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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 PLoS+One
2017 ; 12
(9
): e0180413
Nephropedia Template TP
gab.com Text
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English Wikipedia
LAG-3 potentiates the survival of Mycobacterium tuberculosis in host phagocytes
by modulating mitochondrial signaling in an in-vitro granuloma model
#MMPMID28880895
Phillips BL
; Gautam US
; Bucsan AN
; Foreman TW
; Golden NA
; Niu T
; Kaushal D
; Mehra S
PLoS One
2017[]; 12
(9
): e0180413
PMID28880895
show ga
CD4+ T-cell mediated Th1 immune responses are critical for immunity to TB. The
immunomodulatory protein, lymphocyte activation gene-3 (LAG-3) decreases Th1-type
immune responses in T-cells. LAG-3 expression is significantly induced in the
lungs of macaques with active TB and correlates with increased bacterial burden.
Overproduction of LAG-3 can greatly diminish responses and could lead to
uncontrolled Mtb replication. To assess the effect of LAG-3 on the progression of
Mtb infection, we developed a co-culture system wherein blood-derived macrophages
are infected with Mtb and supplemented with macaque blood or lung derived CD4+
T-cells. Silencing LAG-3 signaling in macaque lung CD4+ T-cells enhanced killing
of Mtb in co-cultures, accompanied by reduced mitochondrial electron transport
and increased IFN-? expression. Thus, LAG-3 may modulate adaptive immunity to Mtb
infection by interfering with the mitochondrial apoptosis pathway. Better
understanding this pathway could allow us to circumvent immune features that
promote disease.