Conventional and new immunotherapies for immune system dysregulation in postpartum mood disorders: comparisons to immune system dysregulations in bipolar disorder, major depression and postpartum autoimmune thyroid disease.

Postpartum mood disorders are heterogenous disorders and comprise postpartum psychosis and postpartum depression. Evidence is accumulating that systemic monocyte/macrophage activation, low grade inflammation and (premature senescence related) T cell defects increase the risk for mood disorders outside pregnancy by affecting the function of microglia and T cells in the emotional brain (the cortico-limbic system) leading to inadequate mood regulation upon stress. The evidence in the literature that similar immune dysregulations are present in postpartum mood disorders. The physiological postpartum period is characterized by a rapid T cell surge and a mild activation of the monocyte/macrophage system. Postpartum mood disorder patients show a diminished T cell surge (including that of T regulatory cells) and an increase in low grade inflammation, i.e. an increased inflammatory state of monocytes/macrophages and higher levels of serum pro-inflammatory cytokines. Anti-inflammatory agents (e.g. COX-2 inhibitors) and T cell boosting agents (e.g. low dose IL-2 therapy) should be further investigated as treatment. The hypothesis should be investigated that postpartum mood disorders are active episodes (triggered by changes in the postpartum immuno-endocrine milieu) in ongoing, dynamically fluctuating aberrant neuro-immune-endocrine trajectories leading to mood disorders in women (inheritably) vulnerable to these disorders.