Thymosin-α1 increases intrahepatic NKT cells and CTLs in patients with chronic hepatitis B

Compartmentalization and its implication for peripheral immunologically‐competent cells to the liver in patients with HBV‐related acute‐on‐chronic liver failure

“…Lymphocyte infiltration into tissue is a multi‐step process mediated by interactions between multiple adhesion molecules, chemokines, and chemokine receptors 21,22 . Lymphocyte trafficking to the liver is a primary immunosurveillance mechanism, but persistent lymphocyte infiltration into the liver results in chronic inflammation, liver damage, and eventually fibrosis and cirrhosis 23,24 . In fact, intrahepatic lymphocyte response is essential for viral clearance or control in HBV infection 25,26 .…”

Impaired function of hepatic natural killer cells from murine chronic HBsAg carriers

“…In addition, intrahepatic NKT cells activated by IL-18 inhibited HBV replication in the liver of HBV transgenic mice [31]. NKT cells augmented in the liver by T-alpha1 may eliminate HBV infected hepatocytes [72]. Recently, other nonclassical NKT cells that are CD1d restricted but nonreactive to a-GalCer are activated in response to hepatocytes expressing hepatitis B viral antigens in a transgenic mouse model of acute HBV infection [73].…”

The efficacy and safety of thymosin alpha‐1 in Japanese patients with chronic hepatitis B; results from a randomized clinical trial

“…Tα1 is a 28‐amino acid polypeptide which was originally isolated from bovine thymus extract (thymosin fraction 5) and is now chemically synthesized [21]. Tα1 treatment leads to the inhibition of chronic viral infection through a mechanism of cellular immune response modulation via an increase in the secretion of interferon‐alpha, interferon‐gamma, and cytokines such as IL‐2, IL‐3, and the differentiation and maturation of T cells [11,19]. Tα1 also increases T‐cell populations by blocking apoptosis [22] and increases natural killer (NK) cell activity in multiple animal models and normal human subjects [11].…”