Neutrophil-plasmacytoid dendritic cell interaction leads to production of type I IFN in response to Mycobacterium tuberculosis.
Eur J Immunol
; 54(3): e2350666, 2024 Mar.
Article
in En
| MEDLINE
| ID: mdl-38161237
ABSTRACT
Mycobacterium tuberculosis (Mtb) can cause a latent infection that sometimes progresses to clinically active tuberculosis (TB). Type I interferons (IFN-I) have been implicated in initiating the progression from latency to active TB, in part because IFN-I stimulated genes are the earliest genes to be upregulated in patients as they advance to active TB. Plasmacytoid dendritic cells (pDCs) are major producers of IFN-I during viral infections and in response to autoimmune-induced neutrophil extracellular traps. pDCs have also been suggested to be the major producers of IFN-I during Mtb infection of mice and nonhuman primates, but direct evidence has been lacking. Here, we found that Mtb did not stimulate isolated human pDCs to produce IFN-I, but human neutrophils infected with Mtb-activated co-cultured pDCs to do so. Mtb-infected neutrophils produced neutrophil extracellular traps, whose exposed DNA is a well-known mechanism to activate pDCs to secrete IFN-I. We conclude that pDCs contribute to the IFN-I response during Mtb infection by interacting with infected neutrophils which may then promote Mtb pathogenesis.
Key words
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Tuberculosis
/
Interferon Type I
/
Mycobacterium tuberculosis
Limits:
Animals
/
Humans
Language:
En
Journal:
Eur J Immunol
Year:
2024
Type:
Article
Affiliation country:
United States