Abstract:
:Inflammation is critical for controlling pathogens, but also responsible for symptoms of infectious diseases. IL-27 is an important regulator of inflammation and can limit development of IFNγ-producing Tbet+ CD4+ T (Th1) cells. IL-27 is thought to do this by stimulating IL-10 production by CD4+ T cells, but the underlying mechanisms of these immunoregulatory pathways are not clear. Here we studied the role of IL-27 signalling in experimental visceral leishmaniasis (VL) caused by infection of C57BL/6 mice with the human pathogen Leishmania donovani. We found IL-27 signalling was critical for the development of IL-10-producing Th1 (Tr1) cells during infection. Furthermore, in the absence of IL-27 signalling, there was improved control of parasite growth, but accelerated splenic pathology characterised by the loss of marginal zone macrophages. Critically, we discovered that IL-27 signalling limited glycolysis in Th1 cells during infection that in turn attenuated inflammation. Furthermore, the modulation of glycolysis in the absence of IL-27 signalling restricted tissue pathology without compromising anti-parasitic immunity. Together, these findings identify a novel mechanism by which IL-27 mediates immune regulation during disease by regulating cellular metabolism.
journal_name
PLoS Pathogjournal_title
PLoS pathogensauthors
Montes de Oca M,de Labastida Rivera F,Winterford C,Frame TCM,Ng SS,Amante FH,Edwards CL,Bukali L,Wang Y,Uzonna JE,Kuns RD,Zhang P,Kabat A,Klein Geltink RI,Pearce EJ,Hill GR,Engwerda CRdoi
10.1371/journal.ppat.1008994subject
Has Abstractpub_date
2020-10-13 00:00:00pages
e1008994issue
10eissn
1553-7366issn
1553-7374pii
PPATHOGENS-D-20-01240journal_volume
16pub_type
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