulation of Treg cells and reduced arginase activity, but also led to an increase in the percentages of Th17 cells in the secondary lymphoid organs of mice. Elevated levels of interferon-γ and decreased levels of interleukin-10 were also noted in the culture supernatants of mouse splenocytes that were treated with neutralizing antibodies. Furthermore, treatment with neutralizing antibodies enhanced the expression of inducible nitric oxide synthase on host macrophages and CD40 on host dendritic cells with concomitant decreased expression of alternative activation markers Arg1, Ym1 and Fizz1, which together lead to reduced parasite burden in treated animals. In summary, administration of neutralizing antibodies helps in breaking the regulatory network in mice and limits parasite-induced immunosuppression at the earliest host-parasite interface.
DOI: 10.1111/imm.12550
PubMed: 26501838
Links to Exploration step
pubmed:26501838Le document en format XML
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Lucknow, India.</nlm:affiliation></affiliation></author><author><name sortKey="Verma, Meenakshi" sort="Verma, Meenakshi" uniqKey="Verma M" first="Meenakshi" last="Verma">Meenakshi Verma</name><affiliation><nlm:affiliation>Parasitology Division, CSIR-Central Drug Research Institute, Lucknow, India.</nlm:affiliation></affiliation></author><author><name sortKey="Srivastava, Mrigank" sort="Srivastava, Mrigank" uniqKey="Srivastava M" first="Mrigank" last="Srivastava">Mrigank Srivastava</name><affiliation><nlm:affiliation>Parasitology Division, CSIR-Central Drug Research Institute, Lucknow, India.</nlm:affiliation></affiliation></author><author><name sortKey="Misra Bhattacharya, Shailja" sort="Misra Bhattacharya, Shailja" uniqKey="Misra Bhattacharya S" first="Shailja" last="Misra-Bhattacharya">Shailja Misra-Bhattacharya</name><affiliation><nlm:affiliation>Parasitology Division, CSIR-Central Drug Research Institute, Lucknow, 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uniqKey="Sharma P" first="Pankaj" last="Sharma">Pankaj Sharma</name><affiliation><nlm:affiliation>Parasitology Division, CSIR-Central Drug Research Institute, Lucknow, India.</nlm:affiliation></affiliation></author><author><name sortKey="Sharma, Aditi" sort="Sharma, Aditi" uniqKey="Sharma A" first="Aditi" last="Sharma">Aditi Sharma</name><affiliation><nlm:affiliation>Parasitology Division, CSIR-Central Drug Research Institute, Lucknow, India.</nlm:affiliation></affiliation></author><author><name sortKey="Verma, Meenakshi" sort="Verma, Meenakshi" uniqKey="Verma M" first="Meenakshi" last="Verma">Meenakshi Verma</name><affiliation><nlm:affiliation>Parasitology Division, CSIR-Central Drug Research Institute, Lucknow, India.</nlm:affiliation></affiliation></author><author><name sortKey="Srivastava, Mrigank" sort="Srivastava, Mrigank" uniqKey="Srivastava M" first="Mrigank" last="Srivastava">Mrigank Srivastava</name><affiliation><nlm:affiliation>Parasitology Division, CSIR-Central Drug 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scheme="MESH" qualifier="immunology" xml:lang="en"><term>Dendritic Cells</term><term>Elephantiasis, Filarial</term><term>Eosinophils</term><term>T-Lymphocytes, Regulatory</term><term>Th17 Cells</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Elephantiasis, Filarial</term><term>T-Lymphocytes, Regulatory</term><term>Th17 Cells</term></keywords><keywords scheme="MESH" qualifier="parasitology" xml:lang="en"><term>Dendritic Cells</term><term>Elephantiasis, Filarial</term><term>Eosinophils</term><term>T-Lymphocytes, Regulatory</term><term>Th17 Cells</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cells, Cultured</term><term>Disease Models, Animal</term><term>Host-Parasite Interactions</term><term>Immunization</term><term>Mice, Inbred BALB C</term><term>Time Factors</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Lymphatic filariasis leads to profound impairment of parasite-specific T helper type 1 (Th1) and Th2 immune responses and significantly increases the expression of regulatory networks and regulatory effectors like transforming growth factor-β, CD25, cytotoxic T-lymphocyte antigen 4, glucocorticoid-induced tumour necrosis factor receptor (GITR) and regulatory T (Treg) cells, which together play an important role in immunosuppression. While Treg cells suppress the activity of effector cells, monocyte dysfunction, characterized by an alternatively activated immunoregulatory phenotype, is one hypothesis that explains the lack of an antigen-specific T-cell response in infected individuals. In the present study, we administered neutralizing antibodies against the Treg cell-associated markers CD25 and GITR and observed its effects on filaria-induced immunosuppression. Our results show that administration of anti-CD25 and anti-GITR in infected animals not only arrested the accumulation of Treg cells and reduced arginase activity, but also led to an increase in the percentages of Th17 cells in the secondary lymphoid organs of mice. Elevated levels of interferon-γ and decreased levels of interleukin-10 were also noted in the culture supernatants of mouse splenocytes that were treated with neutralizing antibodies. Furthermore, treatment with neutralizing antibodies enhanced the expression of inducible nitric oxide synthase on host macrophages and CD40 on host dendritic cells with concomitant decreased expression of alternative activation markers Arg1, Ym1 and Fizz1, which together lead to reduced parasite burden in treated animals. In summary, administration of neutralizing antibodies helps in breaking the regulatory network in mice and limits parasite-induced immunosuppression at the earliest host-parasite interface.