AustralieFrV1, PascalFrancis, Corpus, bibRecord, 001854

Specific maternal microchimeric T cells targeting fetal antigens in β cells predispose to auto-immune diabetes in the child

Identifieur interne : 001854 ( PascalFrancis/Corpus ); précédent : 001853; suivant : 001855

Specific maternal microchimeric T cells targeting fetal antigens in β cells predispose to auto-immune diabetes in the child

Auteurs : Edwige Roy ; Michele Leduc ; Sarah Guegan ; Latif Rachdi ; Nicolas Kluger ; Raphael Scharfmann ; Selim Aractingi ; Kiarash Khosrotehrani

Source :

Journal of autoimmunity : (Print) [ 0896-8411 ] ; 2011.

RBID : Pascal:11-0478881

Descripteurs français

Pascal (Inist)
- Diabète, Insulite, Maladie autoimmune, Lymphocyte T, Enfant, Cellule β, Mère, Antigène, Foetus, Microchimérisme, Gestation, Prédisposition, Immunologie.

English descriptors

KwdEn :
- Antigen, Autoimmune disease, Child, Diabetes mellitus, Fetus, Immunology, Insulitis, Microchimerism, Mother, Predisposition, Pregnancy, T-Lymphocyte, β Cell.

Abstract

Objective: During pregnancy there is an exchange of cells between the fetus and the mother including T lymphocytes that can persist after delivery. Previous studies have described an increased numbers of maternal cells in children with juvenile diabetes as compared to their unaffected siblings. Our objective was to assess the possibility for these chimeric T cells to trigger an anti-beta cell response. Research design and methods: We mated OT2 transgenic female mice having T cells specifically targeting ovalbumin to RIP-OVA males expressing ovalbumin in pancreatic β cells. This allowed us to examine RIP-OVA progeny from OT2 mothers to assess the consequences of maternal T cells acquired during gestation or lactation. We quantitatively analyzed the pancreas of RIP-OVA mice from OT2 mothers for islet infiltration and compared them to RIP-OVA mice not exposed to OT2 mothers or to wild-type mice from OT2 mothers. Results: RIP-OVA mice from OT2 mothers had significantly more peri-insulitis (p = 0.0083) compared to wild-type littermates. Similarly RIP-OVA mice from OT2 mothers had more peri-insulitis as compared to RIP-OVA mice from RIP-OVA mothers (p=0.0073). Presence and specific anti-ovalbumin activity of maternal OT2 cells in the offsprings' peripheral lymphoid tissues was found in a separate group of mice. In animals presenting islet inflammation, CD3+ infiltrating cells in the pancreas were however derived from the offspring and not from OT2 mothers. In accordance, OT2 and RIP-OVA double transgenic mice with high levels of auto-reactive T cells had more peri-insulitis and sometimes intense insulitis when they were from OT2 mothers as compared to RIP-OVA mothers (p = 0.046). Conclusions: In highly specific fetal/maternal combinations, maternal T cells with activity against the offspring pancreatic beta cells, presumably chimeric in fetal organs, initiate islet inflammation and may therefore predispose to auto-immune diabetes.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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A11	`02`	`1`		`@1 LEDUC (Michele)`
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A11	`05`	`1`		`@1 KLUGER (Nicolas)`
A11	`06`	`1`		`@1 SCHARFMANN (Raphael)`
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A14	`05`			`@1 Université Paris Descartes, Faculté de Médecine Necker @2 Paris @3 FRA @Z 4 aut. @Z 6 aut.`
A14	`06`			`@1 The University of Queensland, Centre for Clinical Research (UQCCR) @2 Brisbane @3 AUS @Z 8 aut.`
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C01	`01`		`ENG`	@0 Objective: During pregnancy there is an exchange of cells between the fetus and the mother including T lymphocytes that can persist after delivery. Previous studies have described an increased numbers of maternal cells in children with juvenile diabetes as compared to their unaffected siblings. Our objective was to assess the possibility for these chimeric T cells to trigger an anti-beta cell response. Research design and methods: We mated OT2 transgenic female mice having T cells specifically targeting ovalbumin to RIP-OVA males expressing ovalbumin in pancreatic β cells. This allowed us to examine RIP-OVA progeny from OT2 mothers to assess the consequences of maternal T cells acquired during gestation or lactation. We quantitatively analyzed the pancreas of RIP-OVA mice from OT2 mothers for islet infiltration and compared them to RIP-OVA mice not exposed to OT2 mothers or to wild-type mice from OT2 mothers. Results: RIP-OVA mice from OT2 mothers had significantly more peri-insulitis (p = 0.0083) compared to wild-type littermates. Similarly RIP-OVA mice from OT2 mothers had more peri-insulitis as compared to RIP-OVA mice from RIP-OVA mothers (p=0.0073). Presence and specific anti-ovalbumin activity of maternal OT2 cells in the offsprings' peripheral lymphoid tissues was found in a separate group of mice. In animals presenting islet inflammation, CD3+ infiltrating cells in the pancreas were however derived from the offspring and not from OT2 mothers. In accordance, OT2 and RIP-OVA double transgenic mice with high levels of auto-reactive T cells had more peri-insulitis and sometimes intense insulitis when they were from OT2 mothers as compared to RIP-OVA mothers (p = 0.046). Conclusions: In highly specific fetal/maternal combinations, maternal T cells with activity against the offspring pancreatic beta cells, presumably chimeric in fetal organs, initiate islet inflammation and may therefore predispose to auto-immune diabetes.
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Format Inist (serveur)

