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Related Experiment Video

Updated: May 24, 2026

Generation of Two-color Antigen Microarrays for the Simultaneous Detection of IgG and IgM Autoantibodies

Generation of Two-color Antigen Microarrays for the Simultaneous Detection of IgG and IgM Autoantibodies

Published on: September 15, 2016

[Autoantigen BiP and autoimmune diseases].

Hirofumi Shoda¹, Keishi Fujio, Kazuhiko Yamamoto

¹Department of Allergy and Rheumatology, Graduate School of Medicine, the University of Tokyo, Tokyo, Japan.

Nihon Rinsho Men'Eki Gakkai Kaishi = Japanese Journal of Clinical Immunology

|March 1, 2012

Summary

Immunoglobulin Binding Protein (BiP) is implicated in rheumatoid arthritis (RA). Immune responses to citrullinated BiP can worsen arthritis, while native BiP may regulate it, suggesting a balance is key in autoimmune diseases.

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Area of Science:

Immunology
Autoimmunity
Rheumatology

Context:

Immunoglobulin Binding Protein (BiP), a heat shock protein 70 family member, is an autoantigen in rheumatoid arthritis (RA).
Anti-BiP antibodies are found in up to 60% of RA patients and also in systemic lupus erythematosus.
Anti-citrullinated BiP antibodies are a subset of anti-citrullinated protein/peptide antibodies (ACPAs), strongly linked to RA.

Purpose:

To explore the role of immune responses to BiP, particularly citrullinated BiP, in the pathogenesis of rheumatoid arthritis.
To investigate the dual nature of immune responses to BiP, encompassing both pro-inflammatory and regulatory T cell activities.

Summary:

Immune responses to BiP are diverse, with anti-citrullinated BiP exacerbating inflammatory arthritis in mouse models.
Administration of native BiP in mice induced regulatory CD4+ T cells (IL-4, IL-10) and ameliorated inflammatory arthritis.
Dysregulation of the balance between pro-inflammatory and regulatory immune responses to BiP may contribute to autoimmune diseases like RA.

Impact:

Highlights the complex role of BiP in autoimmune diseases, particularly RA.
Suggests that targeting immune responses to BiP could be a therapeutic strategy for RA.
Provides insights into the mechanisms underlying ACPA-associated autoimmunity.