What question did this study set out to answer?

To determine how intracellular cyclic nucleotide levels are regulated in antigen-presenting myeloid cells and identify the role of phosphodiesterase 1B (Pde1b) in governing immune activation.

September 17, 2026EMBO ReportsOpen Access

Pde1b controls cyclic nucleotide signaling in cDC1 and macrophages to regulate immune responses

View Full Paper

Ask AI

Bookmark

Authors

LRLais L O Rekowsky RSRicardo Luís Louzada da Silva JSJonathan A Seenarine

Discussion

Member takes

Overview

Experimental study demonstrates that Pde1b loss impairs myeloid cyclic nucleotide regulation during infection, indicating an essential role in antimicrobial immunity.

Key Points

To determine how intracellular cyclic nucleotide levels are regulated in antigen-presenting myeloid cells and identify the role of phosphodiesterase 1B (Pde1b) in governing immune activation.
Employed genetic loss-of-function mouse models of Pde1b deficiency during Listeria infection.
Evaluated antigen-specific CD8+ and CD4+ T cell responses, myeloid transcriptional profiles, and the effects of wild-type dendritic cell adoptive transfer.
Assessed intracellular cAMP and cGMP concentrations alongside downstream PKA, PKG, and CREB signaling pathways.
Pde1b deficiency impaired bacterial clearance, suppressed CD8+ and CD4+ T cell expansion, and skewed myeloid transcriptional programs toward immunoregulatory states.
Adoptive transfer of wild-type dendritic cells into Pde1b-deficient hosts partially restored T cell priming.
Loss of Pde1b elevated cAMP and cGMP in cDC1 and macrophages, driving excessive PKA/PKG signaling and CREB-associated transcriptional changes that were not replicated by other phosphodiesterase inhibitors.

Cite This Study

Rekowsky et al. (2026) studied this question.

synapsesocial.com/papers/6aabb7b85f706d05830e7027 https://doi.org/10.1038/s44319-026-00924-z

View Full Paper

Ask AI

Bookmark

September 17, 2026EMBO ReportsOpen Access

Pde1b controls cyclic nucleotide signaling in cDC1 and macrophages to regulate immune responses

View Full Paper

Ask AI

Bookmark

Authors

LRLais L O Rekowsky RSRicardo Luís Louzada da Silva JSJonathan A Seenarine

Discussion

Member takes

Overview

Experimental study demonstrates that Pde1b loss impairs myeloid cyclic nucleotide regulation during infection, indicating an essential role in antimicrobial immunity.

Key Points

To determine how intracellular cyclic nucleotide levels are regulated in antigen-presenting myeloid cells and identify the role of phosphodiesterase 1B (Pde1b) in governing immune activation.
Employed genetic loss-of-function mouse models of Pde1b deficiency during Listeria infection.
Evaluated antigen-specific CD8+ and CD4+ T cell responses, myeloid transcriptional profiles, and the effects of wild-type dendritic cell adoptive transfer.
Assessed intracellular cAMP and cGMP concentrations alongside downstream PKA, PKG, and CREB signaling pathways.
Pde1b deficiency impaired bacterial clearance, suppressed CD8+ and CD4+ T cell expansion, and skewed myeloid transcriptional programs toward immunoregulatory states.
Adoptive transfer of wild-type dendritic cells into Pde1b-deficient hosts partially restored T cell priming.
Loss of Pde1b elevated cAMP and cGMP in cDC1 and macrophages, driving excessive PKA/PKG signaling and CREB-associated transcriptional changes that were not replicated by other phosphodiesterase inhibitors.

Cite This Study

Rekowsky et al. (2026) studied this question.

synapsesocial.com/papers/6aabb7b85f706d05830e7027 https://doi.org/10.1038/s44319-026-00924-z

Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

View Full Paper

Ask AI

Bookmark