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Related Experiment Video

Updated: Feb 13, 2026

The bm12 Inducible Model of Systemic Lupus Erythematosus SLE in C57BL/6 Mice

The bm12 Inducible Model of Systemic Lupus Erythematosus SLE in C57BL/6 Mice

Published on: November 1, 2015

Plasma Cell Differentiation Pathways in Systemic Lupus Erythematosus.

Susan Malkiel¹, Ashley N Barlev^1,2, Yemil Atisha-Fregoso^1,3

¹Center of Autoimmune Musculoskeletal and Hematopoietic Diseases, The Feinstein Institute for Medical Research, Northwell Health, Manhasset, NY, United States.

Frontiers in Immunology

|March 21, 2018

Summary

Plasma cells produce antibodies, but in autoimmune diseases like lupus, they create harmful ones. Understanding whether germinal center or extrafollicular pathways dominate in patients may lead to targeted treatments.

Keywords:

B cells autoantibodies plasma cells systemic lupus erythematosus tolerance

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The bm12 Inducible Model of Systemic Lupus Erythematosus SLE in C57BL/6 Mice

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Area of Science:

Immunology
Autoimmunity
B cell biology

Background:

Plasma cells (PCs) produce antibodies, crucial for immunity but also implicated in autoimmune diseases like systemic lupus erythematosus (SLE).
Traditionally, high-affinity autoantibodies were thought to originate from germinal center (GC) responses, but extrafollicular (EF) pathways are also implicated in SLE.
The origin pathway of PCs may influence their lifespan and therapeutic sensitivity.

Purpose of the Study:

To investigate the hypothesis that either GC or EF pathways dominate in individual SLE patients.
To explore the role of genetic risk factors in driving the predominance of either GC or EF B cell responses.
To identify molecular mechanisms underlying autoreactive PC differentiation in SLE for precision therapy.

Main Methods:

Analysis of B cell differentiation pathways (GC vs. EF).
Investigation of genetic risk factors influencing B cell responses.
Exploration of signaling pathway cross-talk (BCR, TLR, cytokines) in B cells.
Examination of risk variants in interferon and TLR pathways.

Main Results:

Both GC and EF responses are implicated in SLE pathogenesis.
Genetic factors may dictate the predominant B cell differentiation pathway in SLE patients.
Cross-talk between BCR, TLR, and cytokine signaling complicates B cell differentiation analysis.
Specific risk variants may preferentially influence either GC or EF responses.

Conclusions:

Identifying the dominant PC differentiation pathway (GC or EF) in individual SLE patients is crucial.
Understanding the molecular mechanisms and genetic drivers of these pathways is key to developing targeted treatments.
Distinguishing between GC-driven and EF-driven responses can guide precision therapy for SLE heterogeneity.