Risk of celiac disease autoimmunity is modified by interactions between CD247 and environmental exposures

Anna Eurén; Kristian Lynch; Katri Lindfors; Hemang Parikh; Sibylle Koletzko; Edwin Liu; Beena Akolkar; William Hagopian; Jeffrey P. Krischer; Marian Rewers; Jorma Toppari; Anette Ziegler; Daniel Agardh; Kalle Kurppa; on behalf of the TEDDY Study Group; Carin Andrén Aronsson; Rasmus Bennet; Corrado Cilio; Susanne Dahlberg; Malin Goldman Tsubarah; Emelie Ericson-Hallström; Lina Fransson; Thomas Gard; Emina Halilovic; Susanne Hyberg; Berglind Jonsdottir; Naghmeh Karimi; Helena Elding Larsson; Marielle Lindström; Markus Lundgren; Marlena Maziarz; Jessica Melin; Caroline Nilsson; Kobra Rahmati; Anita Ramelius; Falastin Salami; Anette Sjöberg; Terese Wiktorsson

doi:10.1038/s41598-024-75496-w

Risk of celiac disease autoimmunity is modified by interactions between CD247 and environmental exposures

Anna Eurén, Kristian Lynch, Katri Lindfors, Hemang Parikh, Sibylle Koletzko, Edwin Liu, Beena Akolkar, William Hagopian, Jeffrey P. Krischer, Marian Rewers, Jorma Toppari, Anette Ziegler, Daniel Agardh, Kalle Kurppa, on behalf of the TEDDY Study Group, Carin Andrén Aronsson (medarbetare), Rasmus Bennet (medarbetare), Corrado Cilio (medarbetare), Susanne Dahlberg (medarbetare), Malin Goldman Tsubarah (medarbetare)Emelie Ericson-Hallström (medarbetare), Lina Fransson (medarbetare), Thomas Gard (medarbetare), Emina Halilovic (medarbetare), Susanne Hyberg (medarbetare), Berglind Jonsdottir (medarbetare), Naghmeh Karimi (medarbetare), Helena Elding Larsson (medarbetare), Marielle Lindström (medarbetare), Markus Lundgren (medarbetare), Marlena Maziarz (medarbetare), Jessica Melin (medarbetare), Caroline Nilsson (medarbetare), Kobra Rahmati (medarbetare), Anita Ramelius (medarbetare), Falastin Salami (medarbetare), Anette Sjöberg (medarbetare), Terese Wiktorsson (medarbetare)

Forskningsoutput: Tidskriftsbidrag › Artikel i vetenskaplig tidskrift › Peer review

Sammanfattning

Season of birth, viral infections, HLA haplogenotypes and non-HLA variants are implicated in the development of celiac disease and celiac disease autoimmunity, suggesting a combined role of genes and environmental exposures. The aim of the study was to further decipher the biological pathways conveying the season of birth effect in celiac disease autoimmunity to gain novel insights into the early pathogenesis of celiac disease. Interactions between season of birth, genetics, and early-life environmental factors on the risk of celiac autoimmunity were investigated in the multicenter TEDDY birth cohort study. Altogether 6523 genetically predisposed children were enrolled to long-term follow-up with prospective sampling and data collection at six research centers in the USA, Germany, Sweden and Finland. Celiac disease autoimmunity was defined as positive tissue transglutaminase antibodies in two consecutive serum samples. There was a significant season of birth effect on the risk of celiac autoimmunity. The effect was dependent on polymorphisms in CD247 gene encoding for CD3ζ chain of TCR-CD3 complex. In particular, children with major alleles for SNP rs864537A > G, in CD247 (AA genotype) had an excess risk of celiac autoimmunity when born March–August as compared to other months. The interaction of CD247 with season of birth on autoimmunity risk was accompanied by interactions with febrile infections between the ages of 3–6 months. Considering the important role of TCR-CD3 complex in the adaptive immune response and our findings here, CD247 variants and their possible effect of subgroups in autoimmunity development could be of interest in the design of future gene-environment studies of celiac disease. ClinicalTrials.gov Identifier: NCT00279318.

Originalspråk	engelska
Artikelnummer	25463
Sidor (från-till)	1-14
Tidskrift	Scientific Reports
Volym	14
DOI	https://doi.org/10.1038/s41598-024-75496-w
Status	Published - 2024 dec.

Bibliografisk information

Publisher Copyright:
© The Author(s) 2024.

