REGULATORY CYTOKINE ENVIRONMENT AS A PATHOGENIC MECHANISM FOR HBV PERSISTANCE (46.13)

• Published in: The Journal of immunology (1950) 2007-04, Vol.178 (1_Supplement), p.S63-S63
• Main Authors: Berrueta, Lisbeth, Barboza, Luisa, Salmen, Siham, Goncalves, Loredana, Colmenares, Melisa, Peterson, Darrell, Montes, Henry, Cartagirone, Raimondo, Gutierrez, Maria del Carmen
• Format: Article
• Language: English
• ISSN: 0022-1767; 1550-6606
• DOI: 10.4049/jimmunol.178.Supp.46.13

The T cell response to HBV has been shown to be vigorous in patients with acute hepatitis who clear the virus, whereas it is weak and narrowly focused in patients with chronic disease. We hypothesized that inappropriate early activation events of T cells could contribute to viral persistence during chronic infection. Therefore, we investigated the induction of activation receptors and cytokine production in lymphocytes stimulated with HBcAg, in a group of chronically infected patients and naturally immune subjects. Chronic patients did not increase CD40L or CD69 following stimulation, compared to subjects that resolved the infection. The presence of a CD4+CD25+ cell population was observed which produced elevated levels of IL-10 and TGF-β following specific stimulation with HBcAg, cytokines that are known to be suppressors of the immune response. These results suggest that a predominant inhibitory environment may be responsible for altered T cell costimulation, representing a mechanism for viral persistence.