tetano
Editor, Senior Moderator
Vopr Virusol. 2012 Nov-Dec;57(6):5-8.
[Immunosuppression at pregnancy and flu].
[Article in Russian]
[No authors listed]
Abstract
The hypothesis of the development of immunosuppression at the pregnancy is put forward in this review. This hypothesis is explaining the complicated character of the pandemic H1N1pdm09 infection among pregnant women. Physiological immunosuppression at pregnancy is based on suppression of various T-lymphocyte subpopulations using a unique mechanism: dimerization blockade of TcR receptors by special domains known as immunosuppressive sequences. These protein sequences were recognized in placentary Syntcytins and in proteins of pathogenic viruses, including Ebola virus and retroviruses. Among H5N1 and H1N1pdm09 influenza virus homologs of immunosuppressive domains are revealed and identified as the pathogenicity factors. Synthetic peptides, homologs of these domains, suppress an antigen-induced T-lymphocyte proliferation by inhibiting of TcR and NKG2D receptor activation. Integration of immunosuppressive domains into T-lymphocyte membrane leads to electrostatic pair formation and dimerization through interaction with transmembrane domains of TcR and NKG2D receptors.
PMID:
23477246
[PubMed - in process]
http://www.ncbi.nlm.nih.gov/pubmed/23477246
[Immunosuppression at pregnancy and flu].
[Article in Russian]
[No authors listed]
Abstract
The hypothesis of the development of immunosuppression at the pregnancy is put forward in this review. This hypothesis is explaining the complicated character of the pandemic H1N1pdm09 infection among pregnant women. Physiological immunosuppression at pregnancy is based on suppression of various T-lymphocyte subpopulations using a unique mechanism: dimerization blockade of TcR receptors by special domains known as immunosuppressive sequences. These protein sequences were recognized in placentary Syntcytins and in proteins of pathogenic viruses, including Ebola virus and retroviruses. Among H5N1 and H1N1pdm09 influenza virus homologs of immunosuppressive domains are revealed and identified as the pathogenicity factors. Synthetic peptides, homologs of these domains, suppress an antigen-induced T-lymphocyte proliferation by inhibiting of TcR and NKG2D receptor activation. Integration of immunosuppressive domains into T-lymphocyte membrane leads to electrostatic pair formation and dimerization through interaction with transmembrane domains of TcR and NKG2D receptors.
PMID:
23477246
[PubMed - in process]
http://www.ncbi.nlm.nih.gov/pubmed/23477246