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MRL Strains Have a BAFFR Mutation without Functional Consequence.

Windy R Allman1, Lunhua Liu1, Adam S Coleman1

  • 1Laboratory of Bacterial Polysaccharides, Division of Bacterial Parasitic and Allergenic Products, Center for Biologics Evaluation and Research, U.S. Food and Drug Administration, Silver Spring, Maryland, 20993-0002, United States of America.

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A mutation in B cell activating factor receptor (BAFFR) was found in autoimmune-prone mice but did not impair BAFFR function. Other genetic factors likely contribute to B cell hyperactivity and autoimmune disease development.

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Area of Science:

  • Immunology
  • Genetics
  • Autoimmune Diseases

Background:

  • B cell activating factor receptor (BAFFR) is crucial for B cell development and survival.
  • Systemic autoimmune diseases involve dysregulated B cell function.
  • Mouse models are essential for studying autoimmune disease pathogenesis.

Purpose of the Study:

  • To investigate the expression and function of BAFFR in mouse strains with varying autoimmune susceptibility.
  • To identify genetic variations in BAFFR and their functional consequences.
  • To understand the role of BAFFR signaling in B cell hyperactivity.

Main Methods:

  • Comparative analysis of BAFFR expression and function in MRL, MRL/Lpr, and BALB/c mice.
  • Genetic sequencing to identify mutations in the TNFRSF13C gene.
  • Assessment of BAFF-mediated B cell apoptosis, NF-κB2 activation, and MAPK ERK1/2 signaling.
  • Correlation of ERK1/2 basal activity with autoimmune susceptibility.

Main Results:

  • A Pro44Ser substitution mutation in BAFFR (encoded by TNFRSF13C) was identified in MRL and MRL/Lpr mice.
  • Mutant BAFFR was expressed on B cells and responded to BAFF, reducing apoptosis and activating NF-κB2.
  • BAFF failed to significantly induce ERK1/2 signaling in MRL/Lpr B cells due to high basal activity, which correlated with autoimmune susceptibility.
  • Aged MRL/Lpr mice showed high BAFF, low surface BAFFR, and high basal NF-κB2 activation.

Conclusions:

  • The P44S BAFFR mutation does not impair BAFFR function or enhance B cell activity in MRL and MRL/Lpr mice.
  • Other genetic loci on the MRL background likely contribute to B cell hyperactivity and autoimmune susceptibility.
  • BAFFR signaling and its regulation are complex and influenced by multiple genetic factors in autoimmune disease.