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2017 ; 8
(ä): 1055
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RIPK3/Fas-Associated Death Domain Axis Regulates Pulmonary Immunopathology to
Cryptococcal Infection Independent of Necroptosis
#MMPMID28919893
Fa Z
; Xie Q
; Fang W
; Zhang H
; Zhang H
; Xu J
; Pan W
; Xu J
; Olszewski MA
; Deng X
; Liao W
Front Immunol
2017[]; 8
(ä): 1055
PMID28919893
show ga
Fas-associated death domain (FADD) and receptor interacting protein kinase 3
(RIPK3) are multifunctional regulators of cell death and immune response. Using a
mouse model of cryptococcal infection, the roles of FADD and RIPK3 in
anti-cryptococcal defense were investigated. Deletion of RIPK3 alone led to
increased inflammatory cytokine production in the Cryptococcus
neoformans-infected lungs, but in combination with FADD deletion, it led to a
robust Th1-biased response with M1-biased macrophage activation. Rather than
being protective, these responses led to paradoxical C. neoformans expansion and
rapid clinical deterioration in Ripk3(-/-) and Ripk3(-/-)Fadd(-/-) mice. The
increased mortality of Ripk3(-/-) and even more accelerated mortality in
Ripk3(-/-)Fadd(-/-) mice was attributed to profound pulmonary damage due to
neutrophil-dominant infiltration with prominent upregulation of pro-inflammatory
cytokines. This phenomenon was partially associated with selective alterations in
the apoptotic frequency of some leukocyte subsets, such as eosinophils and
neutrophils, in infected Ripk3(-/-)Fadd(-/-) mice. In conclusion, our study shows
that RIPK3 in concert with FADD serve as physiological "brakes," preventing the
development of excessive inflammation and Th1 bias, which in turn contributes to
pulmonary damage and defective fungal clearance. This novel link between the
protective effect of FADD and RIPK3 in antifungal defense and sustenance of
immune homeostasis may be important for the development of novel immunomodulatory
therapies against invasive fungal infections.
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