Ämnesklassifikation (UKÄ)

Endokrinologi och diabetes

FN:s Globala mål

Denna forskningsoutput relaterar till följande Globala mål

Tillgång till dokument

10.1038/s41598-024-75496-wLicens: CC BY-NC-ND

Citera det här

Eurén, A., Lynch, K., Lindfors, K., Parikh, H., Koletzko, S., Liu, E., Akolkar, B., Hagopian, W., Krischer, J. P., Rewers, M., Toppari, J., Ziegler, A., Agardh, D., Kurppa, K., on behalf of the TEDDY Study Group, Aronsson, C. A., Bennet, R., Cilio, C., Dahlberg, S., ... Wiktorsson, T. (2024). Risk of celiac disease autoimmunity is modified by interactions between CD247 and environmental exposures. Scientific Reports, 14, 1-14. Artikel 25463. https://doi.org/10.1038/s41598-024-75496-w

@article{3feeefe032744f5295a79f5956f45447,

title = "Risk of celiac disease autoimmunity is modified by interactions between CD247 and environmental exposures",

abstract = "Season of birth, viral infections, HLA haplogenotypes and non-HLA variants are implicated in the development of celiac disease and celiac disease autoimmunity, suggesting a combined role of genes and environmental exposures. The aim of the study was to further decipher the biological pathways conveying the season of birth effect in celiac disease autoimmunity to gain novel insights into the early pathogenesis of celiac disease. Interactions between season of birth, genetics, and early-life environmental factors on the risk of celiac autoimmunity were investigated in the multicenter TEDDY birth cohort study. Altogether 6523 genetically predisposed children were enrolled to long-term follow-up with prospective sampling and data collection at six research centers in the USA, Germany, Sweden and Finland. Celiac disease autoimmunity was defined as positive tissue transglutaminase antibodies in two consecutive serum samples. There was a significant season of birth effect on the risk of celiac autoimmunity. The effect was dependent on polymorphisms in CD247 gene encoding for CD3ζ chain of TCR-CD3 complex. In particular, children with major alleles for SNP rs864537A > G, in CD247 (AA genotype) had an excess risk of celiac autoimmunity when born March–August as compared to other months. The interaction of CD247 with season of birth on autoimmunity risk was accompanied by interactions with febrile infections between the ages of 3–6 months. Considering the important role of TCR-CD3 complex in the adaptive immune response and our findings here, CD247 variants and their possible effect of subgroups in autoimmunity development could be of interest in the design of future gene-environment studies of celiac disease. ClinicalTrials.gov Identifier: NCT00279318.",

author = "Anna Eur{\'e}n and Kristian Lynch and Katri Lindfors and Hemang Parikh and Sibylle Koletzko and Edwin Liu and Beena Akolkar and William Hagopian and Krischer, {Jeffrey P.} and Marian Rewers and Jorma Toppari and Anette Ziegler and Daniel Agardh and Kalle Kurppa and {on behalf of the TEDDY Study Group} and Aronsson, {Carin Andr{\'e}n} and Rasmus Bennet and Corrado Cilio and Susanne Dahlberg and Tsubarah, {Malin Goldman} and Emelie Ericson-Hallstr{\"o}m and Lina Fransson and Thomas Gard and Emina Halilovic and Susanne Hyberg and Berglind Jonsdottir and Naghmeh Karimi and Larsson, {Helena Elding} and Marielle Lindstr{\"o}m and Markus Lundgren and Marlena Maziarz and Jessica Melin and Caroline Nilsson and Kobra Rahmati and Anita Ramelius and Falastin Salami and Anette Sj{\"o}berg and Terese Wiktorsson",

note = "Publisher Copyright: {\textcopyright} The Author(s) 2024.",

year = "2024",

month = dec,

doi = "10.1038/s41598-024-75496-w",

language = "English",

volume = "14",

pages = "1--14",

journal = "Scientific Reports",

issn = "2045-2322",

publisher = "Nature Publishing Group",

}

Eurén, A, Lynch, K, Lindfors, K, Parikh, H, Koletzko, S, Liu, E, Akolkar, B, Hagopian, W, Krischer, JP, Rewers, M, Toppari, J, Ziegler, A, Agardh, D, Kurppa, K, on behalf of the TEDDY Study Group, Aronsson, CA, Bennet, R, Cilio, C, Dahlberg, S, Tsubarah, MG, Ericson-Hallström, E, Fransson, L, Gard, T, Halilovic, E, Hyberg, S, Jonsdottir, B, Karimi, N, Larsson, HE, Lindström, M, Lundgren, M , Maziarz, M , Melin, J, Nilsson, C, Rahmati, K, Ramelius, A, Salami, F, Sjöberg, A & Wiktorsson, T 2024, 'Risk of celiac disease autoimmunity is modified by interactions between CD247 and environmental exposures', Scientific Reports, vol. 14, 25463, s. 1-14. https://doi.org/10.1038/s41598-024-75496-w

TY - JOUR

T1 - Risk of celiac disease autoimmunity is modified by interactions between CD247 and environmental exposures

AU - Eurén, Anna

AU - Lynch, Kristian

AU - Lindfors, Katri

AU - Parikh, Hemang

AU - Koletzko, Sibylle

AU - Liu, Edwin

AU - Akolkar, Beena

AU - Hagopian, William

AU - Krischer, Jeffrey P.

