Regulatory Rheumatoid Factor is Specific to PD-1 and Uses PD-1 Pathway to Control CD4 T Lymphocytes.

CD4 T lymphocytes IgG Fc fragments control of autoimmunity programmed death-1 regulatory rheumatoid factor

Journal

Immunological investigations
ISSN: 1532-4311
Titre abrégé: Immunol Invest
Pays: England
ID NLM: 8504629

Informations de publication

Date de publication:
Nov 2023
Historique:
medline: 22 9 2023
pubmed: 24 8 2023
entrez: 24 8 2023
Statut: ppublish

Résumé

We have earlier discovered a new factor of autoimmunity downregulation, called regulatory rheumatoid factor (regRF). Being anti-idiotypic antibodies, regRF restricts the expansion of CD4 The specificity of the shared regRF paratope to PD-1 was determined by ELISA. T cell activation was performed with immobilized anti-CD3ε antibodies. Flow cytometry was used to study the effect of regRF on PD-1 We found that regRF binds to PD-1. IgG Fc fragments carrying epitopes specific to the shared paratope of regRF compete with PD-1 for binding to regRF. It follows that regRF recognizes specifically PD-1 by means of a shared paratope. RegRF-containing serum reduced the number of PD-1 RegRF uses PD-1 pathway to control activated CD4

Sections du résumé

BACKGROUND UNASSIGNED
We have earlier discovered a new factor of autoimmunity downregulation, called regulatory rheumatoid factor (regRF). Being anti-idiotypic antibodies, regRF restricts the expansion of CD4
METHODS UNASSIGNED
The specificity of the shared regRF paratope to PD-1 was determined by ELISA. T cell activation was performed with immobilized anti-CD3ε antibodies. Flow cytometry was used to study the effect of regRF on PD-1
RESULTS UNASSIGNED
We found that regRF binds to PD-1. IgG Fc fragments carrying epitopes specific to the shared paratope of regRF compete with PD-1 for binding to regRF. It follows that regRF recognizes specifically PD-1 by means of a shared paratope. RegRF-containing serum reduced the number of PD-1
CONCLUSION UNASSIGNED
RegRF uses PD-1 pathway to control activated CD4

Identifiants

pubmed: 37615124
doi: 10.1080/08820139.2023.2250818
doi:

Substances chimiques

Programmed Cell Death 1 Receptor 0
Rheumatoid Factor 9009-79-4

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

897-908

Auteurs

Tatyana Khramova (T)

Laboratory of Molecular and Cell Immunology, Department of Immunology and Cell Biology, Udmurt State University, Izhevsk, Russian Federation.
Laboratory of Biocompatible Materials, Udmurt Federal Research Center UB RAS, Izhevsk, Russian Federation.

Liubov Beduleva (L)

Laboratory of Molecular and Cell Immunology, Department of Immunology and Cell Biology, Udmurt State University, Izhevsk, Russian Federation.
Laboratory of Biocompatible Materials, Udmurt Federal Research Center UB RAS, Izhevsk, Russian Federation.

Alexandr Sidorov (A)

Laboratory of Molecular and Cell Immunology, Department of Immunology and Cell Biology, Udmurt State University, Izhevsk, Russian Federation.
Laboratory of Biocompatible Materials, Udmurt Federal Research Center UB RAS, Izhevsk, Russian Federation.

Alexey Terentiev (A)

Laboratory of Molecular and Cell Immunology, Department of Immunology and Cell Biology, Udmurt State University, Izhevsk, Russian Federation.
Laboratory of Biocompatible Materials, Udmurt Federal Research Center UB RAS, Izhevsk, Russian Federation.

Igor Menshikov (I)

Laboratory of Molecular and Cell Immunology, Department of Immunology and Cell Biology, Udmurt State University, Izhevsk, Russian Federation.
Laboratory of Biocompatible Materials, Udmurt Federal Research Center UB RAS, Izhevsk, Russian Federation.

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Classifications MeSH