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The hepatitis B virus core and e antigens elicit different Th cell subsets: antigen structure can affect Th cell
D R Milich1, F Schödel, J L Hughes
1Department of Molecular Biology, The Scripps Research Institute, La Jolla, California 92037, USA.
Journal of Virology
|March 1, 1997
Summary
Hepatitis B virus core antigen (HBcAg) preferentially induces Th1 immune responses, while hepatitis B virus e antigen (HBeAg) induces Th2 responses. This structural difference in immunogen influences T helper cell differentiation, potentially impacting chronic HBV infection outcomes.
Area of Science:
- Immunology
- Virology
Background:
- The function of secreted hepatitis B virus e antigen (HBeAg), a viral nucleoprotein, is not fully understood.
- HBeAg is suggested to act as an immunomodulator, potentially influencing T helper cell responses.
Purpose of the Study:
- To investigate whether the particulate hepatitis B virus core antigen (HBcAg) and nonparticulate HBeAg preferentially elicit different T helper (Th) cell subsets.
- To determine the impact of antigen structure on Th cell differentiation and its relevance to chronic HBV infection.
Main Methods:
- Mice were immunized with recombinant HBcAg and HBeAg, with and without adjuvants.
- Immunoglobulin G (IgG) isotype profiles of anti-HBc and anti-HBe antibodies were analyzed.
- In vitro cytokine production by HBcAg- and HBeAg-primed Th cells was measured.
Main Results:
- HBcAg immunization induced primarily IgG2a/IgG2b anti-HBc antibodies and Th1-associated cytokines (IL-2, IFN-gamma).
- HBeAg immunization induced predominantly IgG1 anti-HBe antibodies and Th2-associated cytokine (IL-4).
- Antigen structure, not just specificity, dictated Th cell subset development, though this could be modulated by cytokine treatment.
Conclusions:
- HBcAg preferentially elicits Th1-like cells, while HBeAg preferentially elicits Th2-like cells.
- Circulating HBeAg may suppress antiviral clearance by promoting anti-inflammatory Th2 responses.
- Antigen structure is a key determinant of Th cell phenotype, with implications for HBV pathogenesis and therapy.