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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
2014 ; 9
(9
): e106392
Nephropedia Template TP
gab.com Text
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Twit Text #
English Wikipedia
The interferon-induced gene Ifi27l2a is active in lung macrophages and
lymphocytes after influenza A infection but deletion of Ifi27l2a in mice does not
increase susceptibility to infection
#MMPMID25184786
Tantawy MA
; Hatesuer B
; Wilk E
; Dengler L
; Kasnitz N
; Weiß S
; Schughart K
PLoS One
2014[]; 9
(9
): e106392
PMID25184786
show ga
Interferons represent one of the first and essential host defense mechanisms
after infection, and the activation of the IFN-pathway results in the
transcriptional activation of hundreds of interferon-stimulated genes. The
alpha-inducible protein 27 like 2A (Ifi27l2a) gene (human synonym: ISG12) is
strongly up-regulated in the lung after influenza A infection in mice and has
been shown in gene expression studies to be highly correlated to other activated
genes. Therefore, we investigated the role of Ifi27l2a for the host defense to
influenza A infections in more detail. RT-PCR analyses in non-infected mice
demonstrated that Ifi27l2a was expressed in several tissues, including the lung.
Detailed analyses of reporter gene expression in lungs from Ifi27l2a-LacZ mice
revealed that Ifi27l2a was expressed in macrophages and lymphocytes but not in
alveolar cells or bronchiolar epithelium cells. The number of macrophages and
lymphocyte strongly increased in the lung after infection, but no significant
increase in expression levels of the LacZ reporter gene was found within
individual immune cells. Also, no reporter gene expression was found in
bronchiolar epithelial cells, alveolar cells or infiltrating neutrophils after
infection. Thus, up-regulation of Ifi27l2a in infected lungs is mainly due to the
infiltration of macrophages and lymphocytes. Most surprisingly, deletion of
Ifi27l2a in mouse knock-out lines did not result in increased susceptibility to
infections with H1N1 or H7N7 influenza A virus compared to wild type C57BL/6N
mice, suggesting a less important role of the gene for the host response to
influenza infections than for bacterial infections.
|Animals
[MESH]
|Gene Deletion
[MESH]
|Gene Expression Regulation
[MESH]
|Humans
[MESH]
|Influenza A Virus, H1N1 Subtype/pathogenicity
[MESH]
|Influenza A Virus, H7N7 Subtype/pathogenicity
[MESH]