Hepatitis B Virus Researchers Make Important Discovery in the Field of Immunology

[sorte]

http://hepatitisnewstoday.com/2015/05/19/hepatitis-b-virus-researchers-make-important-discovery-field-immunology/

This week, a group of interdisciplinary researchers from the University College London (UCL) released study findings in which they made a discovery that could have important implications in several clinical disciplines. The study entitled, “Metabolic regulation of hepatitis B immunopathology by myeloid-derived suppressor cells,” focused on the reasons why the immune system cannot control hepatitis B virus (HBV) infection once it becomes established in the liver, and the findings could potentially lead to new therapeutic drug targets to treat HBV infections. The study was published in the latest edition of Nature: Medicine....

[studyforhope]

I also doubt that supplemental arginine can completely restore T cell function, but it might help substantially to improve it. It is well known that nitric oxide in the liver acts as a critical hbv suppressing agent and it is likely also involved in T cell activation mechanisms beyond that. Thus addition of 4 times a gram of oral  l arginine per day might well speed up immune elimination mechanisms.

I don't know about a relationship of arginine to carnitine metabolism.

[stef2011]

http://www.bloodjournal.org/content/109/4/1568?sso-checked=true

l-arginine availability regulates T-lymphocyte cell-cycle progression


http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3519282/

Metabolism of L-Arginine by Myeloid-Derived Suppressor Cells in Cancer: Mechanisms of T cell suppression and Therapeutic Perspectives

[stef2011]

dont know if this has anything to do with our situation.we may try although it sounds to easy to reverse cd8 to full activity by simply taking arginine

http://www.jbc.org/content/277/24/21123.full.html

In addition, the work presented here suggests that the CD3ζ down-regulation induced by L-Arg starvation is not caused by apoptosis but rather through post-transcriptional mechanisms that decrease the half-life of the CD3ζ mRNA. This process is completely reversible by the replenishment of L-Arg.

[stef2011]

has carnitine anything to do with this scenario or with arginine?

i remember that a trial of adv plus peg found lowest carnitine levels on those with hbsag loss
http://www.ncbi.nlm.nih.gov/pubmed/24824278

[studyforhope]

one wonders if orally supplied l arginine might help to activate these t cells.

[studyforhope]

Metabolic regulation of hepatitis B immunopathology by myeloid-derived suppressor cells.
Pallett LJ1, Gill US2, Quaglia A3, Sinclair LV4, Jover-Cobos M5, Schurich A1, Singh KP1, Thomas N1, Das A1, Chen A1, Fusai G5, Bertoletti A6, Cantrell DA4, Kennedy PT2, Davies NA5, Haniffa M7, Maini MK1.
Author information

Abstract
Infection with hepatitis B virus (HBV) results in disparate degrees of tissue injury: the virus can either replicate without pathological consequences or trigger immune-mediated necroinflammatory liver damage. We investigated the potential for myeloid-derived suppressor cells (MDSCs) to suppress T cell-mediated immunopathology in this setting. Granulocytic MDSCs (gMDSCs) expanded transiently in acute resolving HBV, decreasing in frequency prior to peak hepatic injury. In persistent infection, arginase-expressing gMDSCs (and circulating arginase) increased most in disease phases characterized by HBV replication without immunopathology, whilst L-arginine decreased. gMDSCs expressed liver-homing chemokine receptors and accumulated in the liver, their expansion supported by hepatic stellate cells. We provide in vitro and ex vivo evidence that gMDSCs potently inhibited T cells in a partially arginase-dependent manner. L-arginine-deprived T cells upregulated system L amino acid transporters to increase uptake of essential nutrients and attempt metabolic reprogramming. These data demonstrate the capacity of expanded arginase-expressing gMDSCs to regulate liver immunopathology in HBV infection.