Biased TCR repertoire in infiltrating lesional T cells in human Bancroftian filariasis.
Identifieur interne : 00BE08 ( Ncbi/Curation ); précédent : 00BE07; suivant : 00BE09Biased TCR repertoire in infiltrating lesional T cells in human Bancroftian filariasis.
Auteurs : D O Freedman [États-Unis] ; D A Plier ; A. De Almeida ; J. Miranda ; C. Braga ; M C Maia E Silva ; J. Tang ; A. FurtadoSource :
- Journal of immunology (Baltimore, Md. : 1950) [ 0022-1767 ] ; 1999.
Descripteurs français
- KwdFr :
- ARN messager (génétique), Amorces ADN (génétique), Animaux, Antigènes HLA-DR (génétique), Chaines HLA-DRB1, Cytokines (génétique), Expression des gènes, Filariose lymphatique (génétique), Filariose lymphatique (immunologie), Filariose lymphatique (étiologie), Humains, Lymphocytes T (immunologie), RT-PCR, Récepteur lymphocytaire T antigène, alpha-bêta (génétique), Séquence nucléotidique, Wuchereria bancrofti.
- MESH :
- génétique : ARN messager, Amorces ADN, Antigènes HLA-DR, Cytokines, Filariose lymphatique, Récepteur lymphocytaire T antigène, alpha-bêta.
- immunologie : Filariose lymphatique, Lymphocytes T.
- étiologie : Filariose lymphatique.
- Animaux, Chaines HLA-DRB1, Expression des gènes, Humains, RT-PCR, Séquence nucléotidique, Wuchereria bancrofti.
English descriptors
- KwdEn :
- Animals, Base Sequence, Cytokines (genetics), DNA Primers (genetics), Elephantiasis, Filarial (etiology), Elephantiasis, Filarial (genetics), Elephantiasis, Filarial (immunology), Gene Expression, HLA-DR Antigens (genetics), HLA-DRB1 Chains, Humans, RNA, Messenger (genetics), Receptors, Antigen, T-Cell, alpha-beta (genetics), Reverse Transcriptase Polymerase Chain Reaction, T-Lymphocytes (immunology), Wuchereria bancrofti.
- MESH :
- chemical , genetics : Cytokines, DNA Primers, HLA-DR Antigens, RNA, Messenger, Receptors, Antigen, T-Cell, alpha-beta.
- etiology : Elephantiasis, Filarial.
- genetics : Elephantiasis, Filarial.
- immunology : Elephantiasis, Filarial, T-Lymphocytes.
- Animals, Base Sequence, Gene Expression, HLA-DRB1 Chains, Humans, Reverse Transcriptase Polymerase Chain Reaction, Wuchereria bancrofti.
Abstract
To investigate the hypothesis that T cells recognizing specific Ags localize to the site of disease activity in human bancroftian filariasis, we have compared the repertoire of TCR Vbeta gene segments in lesions vs blood in individual patients by RT-PCR ELISA. Vbeta14 and Vbeta24 were overrepresented (5% greater in tissue compared with PBMCs and/or tissue/PBMC ratios in the highest 5% of all tissue/PBMC ratios for all Vbetas for all subjects) in 50% and 40% of study subjects, respectively. Overrepresentation of these two Vbetas did not occur in any control subject. In comparing three patient groups, the proportion of individuals meeting at least one criterion for Vbeta14 overrepresentation was shown to increase in tandem with our current concepts of disease progression (asymptomatic filariasis = 25%; clinical filariasis with active infection = 60%; clinical filariasis without active infection = 71%). In 6 of the 10 individuals with Vbeta14 overrepresentation, Vbeta14 represented >20% of the entire lesional Vbeta repertoire. All but one of the 20 study subjects had at least one Vbeta gene segment that was overrepresented in tissue compared with PBMCs. Only a small number of Vbetas, usually three or less, were overrepresented in any single filariasis patient. However, in the same tissue, no differences between patient groups were found when IFN-gamma, TNF-alpha, IL-4, IL-5, and IL-12 mRNA expression were examined. Taken together, these findings suggest that, in principle, in essentially all patients, whether with subclinical or with clinical filariasis, distinct and limited T cell populations are concentrated in affected tissue.
