Related Experiment Video
Updated: Jan 1, 2026
The bm12 Inducible Model of Systemic Lupus Erythematosus SLE in C57BL/6 Mice
Published on: November 1, 2015
CD22 and CD72 contribute to the development of scleroderma in a murine model
Chunyan Zhao1, Takashi Matsushita1, Vinh Thi Ha Nguyen1
1Department of Dermatology, Faculty of Medicine, Institute of Medical, Pharmaceutical and Health Sciences, Kanazawa University, Ishikawa, Japan.
Background:
Systemic sclerosis (SSc) is a systemic autoimmune disease that is characterized by excessive fibrosis. CD22 and CD72 are B cell-specific cell surface molecules that negatively regulate B cell function.
Objective:
The aim of the present study was to investigate the roles of CD22 and CD72 in a murine scleroderma model.
Methods:
The experimental fibrosis model was generated by subcutaneous injection of bleomycin or hypochlorous acid (HOCL) into wild-type (WT), CD22-deficient (CD22-/-), CD72-deficient (CD72-/-) and CD22 and CD72 double-deficient (CD22-/-/CD72-/-) mice. We histologically assessed skin fibrosis and inflammatory cell infiltration. Cytokine and chemokine expression levels were measured by real-time polymerase chain reaction.
Results:
The severity of fibrosis in the skin and lung was significantly less in CD22-/-, CD72-/-, and CD22-/-/CD72-/- mice than in WT mice in the bleomycin-induced model. In the skin of bleomycin-treated mice, the numbers of CD3+ T cells, CD8+ T cells, and F4/80+ macrophages were significantly lower in CD22-/-, CD72-/-, and CD22-/-/CD72-/- mice than in WT mice. The expression levels of mRNAs for IL-6, TNF-α, TGF-β, CTGF, IL-1β, IL-13, CXCL2, and ICAM-1 were significantly lower in CD22-/-, CD72-/-, and CD22-/-/CD72-/- mice than in WT mice. In the HOCL-induced model, both skin and lung fibrosis were ameliorated in CD22-/-, CD72-/- and CD22-/-/CD72-/- mice compared to WT mice.
Conclusion:
These results indicate that CD22 and CD72 likely play crucial roles in skin and lung fibrosis. Moreover, the inhibition of CD22 and CD72 function has potential as a therapeutic approach to SSc.
Insights
Mice lacking CD22 and CD72 showed reduced skin and lung fibrosis in systemic sclerosis models. Inhibiting CD22 and CD72 may offer a new therapeutic strategy for systemic sclerosis.
Area of Science:
- Immunology
- Rheumatology
- Pathology
Background:
- Systemic sclerosis (SSc) is an autoimmune disease marked by excessive fibrosis.
- CD22 and CD72 are B cell surface molecules that regulate B cell function.
Purpose of the Study:
- Investigate the roles of CD22 and CD72 in a murine model of systemic sclerosis.
- Evaluate the therapeutic potential of targeting CD22 and CD72 in SSc.
Main Methods:
- Generated experimental fibrosis models using bleomycin or hypochlorous acid (HOCL) in wild-type (WT), CD22-deficient, CD72-deficient, and double-deficient mice.
- Histologically assessed skin and lung fibrosis and inflammatory cell infiltration.
- Measured cytokine and chemokine expression levels via real-time PCR.
Main Results:
- CD22-deficient, CD72-deficient, and double-deficient mice exhibited significantly reduced skin and lung fibrosis compared to WT mice in both bleomycin and HOCL models.
- Reduced infiltration of CD3+ T cells, CD8+ T cells, and F4/80+ macrophages was observed in the skin of deficient mice.
- Lowered mRNA expression of key fibrotic and inflammatory mediators, including IL-6, TNF-α, TGF-β, and CTGF, was noted in deficient mice.
Conclusions:
- CD22 and CD72 play significant roles in the development of skin and lung fibrosis.
- Targeting CD22 and CD72 presents a promising therapeutic avenue for treating systemic sclerosis.
