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Autophagy enhances NF?B activity in specific tissue macrophages by sequestering
A20 to boost antifungal immunity
#MMPMID25609235
Kanayama M
; Inoue M
; Danzaki K
; Hammer G
; He YW
; Shinohara ML
Nat Commun
2015[Jan]; 6
(?): 5779
PMID25609235
show ga
Immune responses must be well restrained in a steady state to avoid excessive
inflammation. However, such restraints are quickly removed to exert antimicrobial
responses. Here we report a role of autophagy in an early host antifungal
response by enhancing NF?B activity through A20 sequestration. Enhancement of
NF?B activation is achieved by autophagic depletion of A20, an NF?B inhibitor, in
F4/80(hi) macrophages in the spleen, peritoneum and kidney. We show that p62, an
autophagic adaptor protein, captures A20 to sequester it in the autophagosome.
This allows the macrophages to release chemokines to recruit neutrophils. Indeed,
mice lacking autophagy in myeloid cells show higher susceptibility to Candida
albicans infection due to impairment in neutrophil recruitment. Thus, at least in
the specific aforementioned tissues, autophagy appears to break A20-dependent
suppression in F4/80(hi) macrophages, which express abundant A20 and contribute
to the initiation of efficient innate immune responses.
|*Autophagy
[MESH]
|Animals
[MESH]
|Autophagy-Related Protein 7
[MESH]
|Candida albicans/metabolism
[MESH]
|Candidiasis/*immunology/metabolism
[MESH]
|Chemokine CXCL1/metabolism
[MESH]
|Chemokine CXCL2/metabolism
[MESH]
|Chemokines/metabolism
[MESH]
|Chemotaxis
[MESH]
|Cysteine Endopeptidases/*metabolism
[MESH]
|Down-Regulation
[MESH]
|Female
[MESH]
|Immunity, Innate
[MESH]
|Inflammation
[MESH]
|Intracellular Signaling Peptides and Proteins/*metabolism
[MESH]
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