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">26501838</PMID><DateCreated><Year>2016</Year><Month>01</Month><Day>19</Day></DateCreated><DateCompleted><Year>2016</Year><Month>05</Month><Day>31</Day></DateCompleted><DateRevised><Year>2017</Year><Month>02</Month><Day>01</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1365-2567</ISSN><JournalIssue CitedMedium="Internet"><Volume>147</Volume><Issue>2</Issue><PubDate><Year>2016</Year><Month>Feb</Month></PubDate></JournalIssue><Title>Immunology</Title><ISOAbbreviation>Immunology</ISOAbbreviation></Journal><ArticleTitle>Regulatory T-cell neutralization in mice during filariasis helps in parasite clearance by enhancing T helper type 17-mediated pro-inflammatory response.</ArticleTitle><Pagination><MedlinePgn>190-203</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1111/imm.12550</ELocationID><Abstract><AbstractText>Lymphatic filariasis leads to profound impairment of parasite-specific T helper type 1 (Th1) and Th2 immune responses and significantly increases the expression of regulatory networks and regulatory effectors like transforming growth factor-β, CD25, cytotoxic T-lymphocyte antigen 4, glucocorticoid-induced tumour necrosis factor receptor (GITR) and regulatory T (Treg) cells, which together play an important role in immunosuppression. While Treg cells suppress the activity of effector cells, monocyte dysfunction, characterized by an alternatively activated immunoregulatory phenotype, is one hypothesis that explains the lack of an antigen-specific T-cell response in infected individuals. In the present study, we administered neutralizing antibodies against the Treg cell-associated markers CD25 and GITR and observed its effects on filaria-induced immunosuppression. Our results show that administration of anti-CD25 and anti-GITR in infected animals not only arrested the accumulation of Treg cells and reduced arginase activity, but also led to an increase in the percentages of Th17 cells in the secondary lymphoid organs of mice. Elevated levels of interferon-γ and decreased levels of interleukin-10 were also noted in the culture supernatants of mouse splenocytes that were treated with neutralizing antibodies. Furthermore, treatment with neutralizing antibodies enhanced the expression of inducible nitric oxide synthase on host macrophages and CD40 on host dendritic cells with concomitant decreased expression of alternative activation markers Arg1, Ym1 and Fizz1, which together lead to reduced parasite burden in treated animals. In summary, administration of neutralizing antibodies helps in breaking the regulatory network in mice and limits parasite-induced immunosuppression at the earliest host-parasite interface.</AbstractText><CopyrightInformation>© 2015 John Wiley & Sons Ltd.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Pathak</LastName><ForeName>Manisha</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Parasitology Division, CSIR-Central Drug Research Institute, Lucknow, India.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sharma</LastName><ForeName>Pankaj</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Parasitology Division, CSIR-Central Drug Research Institute, Lucknow, India.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sharma</LastName><ForeName>Aditi</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Parasitology Division, CSIR-Central Drug Research Institute, Lucknow, India.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Academy of Scientific and Innovative Research (AcSIR), New Delhi, India.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Verma</LastName><ForeName>Meenakshi</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Parasitology Division, CSIR-Central Drug Research Institute, Lucknow, India.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Academy of Scientific and Innovative Research (AcSIR), New Delhi, India.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Srivastava</LastName><ForeName>Mrigank</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Parasitology Division, CSIR-Central Drug Research Institute, Lucknow, India.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Academy of Scientific and Innovative Research (AcSIR), New Delhi, India.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Misra-Bhattacharya</LastName><ForeName>Shailja</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Parasitology Division, CSIR-Central Drug Research Institute, Lucknow, India.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Academy of Scientific and Innovative Research (AcSIR), New Delhi, India.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2015</Year><Month>12</Month><Day>09</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Immunology</MedlineTA><NlmUniqueID>0374672</NlmUniqueID><ISSNLinking>0019-2805</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D057134">Antibodies, Neutralizing</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D019013">Antigens, CD40</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001425">Bacterial Outer Membrane Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D053450">Glucocorticoid-Induced TNFR-Related Protein</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C556062">IL10 protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018836">Inflammation Mediators</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D053645">Interleukin-2 Receptor alpha Subunit</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C112171">Wsp protein, Wolbachia</NameOfSubstance></Chemical><Chemical><RegistryNumber>130068-27-8</RegistryNumber><NameOfSubstance UI="D016753">Interleukin-10</NameOfSubstance></Chemical><Chemical><RegistryNumber>82115-62-6</RegistryNumber><NameOfSubstance UI="D007371">Interferon-gamma</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Nat Immunol. 2002 Feb;3(2):135-42</RefSource><PMID Version="1">11812990</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Immunol. 2001 Nov 1;167(9):5348-54</RefSource><PMID Version="1">11673551</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Arch Med Res. 2002 Jul-Aug;33(4):422-4</RefSource><PMID Version="1">12234534</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Immunity. 2003 Jul;19(1):71-82</RefSource><PMID Version="1">12871640</PMID></CommentsCorrections><CommentsCorrections 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