NO :	PASCAL 11-0478881 INIST
ET :	Specific maternal microchimeric T cells targeting fetal antigens in β cells predispose to auto-immune diabetes in the child
AU :	ROY (Edwige); LEDUC (Michele); GUEGAN (Sarah); RACHDI (Latif); KLUGER (Nicolas); SCHARFMANN (Raphael); ARACTINGI (Selim); KHOSROTEHRANI (Kiarash)
AF :	UPMC Univ Paris 6, UMR_S938/Paris/France (1 aut., 2 aut., 3 aut., 5 aut., 7 aut., 8 aut.); INSERM, UMR_S938, Centre de Recherche Saint-Antoine, Fetal Stem Cell Laboratory, 27 rue de Chaligny/75012 Paris/France (1 aut., 2 aut., 3 aut., 5 aut., 7 aut., 8 aut.); Assistance Publique-Hôpitaux de Paris, Hôpital Tenon, Service de Dermatologie/Paris/France (2 aut., 3 aut., 7 aut., 8 aut.); INSERM U845, Centre de Recherche Croissance et Signalisation/Paris/France (4 aut., 6 aut.); Université Paris Descartes, Faculté de Médecine Necker/Paris/France (4 aut., 6 aut.); The University of Queensland, Centre for Clinical Research (UQCCR)/Brisbane/Australie (8 aut.)
DT :	Publication en série; Niveau analytique
SO :	Journal of autoimmunity : (Print); ISSN 0896-8411; Royaume-Uni; Da. 2011; Vol. 36; No. 3-4; Pp. 253-262; Bibl. 45 ref.
LA :	Anglais
EA :	Objective: During pregnancy there is an exchange of cells between the fetus and the mother including T lymphocytes that can persist after delivery. Previous studies have described an increased numbers of maternal cells in children with juvenile diabetes as compared to their unaffected siblings. Our objective was to assess the possibility for these chimeric T cells to trigger an anti-beta cell response. Research design and methods: We mated OT2 transgenic female mice having T cells specifically targeting ovalbumin to RIP-OVA males expressing ovalbumin in pancreatic β cells. This allowed us to examine RIP-OVA progeny from OT2 mothers to assess the consequences of maternal T cells acquired during gestation or lactation. We quantitatively analyzed the pancreas of RIP-OVA mice from OT2 mothers for islet infiltration and compared them to RIP-OVA mice not exposed to OT2 mothers or to wild-type mice from OT2 mothers. Results: RIP-OVA mice from OT2 mothers had significantly more peri-insulitis (p = 0.0083) compared to wild-type littermates. Similarly RIP-OVA mice from OT2 mothers had more peri-insulitis as compared to RIP-OVA mice from RIP-OVA mothers (p=0.0073). Presence and specific anti-ovalbumin activity of maternal OT2 cells in the offsprings' peripheral lymphoid tissues was found in a separate group of mice. In animals presenting islet inflammation, CD3+ infiltrating cells in the pancreas were however derived from the offspring and not from OT2 mothers. In accordance, OT2 and RIP-OVA double transgenic mice with high levels of auto-reactive T cells had more peri-insulitis and sometimes intense insulitis when they were from OT2 mothers as compared to RIP-OVA mothers (p = 0.046). Conclusions: In highly specific fetal/maternal combinations, maternal T cells with activity against the offspring pancreatic beta cells, presumably chimeric in fetal organs, initiate islet inflammation and may therefore predispose to auto-immune diabetes.
CC :	002A06; 002B21E01A
FD :	Diabète; Insulite; Maladie autoimmune; Lymphocyte T; Enfant; Cellule β; Mère; Antigène; Foetus; Microchimérisme; Gestation; Prédisposition; Immunologie
FG :	Homme; Pancréas endocrine; Endocrinopathie; Immunopathologie
ED :	Diabetes mellitus; Insulitis; Autoimmune disease; T-Lymphocyte; Child; β Cell; Mother; Antigen; Fetus; Microchimerism; Pregnancy; Predisposition; Immunology
EG :	Human; Endocrine pancreas; Endocrinopathy; Immunopathology
SD :	Diabetes; Insulitis; Enfermedad autoinmune; Linfocito T; Niño; Célula β; Madre; Antígeno; Feto; Microquimerismo; Gestación; Predisposición; Inmunología
LO :	INIST-22171.354000191507480090
ID :	11-0478881

