Objective: To determine the role of toll-like receptor 4(TLR-4) in eliciting cellular and humoral immune responses against recombinant Mycobacterium bovis bacille Calmette-Guérin(rB CG) expressing the C-terminus ...Objective: To determine the role of toll-like receptor 4(TLR-4) in eliciting cellular and humoral immune responses against recombinant Mycobacterium bovis bacille Calmette-Guérin(rB CG) expressing the C-terminus of merozoite surface protein-1 of Plasmodium falciparum. Methods: Six groups of mice(n=6 per group) were injected with phosphate buffered saline T80, BCG or r BCG intraperitoneally, in the presence or absence of a TLR-4 inhibitor; TAK-242. Enzyme-linked immunosorbent assay was carried out for serum total IgG, IgG 1, Ig G2 a and Ig G2 b determination. Spleens were also harvested and splenocytes cultured for determination of intracellular cytokines; IL-4 and IFN-毭 via enzyme-linked immunosorbent assay. Results: The production of total Ig G, and the subclasses Ig G1, Ig G2 a and Ig G2 b was significantly higher in rB CG-immunised mice than BCG and phosphate buffered saline immunised mice in the absence of TAK-242. A significant rise in total IgG occurred with more booster immunisations. The level of IgG 2 a was highest, followed by IgG 2 b, then IgG 1. The production of both IL-4 and IFN-were inhibited in t毭 was also highest in the rB CG immunised groups. These significant riseshe presence of TAK-242. Conclusions: We present evidence of the role of TLR-4 in the increased production of total IgG, IgG 1, IgG 2 a and IgG 2 b, as well as IL-4 and IFN-毭 in response to our rB CG construct.展开更多
基金supported by the Universiti Sains Malaysia(USM) Fundamental Research Grant Scheme(FRGS)(No.203/PPSK/6171158)
文摘Objective: To determine the role of toll-like receptor 4(TLR-4) in eliciting cellular and humoral immune responses against recombinant Mycobacterium bovis bacille Calmette-Guérin(rB CG) expressing the C-terminus of merozoite surface protein-1 of Plasmodium falciparum. Methods: Six groups of mice(n=6 per group) were injected with phosphate buffered saline T80, BCG or r BCG intraperitoneally, in the presence or absence of a TLR-4 inhibitor; TAK-242. Enzyme-linked immunosorbent assay was carried out for serum total IgG, IgG 1, Ig G2 a and Ig G2 b determination. Spleens were also harvested and splenocytes cultured for determination of intracellular cytokines; IL-4 and IFN-毭 via enzyme-linked immunosorbent assay. Results: The production of total Ig G, and the subclasses Ig G1, Ig G2 a and Ig G2 b was significantly higher in rB CG-immunised mice than BCG and phosphate buffered saline immunised mice in the absence of TAK-242. A significant rise in total IgG occurred with more booster immunisations. The level of IgG 2 a was highest, followed by IgG 2 b, then IgG 1. The production of both IL-4 and IFN-were inhibited in t毭 was also highest in the rB CG immunised groups. These significant riseshe presence of TAK-242. Conclusions: We present evidence of the role of TLR-4 in the increased production of total IgG, IgG 1, IgG 2 a and IgG 2 b, as well as IL-4 and IFN-毭 in response to our rB CG construct.