Subclass restriction of immunoglobulin G in liver cirrhosis

Abstract

The serum immunoglobulin G (IgG) subclasses were determined in 41 patients with liver cirrhosis (LC) and in 15 normal controls. In 19 cases of LC and in 6 normal controls, the IgG subclasses were also determined in lymphocyte culture supernatants. The determinations were performed by enzyme immunoassay. It was found that the absolute mean IgG1 and IgG3 levels were increased in all LC due to various causes. The mean IgG1 increase was most pronounced in post-hepatitic LC, and the mean percentage of IgG1 to total IgG was also increased in this type of LC in comparison with the normal controls and the other types of LC. The IgG3 fraction was significantly increased in primary biliary cirrhosis (PBC). In alcoholic LC, all IgG subclasses were increased significantly in comparison with normal controls. In lymphocyte culture supernatants from PBC patients, the mean IgG1 and IgG3 levels were increased in supernatants from unstimulated cultures, and the mean IgG1, IgG3, and IgG4 were increased after pokeweed mitogen (PWM) stimulation. In post-hepatitic LC, the mean IgG4 level was increased in both unstimulated culture supernatants and after PWM stimulation. In alcoholic LC, the mean IgG4 level was increased in unstimulated culture supernatants, whereas the mean IgG1 level was increased after PWM stimulation. These findings showed that LC of differing aetiologies exhibited different profiles of IgG subclasses. This may be related to the different aetiological agents and the pathogenesis of the different types of LC.

Diverse IgG subclass responses to adeno‐associated virus infection and vector administration

“…Plates were incubated at 37 degrees for two hours. Plates were wa[Akbar et al, 1990]shed four times and then incubated with streptavidin-HRP at a dilution of 1:2000 for two hours at room temperature. Finally, plates were washed four times with wash buffer and developed with an OPD sodium citrate buffer (1mg/mL) (Sigma) containing hydrogen peroxide.…”

“…Antibodies to Hepatitis B vary in subclass specificity based on whether the primary exposure was to recombinant protein (IgG1), recombinant DNA (IgG1 and IgG2) or a natural infection (IgG1 and IgG3) [Borzi et al, 1992; Carotenuto et al, 1995; Wang et al, 2005]. Moreover, carriers of hepatitis (IgG1>IgG3) can be distinguished from hepatitis-infected individuals undergoing liver cirrhosis (IgG3>IgG1) based on IgG subclass profiles [Akbar et al, 1990; Torgano et al, 1995]. Primary and secondary exposure to viruses can also be distinguished by IgG subclasses in the case of herpesvirus, respiratory syncytial virus, measles virus and dengue virus [El Mubarak et al, 2004; Hashido and Kawana, 1997; Koraka et al, 2001; Wagner et al, 1989].…”

Immunoglobulin G subclass antibodies to rubella virus in chronic liver disease, acute rubella and healthy controls

“…No consistent changes of IgG subclass profiles have been described in chronic liver disease, but some patients with alcoholic liver disease may show an increase in all subclasses [37]. The cause of the hypergammaglobulinemias seen in various chronic liver diseases (raised IgG in AICAH and certain cirrhoses, IgM in PBC and IgA in alcoholic liver disease [38]) is not known, but T-lymphocyte dysfunction of B-lymphocyte regulation has been suggested [7,36,39,40].…”