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Pascal:11-0478881

Le document en format XML

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<author><name sortKey="Aractingi, Selim" sort="Aractingi, Selim" uniqKey="Aractingi S" first="Selim" last="Aractingi">Selim Aractingi</name>
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<author><name sortKey="Khosrotehrani, Kiarash" sort="Khosrotehrani, Kiarash" uniqKey="Khosrotehrani K" first="Kiarash" last="Khosrotehrani">Kiarash Khosrotehrani</name>
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Specific maternal microchimeric T cells targeting fetal antigens in β cells predispose to auto-immune diabetes in the child</title>
<author><name sortKey="Roy, Edwige" sort="Roy, Edwige" uniqKey="Roy E" first="Edwige" last="Roy">Edwige Roy</name>
<affiliation><inist:fA14 i1="01"><s1>UPMC Univ Paris 6, UMR_S938</s1>
<s2>Paris</s2>
<s3>FRA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>5 aut.</sZ>
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<affiliation><inist:fA14 i1="02"><s1>INSERM, UMR_S938, Centre de Recherche Saint-Antoine, Fetal Stem Cell Laboratory, 27 rue de Chaligny</s1>
<s2>75012 Paris</s2>
<s3>FRA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>7 aut.</sZ>
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<author><name sortKey="Leduc, Michele" sort="Leduc, Michele" uniqKey="Leduc M" first="Michele" last="Leduc">Michele Leduc</name>
<affiliation><inist:fA14 i1="01"><s1>UPMC Univ Paris 6, UMR_S938</s1>
<s2>Paris</s2>
<s3>FRA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>8 aut.</sZ>
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</affiliation>
<affiliation><inist:fA14 i1="02"><s1>INSERM, UMR_S938, Centre de Recherche Saint-Antoine, Fetal Stem Cell Laboratory, 27 rue de Chaligny</s1>
<s2>75012 Paris</s2>
<s3>FRA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>8 aut.</sZ>
</inist:fA14>
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<affiliation><inist:fA14 i1="03"><s1>Assistance Publique-Hôpitaux de Paris, Hôpital Tenon, Service de Dermatologie</s1>
<s2>Paris</s2>
<s3>FRA</s3>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>8 aut.</sZ>
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</author>
<author><name sortKey="Guegan, Sarah" sort="Guegan, Sarah" uniqKey="Guegan S" first="Sarah" last="Guegan">Sarah Guegan</name>
<affiliation><inist:fA14 i1="01"><s1>UPMC Univ Paris 6, UMR_S938</s1>
<s2>Paris</s2>
<s3>FRA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>8 aut.</sZ>
</inist:fA14>
</affiliation>
<affiliation><inist:fA14 i1="02"><s1>INSERM, UMR_S938, Centre de Recherche Saint-Antoine, Fetal Stem Cell Laboratory, 27 rue de Chaligny</s1>
<s2>75012 Paris</s2>
<s3>FRA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>8 aut.</sZ>
</inist:fA14>
</affiliation>
<affiliation><inist:fA14 i1="03"><s1>Assistance Publique-Hôpitaux de Paris, Hôpital Tenon, Service de Dermatologie</s1>
<s2>Paris</s2>
<s3>FRA</s3>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>8 aut.</sZ>
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</author>
<author><name sortKey="Rachdi, Latif" sort="Rachdi, Latif" uniqKey="Rachdi L" first="Latif" last="Rachdi">Latif Rachdi</name>
<affiliation><inist:fA14 i1="04"><s1>INSERM U845, Centre de Recherche Croissance et Signalisation</s1>
<s2>Paris</s2>
<s3>FRA</s3>
<sZ>4 aut.</sZ>
<sZ>6 aut.</sZ>
</inist:fA14>
</affiliation>