AU - Rewers, Marian

AU - Toppari, Jorma

AU - Ziegler, Anette

AU - Agardh, Daniel

AU - Kurppa, Kalle

AU - on behalf of the TEDDY Study Group

A2 - Aronsson, Carin Andrén

A2 - Bennet, Rasmus

A2 - Cilio, Corrado

A2 - Dahlberg, Susanne

A2 - Tsubarah, Malin Goldman

A2 - Ericson-Hallström, Emelie

A2 - Fransson, Lina

A2 - Gard, Thomas

A2 - Halilovic, Emina

A2 - Hyberg, Susanne

A2 - Jonsdottir, Berglind

A2 - Karimi, Naghmeh

A2 - Larsson, Helena Elding

A2 - Lindström, Marielle

A2 - Lundgren, Markus

A2 - Maziarz, Marlena

A2 - Melin, Jessica

A2 - Nilsson, Caroline

A2 - Rahmati, Kobra

A2 - Ramelius, Anita

A2 - Salami, Falastin

A2 - Sjöberg, Anette

A2 - Wiktorsson, Terese

PY - 2024/12

Y1 - 2024/12

N2 - Season of birth, viral infections, HLA haplogenotypes and non-HLA variants are implicated in the development of celiac disease and celiac disease autoimmunity, suggesting a combined role of genes and environmental exposures. The aim of the study was to further decipher the biological pathways conveying the season of birth effect in celiac disease autoimmunity to gain novel insights into the early pathogenesis of celiac disease. Interactions between season of birth, genetics, and early-life environmental factors on the risk of celiac autoimmunity were investigated in the multicenter TEDDY birth cohort study. Altogether 6523 genetically predisposed children were enrolled to long-term follow-up with prospective sampling and data collection at six research centers in the USA, Germany, Sweden and Finland. Celiac disease autoimmunity was defined as positive tissue transglutaminase antibodies in two consecutive serum samples. There was a significant season of birth effect on the risk of celiac autoimmunity. The effect was dependent on polymorphisms in CD247 gene encoding for CD3ζ chain of TCR-CD3 complex. In particular, children with major alleles for SNP rs864537A > G, in CD247 (AA genotype) had an excess risk of celiac autoimmunity when born March–August as compared to other months. The interaction of CD247 with season of birth on autoimmunity risk was accompanied by interactions with febrile infections between the ages of 3–6 months. Considering the important role of TCR-CD3 complex in the adaptive immune response and our findings here, CD247 variants and their possible effect of subgroups in autoimmunity development could be of interest in the design of future gene-environment studies of celiac disease. ClinicalTrials.gov Identifier: NCT00279318.

AB - Season of birth, viral infections, HLA haplogenotypes and non-HLA variants are implicated in the development of celiac disease and celiac disease autoimmunity, suggesting a combined role of genes and environmental exposures. The aim of the study was to further decipher the biological pathways conveying the season of birth effect in celiac disease autoimmunity to gain novel insights into the early pathogenesis of celiac disease. Interactions between season of birth, genetics, and early-life environmental factors on the risk of celiac autoimmunity were investigated in the multicenter TEDDY birth cohort study. Altogether 6523 genetically predisposed children were enrolled to long-term follow-up with prospective sampling and data collection at six research centers in the USA, Germany, Sweden and Finland. Celiac disease autoimmunity was defined as positive tissue transglutaminase antibodies in two consecutive serum samples. There was a significant season of birth effect on the risk of celiac autoimmunity. The effect was dependent on polymorphisms in CD247 gene encoding for CD3ζ chain of TCR-CD3 complex. In particular, children with major alleles for SNP rs864537A > G, in CD247 (AA genotype) had an excess risk of celiac autoimmunity when born March–August as compared to other months. The interaction of CD247 with season of birth on autoimmunity risk was accompanied by interactions with febrile infections between the ages of 3–6 months. Considering the important role of TCR-CD3 complex in the adaptive immune response and our findings here, CD247 variants and their possible effect of subgroups in autoimmunity development could be of interest in the design of future gene-environment studies of celiac disease. ClinicalTrials.gov Identifier: NCT00279318.

U2 - 10.1038/s41598-024-75496-w

DO - 10.1038/s41598-024-75496-w

M3 - Article

C2 - 39462122

AN - SCOPUS:85207848859

SN - 2045-2322

VL - 14

SP - 1

EP - 14

JO - Scientific Reports

JF - Scientific Reports

M1 - 25463

ER -

Risk of celiac disease autoimmunity is modified by interactions between CD247 and environmental exposures

Sammanfattning

Bibliografisk information

Ämnesklassifikation (UKÄ)

FN:s Globala mål

Tillgång till dokument

Fingeravtryck

Citera det här