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Beta2-glycoprotein I (beta2-GPI) mRNA is expressed by several cell types involved in anti-phospholipid
B Caronti1, C Calderaro, C Alessandri
1Dipartimento di Scienze Neurologiche, Immunologia Clinica III, Università 'La Sapienza', Roma, Italy.
Abstract:
We report here the expression of beta2-GPI mRNA by cell types involved in the pathophysiology of the anti-phospholipid syndrome (APS), i.e. endothelial cells as a target of autoantibodies in the APS, astrocytes and neurones involved in APS of the central nervous system (CNS). Lymphocytes were also included in the study, as it has been demonstrated that patients with systemic lupus erythematosus-associated CNS diseases have serum anti-lymphocyte antibodies cross-reacting with brain antigens, and intrathecally synthesized anti-neurone antibodies. Reverse transcriptase-polymerase chain reaction followed by restriction enzyme digestion of the product obtained demonstrated the presence of beta2-GPI mRNA in all cell types here tested, cultured both in presence and absence of fetal calf serum. In both culture conditions, the same cell types were immunoreactive to an anti-beta2-GPI MoAb, as determined by indirect immunofluorescence technique. Taken together, these results indicate a direct cell synthesis of beta2-GPI, suggesting an antigenic function of beta2-GPI in the APS, including the CNS disease that occurs in this syndrome.
Insights
Beta2-glycoprotein I (beta2-GPI) mRNA is expressed by cells implicated in anti-phospholipid syndrome (APS). This suggests beta2-GPI plays a direct antigenic role in APS pathogenesis, including central nervous system involvement.
Area of Science:
- Immunology
- Molecular Biology
- Neuroscience
Background:
- Anti-phospholipid syndrome (APS) involves autoantibodies targeting various cells.
- Central nervous system (CNS) involvement in APS is linked to cross-reacting antibodies.
Purpose of the Study:
- To investigate the expression of beta2-glycoprotein I (beta2-GPI) mRNA in cells relevant to APS pathophysiology.
- To determine if these cells synthesize beta2-GPI, suggesting a potential antigenic role.
Main Methods:
- Reverse transcriptase-polymerase chain reaction (RT-PCR) to detect beta2-GPI mRNA.
- Indirect immunofluorescence using anti-beta2-GPI monoclonal antibody (MoAb) to assess protein expression.
- Cell cultures of endothelial cells, astrocytes, neurons, and lymphocytes.
Main Results:
- Beta2-GPI mRNA was detected in endothelial cells, astrocytes, neurons, and lymphocytes.
- All tested cell types showed immunoreactivity to anti-beta2-GPI MoAb.
- Cellular expression of beta2-GPI was confirmed in both fetal calf serum-supplemented and unsupplemented cultures.
Conclusions:
- Cells involved in APS pathophysiology, including CNS cells, directly synthesize beta2-GPI.
- Beta2-GPI likely functions as an antigen in APS, contributing to disease mechanisms.
- This finding has implications for understanding APS pathogenesis, particularly CNS manifestations.