<affiliation><inist:fA14 i1="05"><s1>Université Paris Descartes, Faculté de Médecine Necker</s1>
<s2>Paris</s2>
<s3>FRA</s3>
<sZ>4 aut.</sZ>
<sZ>6 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Kluger, Nicolas" sort="Kluger, Nicolas" uniqKey="Kluger N" first="Nicolas" last="Kluger">Nicolas Kluger</name>
<affiliation><inist:fA14 i1="01"><s1>UPMC Univ Paris 6, UMR_S938</s1>
<s2>Paris</s2>
<s3>FRA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>8 aut.</sZ>
</inist:fA14>
</affiliation>
<affiliation><inist:fA14 i1="02"><s1>INSERM, UMR_S938, Centre de Recherche Saint-Antoine, Fetal Stem Cell Laboratory, 27 rue de Chaligny</s1>
<s2>75012 Paris</s2>
<s3>FRA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>8 aut.</sZ>
</inist:fA14>
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</author>
<author><name sortKey="Scharfmann, Raphael" sort="Scharfmann, Raphael" uniqKey="Scharfmann R" first="Raphael" last="Scharfmann">Raphael Scharfmann</name>
<affiliation><inist:fA14 i1="04"><s1>INSERM U845, Centre de Recherche Croissance et Signalisation</s1>
<s2>Paris</s2>
<s3>FRA</s3>
<sZ>4 aut.</sZ>
<sZ>6 aut.</sZ>
</inist:fA14>
</affiliation>
<affiliation><inist:fA14 i1="05"><s1>Université Paris Descartes, Faculté de Médecine Necker</s1>
<s2>Paris</s2>
<s3>FRA</s3>
<sZ>4 aut.</sZ>
<sZ>6 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Aractingi, Selim" sort="Aractingi, Selim" uniqKey="Aractingi S" first="Selim" last="Aractingi">Selim Aractingi</name>
<affiliation><inist:fA14 i1="01"><s1>UPMC Univ Paris 6, UMR_S938</s1>
<s2>Paris</s2>
<s3>FRA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>8 aut.</sZ>
</inist:fA14>
</affiliation>
<affiliation><inist:fA14 i1="02"><s1>INSERM, UMR_S938, Centre de Recherche Saint-Antoine, Fetal Stem Cell Laboratory, 27 rue de Chaligny</s1>
<s2>75012 Paris</s2>
<s3>FRA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>8 aut.</sZ>
</inist:fA14>
</affiliation>
<affiliation><inist:fA14 i1="03"><s1>Assistance Publique-Hôpitaux de Paris, Hôpital Tenon, Service de Dermatologie</s1>
<s2>Paris</s2>
<s3>FRA</s3>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>8 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Khosrotehrani, Kiarash" sort="Khosrotehrani, Kiarash" uniqKey="Khosrotehrani K" first="Kiarash" last="Khosrotehrani">Kiarash Khosrotehrani</name>
<affiliation><inist:fA14 i1="01"><s1>UPMC Univ Paris 6, UMR_S938</s1>
<s2>Paris</s2>
<s3>FRA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>8 aut.</sZ>
</inist:fA14>
</affiliation>
<affiliation><inist:fA14 i1="02"><s1>INSERM, UMR_S938, Centre de Recherche Saint-Antoine, Fetal Stem Cell Laboratory, 27 rue de Chaligny</s1>
<s2>75012 Paris</s2>
<s3>FRA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>8 aut.</sZ>
</inist:fA14>
</affiliation>
<affiliation><inist:fA14 i1="03"><s1>Assistance Publique-Hôpitaux de Paris, Hôpital Tenon, Service de Dermatologie</s1>
<s2>Paris</s2>
<s3>FRA</s3>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>8 aut.</sZ>
</inist:fA14>
</affiliation>
<affiliation><inist:fA14 i1="06"><s1>The University of Queensland, Centre for Clinical Research (UQCCR)</s1>
<s2>Brisbane</s2>
<s3>AUS</s3>
<sZ>8 aut.</sZ>
</inist:fA14>
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</author>
</analytic>
<series><title level="j" type="main">Journal of autoimmunity : (Print)</title>
<title level="j" type="abbreviated">J. autoimmun. : (Print)</title>
<idno type="ISSN">0896-8411</idno>
