Samenvatting
Objective: Mounting data support the hypothesis for a role of the immune system in the pathophysiology of bipolar disorder. The aim of this study was to examine immune alterations in two unique familial high-risk cohorts for bipolar disorder.
Methods: The study population comprised bipolar offspring, bipolar twins and controls from the Dutch Bipolar Offspring Study and the Dutch Bipolar Twins Study. T-cell percentages were measuredby FACS analysis and serum levels of several hematopoietic/neuronal growth and differentiation factors were measured using aLuminex or Cytometric Bead Array kits.
Results: In bipolar offspring, of who 13% developed a bipolar disorder and 54% a life time mood disorder, partial T cell defects are observed, i.e. lower numbers of circulating CD3+ and/or CD4+ Tcells, from adolescence through adulthood. Inflammatory and regulatory T cells followed a dynamic course over time with reduced levels of natural T regulatory cells in adolescence and a reduced number of Th-1 and -17 cells in young adulthood in bipolar off-spring. Bipolar twin studies show that the genetic background of the individual mainly determined these T cell defects. During adolescence lymphoid and myeloid growth factors (IL-7, IGFBP-2 andSCF) are increased, while general (neuronal) factors (EGF, BDNF,S100B) are decreased in serum of bipolar offspring. No significant association between these immune abnormalities and bipolar disorder was found.
Conclusion: These studies demonstrate a dysregulation of peripheralimmune cells and factors in familial high-risk populations forbipolar disorder that may represent a vulnerability factor for thedevelopment of mood symptomatology
Methods: The study population comprised bipolar offspring, bipolar twins and controls from the Dutch Bipolar Offspring Study and the Dutch Bipolar Twins Study. T-cell percentages were measuredby FACS analysis and serum levels of several hematopoietic/neuronal growth and differentiation factors were measured using aLuminex or Cytometric Bead Array kits.
Results: In bipolar offspring, of who 13% developed a bipolar disorder and 54% a life time mood disorder, partial T cell defects are observed, i.e. lower numbers of circulating CD3+ and/or CD4+ Tcells, from adolescence through adulthood. Inflammatory and regulatory T cells followed a dynamic course over time with reduced levels of natural T regulatory cells in adolescence and a reduced number of Th-1 and -17 cells in young adulthood in bipolar off-spring. Bipolar twin studies show that the genetic background of the individual mainly determined these T cell defects. During adolescence lymphoid and myeloid growth factors (IL-7, IGFBP-2 andSCF) are increased, while general (neuronal) factors (EGF, BDNF,S100B) are decreased in serum of bipolar offspring. No significant association between these immune abnormalities and bipolar disorder was found.
Conclusion: These studies demonstrate a dysregulation of peripheralimmune cells and factors in familial high-risk populations forbipolar disorder that may represent a vulnerability factor for thedevelopment of mood symptomatology
| Originele taal-2 | English |
|---|---|
| Artikelnummer | P-336 |
| Pagina's (van-tot) | 175 |
| Aantal pagina's | 1 |
| Tijdschrift | Bipolar Disorders |
| Volume | 18 |
| Nummer van het tijdschrift | Supplement 1 |
| DOI's | |
| Status | Published - jul-2016 |
| Evenement | 18th Annual Conference of the International-Society-for-Bipolar-Disorders / 8th Biennial Conference of the International-Society-for-Affective-Disorders - Amsterdam, Netherlands Duur: 13-jul-2016 → 16-jul-2016 |