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The bm12 Inducible Model of Systemic Lupus Erythematosus (SLE) in C57BL/6 Mice
Published on: November 1, 2015
Chemokine blockade for lupus model mice.
1Department of Bioregulatory Medicine, Ehime University Graduate School of Medicine, Shitsukawa 454, Toon city, Ehime 791-0295, Japan. hitoshih@m.ehime-u.ac.jp
Frontiers in Bioscience : a Journal and Virtual Library
|November 6, 2007
Summary
Chemokines and their receptors drive autoimmune diseases by recruiting leukocytes. Blocking these interactions offers a novel therapeutic strategy for conditions like systemic lupus erythematosus (SLE).
Area of Science:
- Immunology
- Pathogenesis of Autoimmune Diseases
Background:
- Chemokines and chemokine receptors are key mediators in leukocyte recruitment to tissues.
- Their involvement is critical in the initiation and progression of autoimmune diseases.
Purpose of the Study:
- To review the role of chemokines and chemokine receptors in autoimmune disease pathogenesis.
- To discuss the therapeutic potential of chemokine blockade in lupus models.
Main Methods:
- Utilizing MRL/MpJ-lpr/lpr (MRL/lpr) and (NZB X NZW) F1 mice as models for systemic lupus erythematosus (SLE).
- Analyzing chemokine and chemokine receptor expression patterns in inflamed organs of lupus model mice and humans.
Main Results:
- Evidence indicates a crucial role for chemokines and receptors in autoimmune disease pathogenesis.
- Similar expression patterns observed in humans and lupus model mice, particularly MRL/lpr mice.
Conclusions:
- Chemokine blockade presents a promising therapeutic strategy for autoimmune diseases.
- Findings from lupus model mice are potentially applicable to human SLE treatment.
