Abstract
B cell activation mediated by cluster of differentiation (CD) molecules plays an important role in B cell-related autoimmune diseases. CD22 and CD72 have been demonstrated to act as B cell inhibitory receptors in many autoimmune diseases. Activated B cells are involved in the pathogenesis of myasthenia gravis (MG) by secretion of anti-acetylcholine receptor (AchR) antibodies. However, the roles of CD22 and CD72 on B cells of MG are unknown. In this study, we detected the expression of CD22 and CD72 on B cells of MG, compared to multiple sclerosis (MS) patient controls and healthy controls by flow cytometry and quantitative real-time polymerase transcription chain reaction. Our data demonstrated that aberrant expression of CD72 exists on B cells of MG and MS patients and expression level of CD72 molecule has a significantly negative correlation with anti-AchR antibody levels in MG, which suggests that CD72 may be involved in the pathogenesis of MG and MS. There were no significant differences between study patients (MG, ocular MG, generalized MG, and MS) and healthy controls.
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Abbreviations
- MG:
-
Myasthenia gravis
- MS:
-
Multiple sclerosis
- BCR:
-
B cell receptor
- AchR:
-
Acetylcholine receptor
- CSF:
-
Cerebrospinal fluid
- OMG:
-
Ocular myasthenia gravis
- GMG:
-
Generalized myasthenia gravis
- MP-RT-PCR:
-
Multiplex reverse transcriptase polymerase chain reaction
- HC:
-
Healthy controls
- MuSK:
-
Muscle-specific kinase
- CNS:
-
Central nervous system
- RA:
-
Rheumatoid arthritis
- SLE:
-
Systemic lupus erythematosus
- pSS:
-
Primary Sjögren’s syndrome
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Acknowledgments
The present work was supported by a research grant from the National Natural Science Foundation of China (30971033). We appreciate the support provided by all the colleagues in the study department.
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All the authors declared no competing interests.
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Lu, J., Li, J., Zhu, Tq. et al. Modulation of B Cell Regulatory Molecules CD22 and CD72 in Myasthenia Gravis and Multiple Sclerosis. Inflammation 36, 521–528 (2013). https://doi.org/10.1007/s10753-012-9573-z
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DOI: https://doi.org/10.1007/s10753-012-9573-z