Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\28408984
.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 F1000Res
2017 ; 6
(ä): 391
Nephropedia Template TP
gab.com Text
Twit Text FOAVip
Twit Text #
English Wikipedia
B-cell tolerance and autoimmunity
#MMPMID28408984
Tsubata T
F1000Res
2017[]; 6
(ä): 391
PMID28408984
show ga
Self-reactive B cells are tolerized at various stages of B-cell development and
differentiation, including the immature B-cell stage (central tolerance) and the
germinal center (GC) B-cell stage, and B-cell tolerance involves various
mechanisms such as deletion, anergy, and receptor editing. Self-reactive B cells
generated by random immunoglobulin variable gene rearrangements are tolerized by
central tolerance and anergy in the periphery, and these processes involve
apoptosis regulated by Bim, a pro-apoptotic member of the Bcl-2 family, and
regulation of B-cell signaling by various phosphatases, including SHIP-1 and
SHP-1. Self-reactive B cells generated by somatic mutations during GC reaction
are also eliminated. Fas is not directly involved in this process but prevents
persistence of GC reaction that allows generation of less stringently regulated B
cells, including self-reactive B cells. Defects in self-tolerance preferentially
cause lupus-like disease with production of anti-nuclear antibodies, probably due
to the presence of a large potential B-cell repertoire reactive to nucleic acids
and the presence of nucleic acid-induced activation mechanisms in various immune
cells, including B cells and dendritic cells. A feed-forward loop composed of
anti-nuclear antibodies produced by B cells and type 1 interferons secreted from
nucleic acid-activated dendritic cells plays a crucial role in the development of
systemic lupus erythematosus.
free
free
free