<imprint><date when="2011">2011</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
<seriesStmt><title level="j" type="main">Journal of autoimmunity : (Print)</title>
<title level="j" type="abbreviated">J. autoimmun. : (Print)</title>
<idno type="ISSN">0896-8411</idno>
</seriesStmt>
</fileDesc>
<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Antigen</term>
<term>Autoimmune disease</term>
<term>Child</term>
<term>Diabetes mellitus</term>
<term>Fetus</term>
<term>Immunology</term>
<term>Insulitis</term>
<term>Microchimerism</term>
<term>Mother</term>
<term>Predisposition</term>
<term>Pregnancy</term>
<term>T-Lymphocyte</term>
<term>β Cell</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr"><term>Diabète</term>
<term>Insulite</term>
<term>Maladie autoimmune</term>
<term>Lymphocyte T</term>
<term>Enfant</term>
<term>Cellule β</term>
<term>Mère</term>
<term>Antigène</term>
<term>Foetus</term>
<term>Microchimérisme</term>
<term>Gestation</term>
<term>Prédisposition</term>
<term>Immunologie</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">Objective: During pregnancy there is an exchange of cells between the fetus and the mother including T lymphocytes that can persist after delivery. Previous studies have described an increased numbers of maternal cells in children with juvenile diabetes as compared to their unaffected siblings. Our objective was to assess the possibility for these chimeric T cells to trigger an anti-beta cell response. Research design and methods: We mated OT2 transgenic female mice having T cells specifically targeting ovalbumin to RIP-OVA males expressing ovalbumin in pancreatic β cells. This allowed us to examine RIP-OVA progeny from OT2 mothers to assess the consequences of maternal T cells acquired during gestation or lactation. We quantitatively analyzed the pancreas of RIP-OVA mice from OT2 mothers for islet infiltration and compared them to RIP-OVA mice not exposed to OT2 mothers or to wild-type mice from OT2 mothers. Results: RIP-OVA mice from OT2 mothers had significantly more peri-insulitis (p = 0.0083) compared to wild-type littermates. Similarly RIP-OVA mice from OT2 mothers had more peri-insulitis as compared to RIP-OVA mice from RIP-OVA mothers (p=0.0073). Presence and specific anti-ovalbumin activity of maternal OT2 cells in the offsprings' peripheral lymphoid tissues was found in a separate group of mice. In animals presenting islet inflammation, CD3+ infiltrating cells in the pancreas were however derived from the offspring and not from OT2 mothers. In accordance, OT2 and RIP-OVA double transgenic mice with high levels of auto-reactive T cells had more peri-insulitis and sometimes intense insulitis when they were from OT2 mothers as compared to RIP-OVA mothers (p = 0.046). Conclusions: In highly specific fetal/maternal combinations, maternal T cells with activity against the offspring pancreatic beta cells, presumably chimeric in fetal organs, initiate islet inflammation and may therefore predispose to auto-immune diabetes.</div>
</front>
</TEI>
<inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0896-8411</s0>
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<fA05><s2>36</s2>
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<fA06><s2>3-4</s2>
</fA06>
<fA08 i1="01" i2="1" l="ENG"><s1>Specific maternal microchimeric T cells targeting fetal antigens in β cells predispose to auto-immune diabetes in the child</s1>
