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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 J+Immunol+Res
2017 ; 2017
(ä): 3475926
Nephropedia Template TP
gab.com Text
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English Wikipedia
HLA Class Ia and Ib Polyreactive Anti-HLA-E IgG2a Monoclonal Antibodies (TFL-006
and TFL-007) Suppress Anti-HLA IgG Production by CD19+ B Cells and Proliferation
of CD4+ T Cells While Upregulating Tregs
#MMPMID28634589
Ravindranath MH
J Immunol Res
2017[]; 2017
(ä): 3475926
PMID28634589
show ga
The anti-HLA-E IgG2a mAbs, TFL-006 and TFL-007, reacted with all HLA-I antigens,
similar to the therapeutic preparations of IVIg. Indeed, IVIg lost its HLA
reactivity, when its HLA-E reactivity was adsorbed out. US-FDA approved IVIg to
reduce antibodies in autoimmune diseases. But the mechanism underlying
IVIg-mediated antibody reduction could not be ascertained due to the presence of
other polyclonal antibodies. In spite of it, the cost prohibitive high or low
IVIg is administered to patients waiting for donor organ and for allograft
recipients for lowering antiallograft antibodies. A mAb that could mimic IVIg in
lowering Abs, with defined mechanism of action, would be highly beneficial for
patients. Demonstrably, the anti-HLA-E mAbs mimicked several functions of IVIg
relevant to suppressing the antiallograft Abs. The mAbs suppressed activated T
cells and anti-HLA antibody production by activated B cells, which were dose-wise
superior to IVIg. The anti-HLA-E mAb expanded CD4+, CD25+, and Foxp(3)+ Tregs,
which are known to suppress T and B cells involved in antibody production. These
defined functions of the anti-HLA-E IgG2a mAbs at a level superior to IVIg
encourage developing their humanized version to lower antibodies in allograft
recipients, to promote graft survival, and to control autoimmune diseases.
|Adult
[MESH]
|Antibodies, Monoclonal/metabolism
[MESH]
|Antibody Formation
[MESH]
|Antigens, CD19/metabolism
[MESH]
|Autoimmune Diseases/immunology/*therapy
[MESH]
|B-Lymphocytes/*immunology
[MESH]
|CD4-Positive T-Lymphocytes/*immunology
[MESH]
|Cell Proliferation
[MESH]
|Cost-Benefit Analysis
[MESH]
|Female
[MESH]
|Forkhead Transcription Factors/metabolism
[MESH]
|Graft Rejection/immunology/*prevention & control
[MESH]
|HLA Antigens/immunology
[MESH]
|HLA-E Antigens
[MESH]
|Histocompatibility Antigens Class I/immunology
[MESH]
|Humans
[MESH]
|Hybridomas
[MESH]
|Immunoglobulin G/metabolism
[MESH]
|Immunoglobulins, Intravenous/*therapeutic use
[MESH]