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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Nat+Commun
2018 ; 9
(1
): 1603
Nephropedia Template TP
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The IL-33-PIN1-IRAK-M axis is critical for type 2 immunity in IL-33-induced
allergic airway inflammation
#MMPMID29686383
Nechama M
; Kwon J
; Wei S
; Kyi AT
; Welner RS
; Ben-Dov IZ
; Arredouani MS
; Asara JM
; Chen CH
; Tsai CY
; Nelson KF
; Kobayashi KS
; Israel E
; Zhou XZ
; Nicholson LK
; Lu KP
Nat Commun
2018[Apr]; 9
(1
): 1603
PMID29686383
show ga
Interleukin 33 (IL-33) is among the earliest-released cytokines in response to
allergens that orchestrate type 2 immunity. The prolyl cis-trans isomerase PIN1
is known to induce cytokines for eosinophil survival and activation by
stabilizing cytokines mRNAs, but the function of PIN1 in upstream signaling
pathways in asthma is unknown. Here we show that interleukin receptor associated
kinase M (IRAK-M) is a PIN1 target critical for IL-33 signaling in allergic
asthma. NMR analysis and docking simulations suggest that PIN1 might regulate
IRAK-M conformation and function in IL-33 signaling. Upon IL-33-induced airway
inflammation, PIN1 is activated for binding with and isomerization of IRAK-M,
resulting in IRAK-M nuclear translocation and induction of selected
proinflammatory genes in dendritic cells. Thus, the IL-33-PIN1-IRAK-M is an axis
critical for dendritic cell activation, type 2 immunity and IL-33 induced airway
inflammation.