</fA08>
<fA11 i1="01" i2="1"><s1>ROY (Edwige)</s1>
</fA11>
<fA11 i1="02" i2="1"><s1>LEDUC (Michele)</s1>
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<fA11 i1="03" i2="1"><s1>GUEGAN (Sarah)</s1>
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<fA11 i1="04" i2="1"><s1>RACHDI (Latif)</s1>
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<fA11 i1="05" i2="1"><s1>KLUGER (Nicolas)</s1>
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<fA11 i1="06" i2="1"><s1>SCHARFMANN (Raphael)</s1>
</fA11>
<fA11 i1="07" i2="1"><s1>ARACTINGI (Selim)</s1>
</fA11>
<fA11 i1="08" i2="1"><s1>KHOSROTEHRANI (Kiarash)</s1>
</fA11>
<fA14 i1="01"><s1>UPMC Univ Paris 6, UMR_S938</s1>
<s2>Paris</s2>
<s3>FRA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>8 aut.</sZ>
</fA14>
<fA14 i1="02"><s1>INSERM, UMR_S938, Centre de Recherche Saint-Antoine, Fetal Stem Cell Laboratory, 27 rue de Chaligny</s1>
<s2>75012 Paris</s2>
<s3>FRA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>8 aut.</sZ>
</fA14>
<fA14 i1="03"><s1>Assistance Publique-Hôpitaux de Paris, Hôpital Tenon, Service de Dermatologie</s1>
<s2>Paris</s2>
<s3>FRA</s3>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>8 aut.</sZ>
</fA14>
<fA14 i1="04"><s1>INSERM U845, Centre de Recherche Croissance et Signalisation</s1>
<s2>Paris</s2>
<s3>FRA</s3>
<sZ>4 aut.</sZ>
<sZ>6 aut.</sZ>
</fA14>
<fA14 i1="05"><s1>Université Paris Descartes, Faculté de Médecine Necker</s1>
<s2>Paris</s2>
<s3>FRA</s3>
<sZ>4 aut.</sZ>
<sZ>6 aut.</sZ>
</fA14>
<fA14 i1="06"><s1>The University of Queensland, Centre for Clinical Research (UQCCR)</s1>
<s2>Brisbane</s2>
<s3>AUS</s3>
<sZ>8 aut.</sZ>
</fA14>
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<fA64 i1="01" i2="1"><s0>Journal of autoimmunity : (Print)</s0>
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</fA66>
<fC01 i1="01" l="ENG"><s0>Objective: During pregnancy there is an exchange of cells between the fetus and the mother including T lymphocytes that can persist after delivery. Previous studies have described an increased numbers of maternal cells in children with juvenile diabetes as compared to their unaffected siblings. Our objective was to assess the possibility for these chimeric T cells to trigger an anti-beta cell response. Research design and methods: We mated OT2 transgenic female mice having T cells specifically targeting ovalbumin to RIP-OVA males expressing ovalbumin in pancreatic β cells. This allowed us to examine RIP-OVA progeny from OT2 mothers to assess the consequences of maternal T cells acquired during gestation or lactation. We quantitatively analyzed the pancreas of RIP-OVA mice from OT2 mothers for islet infiltration and compared them to RIP-OVA mice not exposed to OT2 mothers or to wild-type mice from OT2 mothers. Results: RIP-OVA mice from OT2 mothers had significantly more peri-insulitis (p = 0.0083) compared to wild-type littermates. Similarly RIP-OVA mice from OT2 mothers had more peri-insulitis as compared to RIP-OVA mice from RIP-OVA mothers (p=0.0073). Presence and specific anti-ovalbumin activity of maternal OT2 cells in the offsprings' peripheral lymphoid tissues was found in a separate group of mice. In animals presenting islet inflammation, CD3+ infiltrating cells in the pancreas were however derived from the offspring and not from OT2 mothers. In accordance, OT2 and RIP-OVA double transgenic mice with high levels of auto-reactive T cells had more peri-insulitis and sometimes intense insulitis when they were from OT2 mothers as compared to RIP-OVA mothers (p = 0.046). Conclusions: In highly specific fetal/maternal combinations, maternal T cells with activity against the offspring pancreatic beta cells, presumably chimeric in fetal organs, initiate islet inflammation and may therefore predispose to auto-immune diabetes.</s0>
