Deficit in dendritic cell-T cell interaction crucial in hepatitis B.

2004 AUG 4 - (NewsRx.com & NewsRx.net) -- A selective functional deficit in dendritic cell-T cell interactions is a crucial mechanism in chronic hepatitis B virus infection.

"A defect in specific T cell immunity has long been assumed to be the central mechanism of persistent Hepatitis B virus (HBV) infection. Recent studies on HBV transgenic mice have suggested. However, that functional deficit of dendritic cells (DC) was an underlying cause for the T cell dysfunction," investigators in China report.

"The functions of monocyte-derived DC were determined by studying 75 subjects that included chronic hepatitis B patients with low or high HBV load; antibody to hepatitis B surface antigen (anti-HBs)-positive individuals who had recovered completely from previous acute HBV infection; healthy donors who had received hepatitis B vaccination and were anti-HBs positive; and immunologically naive to HBV or the vaccine individual," said B. J. Zheng and collaborators at Fudan University, the University of Hong Kong, and Queen Elizabeth Hospital in Hong Kong. "Impaired interactions between monocyte-derived DC and T cells were shown in chronic HBV infection patients, especially in those with active virus replication."

The researchers reported, "The dysfunctions included: failure of DC to increase human leukocyte antigen (HLA-II), B7 expression and interleukin-12 secretion in responses to hepatitis B surface antigen (HBsAg); defective induction of T cell proliferative response to HbsAg; and failure to ...