| Summary: | In Brucellosis, the role of hepatic stellate cells (HSCs) in the induction of liver fibrosis has been elucidated recently. Here, we study how the infection modulates the antigen-presenting capacity of LX-2 cells. <i>Brucella abortus</i> infection induces the upregulation of class II transactivator protein (CIITA) with concomitant MHC-I and -II expression in LX-2 cells in a manner that is independent from the expression of the type 4 secretion system (T4SS). In concordance, <i>B. abortus</i> infection increases the phagocytic ability of LX-2 cells and induces MHC-II-restricted antigen processing and presentation. In view of the ability of <i>B. abortus</i>-infected LX-2 cells to produce monocyte-attracting factors, we tested the capacity of culture supernatants from <i>B. abortus</i>-infected monocytes on MHC-I and –II expression in LX-2 cells. Culture supernatants from <i>B. abortus</i>-infected monocytes do not induce MHC-I and -II expression. However, these supernatants inhibit MHC-II expression induced by IFN-γ in an IL-10 dependent mechanism. Since hepatocytes constitute the most abundant epithelial cell in the liver, experiments were conducted to determine the contribution of these cells in antigen presentation in the context of <i>B. abortus</i> infection. Our results indicated that <i>B. abortus</i>-infected hepatocytes have an increased MHC-I expression, but MHC-II levels remain at basal levels. Overall, <i>B. abortus</i> infection induces MHC-I and -II expression in LX-2 cells, increasing the antigen presentation. Nevertheless, this response could be modulated by resident or infiltrating monocytes/macrophages.
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