Tu148 - Effects of Parathyroid Hormone in Peripheral B-cell Tolerance

Abstract Text:

Introduction: Hormones like prolactin and estrogens influence transitional B cells by promoting activation, rescuing them from apoptosis, and enhancing their survival. This immune modulation can contribute to loss of tolerance and the emergence of autoreactive B cells. While these hormonal effects are well-studied, the impact of parathyroid hormone (PTH) on transitional B cells remains poorly understood.

Methods: To investigate the effects of PTH on B-cell peripheral tolerance, we used the transitional mouse B-cell line WEHI-231. Cells were stimulated with increasing concentrations of PTH for 24–96 hours, stained with Annexin V/PI or MHC II antibodies, and analyzed by flow cytometry.

Results: Stimulation with high concentrations of PTH (32 and 64 ng/uL) significantly increased WEHI-231 viability at 72 and 96 hours compared to controls, with no similar effect observed at lower concentrations. This viability enhancement was absent in the mature B-cell line A20. Furthermore, high PTH levels rescued WEHI-231 cells from anti-IgM-induced apoptosis at 48 and 72 hours and significantly increased MHC class II expression after 48 hours. All findings were statistically significant (p < 0.05).

Conclusion: Our data propose that PTH may rescue transitional B cells from apoptosis, enhancing their survival. Additionally, the observed activation of transitional B cells with increasing PTH concentrations in vitro highlights a potential role in loss of tolerance and autoimmunity.