TY - JOUR
T1 - Conventional and new immunotherapies for immune system dysregulation in postpartum mood disorders
T2 - comparisons to immune system dysregulations in bipolar disorder, major depression, and postpartum autoimmune thyroid disease
AU - Drexhage, Hemmo A.
AU - Bergink, Veerle
AU - Poletti, Sara
AU - Benedetti, Francesco
AU - Osborne, Lauren M.
N1 - Publisher Copyright:
© 2024 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group.
PY - 2024
Y1 - 2024
N2 - Introduction: 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. Areas covered: The evidence in the literature that similar immune dysregulations are present in postpartum mood disorders. Results: 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, that is, an increased inflammatory state of monocytes/macrophages and higher levels of serum pro-inflammatory cytokines. Expert opinion: 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.
AB - Introduction: 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. Areas covered: The evidence in the literature that similar immune dysregulations are present in postpartum mood disorders. Results: 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, that is, an increased inflammatory state of monocytes/macrophages and higher levels of serum pro-inflammatory cytokines. Expert opinion: 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.
KW - Postpartum psychosis
KW - T cells
KW - monocytes
KW - pathogenesis
KW - postpartum depression
KW - postpartum thyroiditis
KW - therapy
UR - http://www.scopus.com/inward/record.url?scp=85208217572&partnerID=8YFLogxK
U2 - 10.1080/1744666X.2024.2420053
DO - 10.1080/1744666X.2024.2420053
M3 - Review article
C2 - 39441185
AN - SCOPUS:85208217572
SN - 1744-666X
JO - Expert Review of Clinical Immunology
JF - Expert Review of Clinical Immunology
ER -