</fC01>
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<fC03 i1="01" i2="X" l="ENG"><s0>Diabetes mellitus</s0>
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<fC03 i1="01" i2="X" l="SPA"><s0>Diabetes</s0>
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<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE"><s0>Insulite</s0>
<s2>NM</s2>
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<fC03 i1="02" i2="X" l="SPA"><s0>Insulitis</s0>
<s2>NM</s2>
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<fC03 i1="03" i2="X" l="FRE"><s0>Maladie autoimmune</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG"><s0>Autoimmune disease</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA"><s0>Enfermedad autoinmune</s0>
<s5>03</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE"><s0>Lymphocyte T</s0>
<s5>05</s5>
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<fC03 i1="04" i2="X" l="ENG"><s0>T-Lymphocyte</s0>
<s5>05</s5>
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<fC03 i1="04" i2="X" l="SPA"><s0>Linfocito T</s0>
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<fC03 i1="05" i2="X" l="FRE"><s0>Enfant</s0>
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<s5>09</s5>
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<s5>09</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA"><s0>Madre</s0>
<s5>09</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE"><s0>Antigène</s0>
<s5>11</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG"><s0>Antigen</s0>
<s5>11</s5>
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<fC03 i1="08" i2="X" l="SPA"><s0>Antígeno</s0>
<s5>11</s5>
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<fC03 i1="09" i2="X" l="FRE"><s0>Foetus</s0>
<s5>12</s5>
</fC03>
<fC03 i1="09" i2="X" l="ENG"><s0>Fetus</s0>
<s5>12</s5>
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</fC03>
<fC03 i1="10" i2="X" l="FRE"><s0>Microchimérisme</s0>
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<fC03 i1="10" i2="X" l="ENG"><s0>Microchimerism</s0>
<s5>17</s5>
</fC03>
<fC03 i1="10" i2="X" l="SPA"><s0>Microquimerismo</s0>
<s5>17</s5>
</fC03>
<fC03 i1="11" i2="X" l="FRE"><s0>Gestation</s0>
<s5>18</s5>
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<server><NO>PASCAL 11-0478881 INIST</NO>
<ET>Specific maternal microchimeric T cells targeting fetal antigens in β cells predispose to auto-immune diabetes in the child</ET>
<AU>ROY (Edwige); LEDUC (Michele); GUEGAN (Sarah); RACHDI (Latif); KLUGER (Nicolas); SCHARFMANN (Raphael); ARACTINGI (Selim); KHOSROTEHRANI (Kiarash)</AU>
<AF>UPMC Univ Paris 6, UMR_S938/Paris/France (1 aut., 2 aut., 3 aut., 5 aut., 7 aut., 8 aut.); INSERM, UMR_S938, Centre de Recherche Saint-Antoine, Fetal Stem Cell Laboratory, 27 rue de Chaligny/75012 Paris/France (1 aut., 2 aut., 3 aut., 5 aut., 7 aut., 8 aut.); Assistance Publique-Hôpitaux de Paris, Hôpital Tenon, Service de Dermatologie/Paris/France (2 aut., 3 aut., 7 aut., 8 aut.); INSERM U845, Centre de Recherche Croissance et Signalisation/Paris/France (4 aut., 6 aut.); Université Paris Descartes, Faculté de Médecine Necker/Paris/France (4 aut., 6 aut.); The University of Queensland, Centre for Clinical Research (UQCCR)/Brisbane/Australie (8 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Journal of autoimmunity : (Print); ISSN 0896-8411; Royaume-Uni; Da. 2011; Vol. 36; No. 3-4; Pp. 253-262; Bibl. 45 ref.</SO>
