Pde4 mediates MHCII expression in oligodendroglia

M Miguel M. Madeira (Molecular and Cellular Pharmacology Graduate Program, Renaissance School of Medicine at Stony Brook University) Z Zachary Hage (Molecular and Cellular Pharmacology Graduate Program, Renaissance School of Medicine at Stony Brook University) D Dimitris Koliatsis (Molecular and Cellular Pharmacology Graduate Program, Renaissance School of Medicine at Stony Brook University) A Alexandros G. Kokkosis (Molecular and Cellular Pharmacology Graduate Program, Renaissance School of Medicine at Stony Brook University) K Kimberly Nnah (Scholars in Biomedical Sciences Program, Renaissance School of Medicine at Stony Brook University) A Alexander J. Rhee (Molecular and Cellular Pharmacology Graduate Program, Renaissance School of Medicine at Stony Brook University) G Gilbert J. Rahme (Molecular and Cellular Pharmacology Graduate Program, Renaissance School of Medicine at Stony Brook University) K Katherine Kamvisios (Department of Pharmacological Sciences, Renaissance School of Medicine at Stony Brook University) A Antonis E. Koromilas B Barbara Rosati (Department of Physiology and Biophysics Renaissance School of Medicine at Stony Brook University) D David McKinnon (Program in Neuroscience, Stony Brook University) S Stella E. Tsirka (Molecular and Cellular Pharmacology Graduate Program, Renaissance School of Medicine at Stony Brook University)

Abstract

Chronic psychosocial stress is a major precipitant of Major Depressive Disorder (MDD), yet the glial mechanisms that translate sustained stress into maladaptive myelin and immune changes remain unclear. Using chronic social defeat stress and single-nucleus RNA sequencing of anterior medial PFC (mPFC) oligodendroglia, we identified a mature-oligodendrocyte cluster almost exclusively from stress-susceptible animals, marked by immune genes (MHCII) and upregulated Pde4b. Integration with a human MDD single-nucleus RNA sequencing dataset confirmed a conserved immune-like oligodendrocyte (ImOL) subset coexpressing Plp1 and Cd74 and enriched for Pde4b. Mechanistically, PDE4 inhibition with crisaborole elevated cAMP–PKA–CREB signaling, blocked IFNγ-induced MHCII expression, and engaged the eIF2α–ATF4/CHOP arm of the integrated stress response (ISR). In vivo modulation of the ISR with ISRIB or guanabenz bidirectionally controlled ImOL prevalence and stress-related behaviors. These findings position Pde4b–cAMP–ISR signaling as a regulator of oligodendroglial immune phenotypes and a promising target to modulate myelination and neuroinflammation in stress-related disorders.

Article Details

Volume / Issue Vol. 123, Issue 19
Published May 12, 2026
ISSN 0027-8424
Publisher National Academy of Sciences

Authors (12)

M

Miguel M. Madeira

Molecular and Cellular Pharmacology Graduate Program, Renaissance School of Medicine at Stony Brook University

Z

Zachary Hage

Molecular and Cellular Pharmacology Graduate Program, Renaissance School of Medicine at Stony Brook University

D

Dimitris Koliatsis

Molecular and Cellular Pharmacology Graduate Program, Renaissance School of Medicine at Stony Brook University

A

Alexandros G. Kokkosis

Molecular and Cellular Pharmacology Graduate Program, Renaissance School of Medicine at Stony Brook University

K

Kimberly Nnah

Scholars in Biomedical Sciences Program, Renaissance School of Medicine at Stony Brook University

A

Alexander J. Rhee

Molecular and Cellular Pharmacology Graduate Program, Renaissance School of Medicine at Stony Brook University

G

Gilbert J. Rahme

Molecular and Cellular Pharmacology Graduate Program, Renaissance School of Medicine at Stony Brook University

K

Katherine Kamvisios

Department of Pharmacological Sciences, Renaissance School of Medicine at Stony Brook University

A

Antonis E. Koromilas

B

Barbara Rosati

Department of Physiology and Biophysics Renaissance School of Medicine at Stony Brook University

D

David McKinnon

Program in Neuroscience, Stony Brook University

S

Stella E. Tsirka

Molecular and Cellular Pharmacology Graduate Program, Renaissance School of Medicine at Stony Brook University