Seven-chain adaptive immune receptor repertoire analysis in rheumatoid arthritis reveals novel features associated with disease and clinically relevant phenotypes.


Journal

Genome biology
ISSN: 1474-760X
Titre abrégé: Genome Biol
Pays: England
ID NLM: 100960660

Informations de publication

Date de publication:
11 Mar 2024
Historique:
received: 04 03 2022
accepted: 04 03 2024
medline: 12 3 2024
pubmed: 12 3 2024
entrez: 12 3 2024
Statut: epublish

Résumé

In rheumatoid arthritis (RA), the activation of T and B cell clones specific for self-antigens leads to the chronic inflammation of the synovium. Here, we perform an in-depth quantitative analysis of the seven chains that comprise the adaptive immune receptor repertoire (AIRR) in RA. In comparison to controls, we show that RA patients have multiple and strong differences in the B cell receptor repertoire including reduced diversity as well as altered isotype, chain, and segment frequencies. We demonstrate that therapeutic tumor necrosis factor inhibition partially restores this alteration but find a profound difference in the underlying biochemical reactivities between responders and non-responders. Combining the AIRR with HLA typing, we identify the specific T cell receptor repertoire associated with disease risk variants. Integrating these features, we further develop a molecular classifier that shows the utility of the AIRR as a diagnostic tool. Simultaneous sequencing of the seven chains of the human AIRR reveals novel features associated with the disease and clinically relevant phenotypes, including response to therapy. These findings show the unique potential of AIRR to address precision medicine in immune-related diseases.

Sections du résumé

BACKGROUND BACKGROUND
In rheumatoid arthritis (RA), the activation of T and B cell clones specific for self-antigens leads to the chronic inflammation of the synovium. Here, we perform an in-depth quantitative analysis of the seven chains that comprise the adaptive immune receptor repertoire (AIRR) in RA.
RESULTS RESULTS
In comparison to controls, we show that RA patients have multiple and strong differences in the B cell receptor repertoire including reduced diversity as well as altered isotype, chain, and segment frequencies. We demonstrate that therapeutic tumor necrosis factor inhibition partially restores this alteration but find a profound difference in the underlying biochemical reactivities between responders and non-responders. Combining the AIRR with HLA typing, we identify the specific T cell receptor repertoire associated with disease risk variants. Integrating these features, we further develop a molecular classifier that shows the utility of the AIRR as a diagnostic tool.
CONCLUSIONS CONCLUSIONS
Simultaneous sequencing of the seven chains of the human AIRR reveals novel features associated with the disease and clinically relevant phenotypes, including response to therapy. These findings show the unique potential of AIRR to address precision medicine in immune-related diseases.

Identifiants

pubmed: 38468286
doi: 10.1186/s13059-024-03210-0
pii: 10.1186/s13059-024-03210-0
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

68

Subventions

Organisme : Instituto de Salud Carlos III
ID : PI17/00019
Organisme : Ministerio de Economía y Competitividad
ID : IPT010000-2010-36

Informations de copyright

© 2024. The Author(s).

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Auteurs

Adrià Aterido (A)

Rheumatology Research Group, Vall Hebron Research Institute, 08035, Barcelona, Spain.

María López-Lasanta (M)

Rheumatology Research Group, Vall Hebron Research Institute, 08035, Barcelona, Spain.

Francisco Blanco (F)

Rheumatology Department, Hospital Juan Canalejo, A Coruña, Spain.

Antonio Juan-Mas (A)

Rheumatology Department, Hospital Son Llatzer, Palma, Spain.

María Luz García-Vivar (ML)

Rheumatology Department, Hospital Universitario Barsuto, Bilbao, Spain.

Alba Erra (A)

Rheumatology Research Group, Vall Hebron Research Institute, 08035, Barcelona, Spain.
Rheumatology Department, Hospital Sant Rafael, Barcelona, Spain.

Carolina Pérez-García (C)

Rheumatology Department, Parc de Salut Mar, Barcelona, Spain.

Simón Ángel Sánchez-Fernández (SÁ)

Rheumatology Department, Hospital La Mancha Centro, Alcázar de San Juan, Spain.

Raimon Sanmartí (R)

Rheumatology Department, Hospital Clínic de Barcelona and IDIBAPS, Barcelona, Spain.

Antonio Fernández-Nebro (A)

Rheumatology Department, Hospital Regional Universitario de Málaga, Málaga, Spain.

Mercedes Alperi-López (M)

Rheumatology Department, Hospital Universitario Central de Asturias, Oviedo, Spain.

Jesús Tornero (J)

Rheumatology Department, Hospital Universitario Guadalajara, Guadalajara, Spain.

Ana María Ortiz (AM)

Rheumatology Department, Hospital Universitario La Princesa, IIS La Princesa, Madrid, Spain.

Carlos Marras Fernández-Cid (CM)

Rheumatology Department, Hospital Universitario Virgen de La Arrixaca, Murcia, Spain.

Núria Palau (N)

Rheumatology Research Group, Vall Hebron Research Institute, 08035, Barcelona, Spain.

Wenjing Pan (W)

iRepertoire Inc, Huntsville, AL, USA.

Miranda Byrne-Steele (M)

iRepertoire Inc, Huntsville, AL, USA.

Dmytro Starenki (D)

iRepertoire Inc, Huntsville, AL, USA.

Daniel Weber (D)

iRepertoire Inc, Huntsville, AL, USA.

Ivan Rodriguez-Nunez (I)

HudsonAlpha Institute for Biotechnology, Huntsville, AL, USA.

Jian Han (J)

iRepertoire Inc, Huntsville, AL, USA.

Richard M Myers (RM)

HudsonAlpha Institute for Biotechnology, Huntsville, AL, USA.

Sara Marsal (S)

Rheumatology Research Group, Vall Hebron Research Institute, 08035, Barcelona, Spain.

Antonio Julià (A)

Rheumatology Research Group, Vall Hebron Research Institute, 08035, Barcelona, Spain. toni.julia@vhir.org.

Classifications MeSH