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Cited by 32Systemic Lupus Erythematosus ResearchT-cell and B-cell ImmunologyImmune Response and Inflammation

Role of PIR‐B in Autoimmune Glomerulonephritis

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Takai, Toshiyuki, Nakamura, Akira, Endo, Shota·2011·BioMed Research International
DOI 10.1155/2011/275302PMC PMC2952822
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Abstract

PIR‐B, an inhibitory receptor expressed on murine B cells and myeloid cells, regulates humoral and cellular immune responses via its constitutive binding to the ligand, MHC class I molecules, on the same cells (cis) or on different cells (trans). Although it has been speculated that PIR‐B is important for maintaining peripheral tolerance, PIR‐B single deficiency does not cause overt autoimmune diseases. Recently, however, the combination of its deficiency with the Fas lpr mutation was found to result in augmented production of autoantibodies such as IgG rheumatoid factor and anti‐DNA IgG, leading to glomerulonephritis in mice. Although the precise molecular mechanism for the overall scenario is unclear, PIR‐B was found to suppress TLR9‐mediated production of naturally autoreactive antibodies by innate B cells or B‐1 cells by inhibiting the activation of Bruton′s tyrosine kinase. Thus, PIR‐B is an important regulator of innate immunity mediated by TLR9 in B‐1 cells, which can otherwise provoke autoimmunity when overactivated.

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  • LILRB proteins are type I transmembrane receptors predominantly expressed on hematopoietic cells.

    “The LILRB proteins are type I transmembrane receptors predominantly expressed on hematopoietic cells14–20.”

    From Oligomeric cystatin C supports the immunosuppressive activity of myeloid cells through interaction with inhibitory receptors (2025) · cites this paper as [16]

    Section 2.1 identifies LILRB1 and LILRB2 as human receptors associated with B cells and myeloid-lineage cells, supporting their expression on hematopoietic cells. Section 2.2 describes PIR-B—not LILRB proteins—as a type I transmembrane receptor. The paper does not establish that LILRB proteins as a group have that structure or are predominantly expressed on hematopoietic cells. (LLM, conf=0.83)

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Cited by

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Authors
Takai, T., Nakamura, A., & Endo, S.
Affiliations
Tohoku University (JP)
Corresponding author
Takai, Toshiyuki
ORCID
Venue
BioMed Research International
Publisher
Wiley
Published
2010-10-04
Volume
2011
Issue
1
Pages
275302-275302
ISSN
  • 1110-7243 (ISSN-L)
  • 2314-6133
  • 2314-6141
DOI
10.1155/2011/275302
PMC
PMC2952822
OpenAlex
W2075218090
Cited by
32
References
1
Citations by year
2026: 1 · 2025: 1 · 2024: 1 · 2022: 1 · 2021: 3 · 2019: 2 · 2018: 4 · 2017: 3 · 2016: 3 · 2015: 4 · 2014: 4 · 2013: 1 · 2012: 4
FWCI
0.21
Type
journal article
Language
en
Open access
Licence
Locations
  • BioMed Research International (publishedVersion, cc-by)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
Funders
  • Ministry of Education, Culture, Sports, Science and Technology
  • Japan Society for the Promotion of Science (22590431)
  • Japan Science and Technology Agency
  • Core Research for Evolutional Science and Technology
Topics
  • Health Sciences › Medicine › Rheumatology › Systemic Lupus Erythematosus Research
  • Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
  • Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
Keywords
PirB, autoimmune glomerulonephritis, inhibitory receptors, peripheral tolerance, autoantibodies, rheumatoid factor, TLR9, B-1 cells, Bruton's tyrosine kinase, autoimmunity
MeSH terms
Agammaglobulinaemia Tyrosine Kinase, Animals, Antibodies, Antinuclear, B-Lymphocytes, Disease Models, Animal, Glomerulonephritis, Immune Tolerance, Immunity, Innate, Leukocytes, Mononuclear, Protein Binding, Protein-Tyrosine Kinases, Receptors, Immunologic, Rheumatoid Factor, Histocompatibility Antigens Class I, Signal Transduction, Autoimmunity, fas Receptor, Toll-Like Receptor 9, Mice

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