PubMed: 9973439
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De Almeida</name></author><author><name sortKey="Miranda, J" sort="Miranda, J" uniqKey="Miranda J" first="J" last="Miranda">J. Miranda</name></author><author><name sortKey="Braga, C" sort="Braga, C" uniqKey="Braga C" first="C" last="Braga">C. Braga</name></author><author><name sortKey="Maia E Silva, M C" sort="Maia E Silva, M C" uniqKey="Maia E Silva M" first="M C" last="Maia E Silva">M C Maia E Silva</name></author><author><name sortKey="Tang, J" sort="Tang, J" uniqKey="Tang J" first="J" last="Tang">J. Tang</name></author><author><name sortKey="Furtado, A" sort="Furtado, A" uniqKey="Furtado A" first="A" last="Furtado">A. 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De Almeida</name></author><author><name sortKey="Miranda, J" sort="Miranda, J" uniqKey="Miranda J" first="J" last="Miranda">J. Miranda</name></author><author><name sortKey="Braga, C" sort="Braga, C" uniqKey="Braga C" first="C" last="Braga">C. Braga</name></author><author><name sortKey="Maia E Silva, M C" sort="Maia E Silva, M C" uniqKey="Maia E Silva M" first="M C" last="Maia E Silva">M C Maia E Silva</name></author><author><name sortKey="Tang, J" sort="Tang, J" uniqKey="Tang J" first="J" last="Tang">J. Tang</name></author><author><name sortKey="Furtado, A" sort="Furtado, A" uniqKey="Furtado A" first="A" last="Furtado">A. Furtado</name></author></analytic><series><title level="j">Journal of immunology (Baltimore, Md. : 1950)</title><idno type="ISSN">0022-1767</idno><imprint><date when="1999" type="published">1999</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Base Sequence</term><term>Cytokines (genetics)</term><term>DNA Primers (genetics)</term><term>Elephantiasis, Filarial (etiology)</term><term>Elephantiasis, Filarial (genetics)</term><term>Elephantiasis, Filarial (immunology)</term><term>Gene Expression</term><term>HLA-DR Antigens (genetics)</term><term>HLA-DRB1 Chains</term><term>Humans</term><term>RNA, Messenger (genetics)</term><term>Receptors, Antigen, T-Cell, alpha-beta (genetics)</term><term>Reverse Transcriptase Polymerase Chain Reaction</term><term>T-Lymphocytes (immunology)</term><term>Wuchereria bancrofti</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>ARN messager (génétique)</term><term>Amorces ADN (génétique)</term><term>Animaux</term><term>Antigènes HLA-DR (génétique)</term><term>Chaines HLA-DRB1</term><term>Cytokines (génétique)</term><term>Expression des gènes</term><term>Filariose lymphatique (génétique)</term><term>Filariose lymphatique (immunologie)</term><term>Filariose lymphatique (étiologie)</term><term>Humains</term><term>Lymphocytes T (immunologie)</term><term>RT-PCR</term><term>Récepteur lymphocytaire T antigène, alpha-bêta (génétique)</term><term>Séquence nucléotidique</term><term>Wuchereria bancrofti</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Cytokines</term><term>DNA Primers</term><term>HLA-DR Antigens</term><term>RNA, Messenger</term><term>Receptors, Antigen, T-Cell, alpha-beta</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Elephantiasis, Filarial</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Elephantiasis, Filarial</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>ARN messager</term><term>Amorces ADN</term><term>Antigènes HLA-DR</term><term>Cytokines</term><term>Filariose lymphatique</term><term>Récepteur lymphocytaire T antigène, alpha-bêta</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Filariose lymphatique</term><term>Lymphocytes T</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Elephantiasis, Filarial</term><term>T-Lymphocytes</term></keywords><keywords scheme="MESH" qualifier="étiologie" xml:lang="fr"><term>Filariose lymphatique</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Base Sequence</term><term>Gene Expression</term><term>HLA-DRB1 Chains</term><term>Humans</term><term>Reverse Transcriptase Polymerase Chain Reaction</term><term>Wuchereria bancrofti</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Chaines HLA-DRB1</term><term>Expression des gènes</term><term>Humains</term><term>RT-PCR</term><term>Séquence nucléotidique</term><term>Wuchereria bancrofti</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">To investigate the hypothesis that T cells recognizing specific Ags localize to the site of disease activity in human bancroftian filariasis, we have compared the repertoire of TCR Vbeta gene segments in lesions vs blood in individual patients by RT-PCR ELISA. Vbeta14 and Vbeta24 were overrepresented (5% greater in tissue compared with PBMCs and/or tissue/PBMC ratios in the highest 5% of all tissue/PBMC ratios for all Vbetas for all subjects) in 50% and 40% of study subjects, respectively. Overrepresentation of these two Vbetas did not occur in any control subject. In comparing three patient groups, the proportion of individuals meeting at least one criterion for Vbeta14 overrepresentation was shown to increase in tandem with our current concepts of disease progression (asymptomatic filariasis = 25%; clinical filariasis with active infection = 60%; clinical filariasis without active infection = 71%). In 6 of the 10 individuals with Vbeta14 overrepresentation, Vbeta14 represented >20% of the entire lesional Vbeta repertoire. All but one of the 20 study subjects had at least one Vbeta gene segment that was overrepresented in tissue compared with PBMCs. Only a small number of Vbetas, usually three or less, were overrepresented in any single filariasis patient. However, in the same tissue, no differences between patient groups were found when IFN-gamma, TNF-alpha, IL-4, IL-5, and IL-12 mRNA expression were examined. Taken together, these findings suggest that, in principle, in essentially all patients, whether with subclinical or with clinical filariasis, distinct and limited T cell populations are concentrated in affected tissue.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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