<LA>Anglais</LA>
<EA>Objective: During pregnancy there is an exchange of cells between the fetus and the mother including T lymphocytes that can persist after delivery. Previous studies have described an increased numbers of maternal cells in children with juvenile diabetes as compared to their unaffected siblings. Our objective was to assess the possibility for these chimeric T cells to trigger an anti-beta cell response. Research design and methods: We mated OT2 transgenic female mice having T cells specifically targeting ovalbumin to RIP-OVA males expressing ovalbumin in pancreatic β cells. This allowed us to examine RIP-OVA progeny from OT2 mothers to assess the consequences of maternal T cells acquired during gestation or lactation. We quantitatively analyzed the pancreas of RIP-OVA mice from OT2 mothers for islet infiltration and compared them to RIP-OVA mice not exposed to OT2 mothers or to wild-type mice from OT2 mothers. Results: RIP-OVA mice from OT2 mothers had significantly more peri-insulitis (p = 0.0083) compared to wild-type littermates. Similarly RIP-OVA mice from OT2 mothers had more peri-insulitis as compared to RIP-OVA mice from RIP-OVA mothers (p=0.0073). Presence and specific anti-ovalbumin activity of maternal OT2 cells in the offsprings' peripheral lymphoid tissues was found in a separate group of mice. In animals presenting islet inflammation, CD3+ infiltrating cells in the pancreas were however derived from the offspring and not from OT2 mothers. In accordance, OT2 and RIP-OVA double transgenic mice with high levels of auto-reactive T cells had more peri-insulitis and sometimes intense insulitis when they were from OT2 mothers as compared to RIP-OVA mothers (p = 0.046). Conclusions: In highly specific fetal/maternal combinations, maternal T cells with activity against the offspring pancreatic beta cells, presumably chimeric in fetal organs, initiate islet inflammation and may therefore predispose to auto-immune diabetes.</EA>
<CC>002A06; 002B21E01A</CC>
<FD>Diabète; Insulite; Maladie autoimmune; Lymphocyte T; Enfant; Cellule β; Mère; Antigène; Foetus; Microchimérisme; Gestation; Prédisposition; Immunologie</FD>
<FG>Homme; Pancréas endocrine; Endocrinopathie; Immunopathologie</FG>
<ED>Diabetes mellitus; Insulitis; Autoimmune disease; T-Lymphocyte; Child; β Cell; Mother; Antigen; Fetus; Microchimerism; Pregnancy; Predisposition; Immunology</ED>
<EG>Human; Endocrine pancreas; Endocrinopathy; Immunopathology</EG>
<SD>Diabetes; Insulitis; Enfermedad autoinmune; Linfocito T; Niño; Célula β; Madre; Antígeno; Feto; Microquimerismo; Gestación; Predisposición; Inmunología</SD>
<LO>INIST-22171.354000191507480090</LO>
<ID>11-0478881</ID>
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Specific maternal microchimeric T cells targeting fetal antigens in β cells predispose to auto-immune diabetes in the child

Specific maternal microchimeric T cells targeting fetal antigens in β cells predispose to auto-immune diabetes in the child

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