TLR2 Mediates Immunity to Experimental Cysticercosis

• Main Author: José L. Reyes, Marisol I. González, Yadira Ledesma-Soto, Abhay R. Satoskar, Luis I. Terrazas
• Format: Article
• Language: English
• Published: Ivyspring International Publisher 2011-01-01
• Series: International Journal of Biological Sciences
• Online Access: http://www.biolsci.org/v07p1323.htm

<p>Information concerning TLR-mediated antigen recognition and regulation of immune responses during helminth infections is scarce. TLR2 is a key molecule required for innate immunity and is involved in the recognition of a wide range of viruses, bacteria, fungi and parasites. Here, we evaluated the role of TLR2 in a <i>Taenia crassiceps</i> cysticercosis model. We compared the course of <i>T. crassiceps</i> infection in C57BL/6 TLR2 knockout mice (TLR2^-/-) with that in wild type C57BL/6 (TLR2^+/+) mice. In addition, we assessed serum antibody and cytokine profiles, splenic cellular responses and cytokine profiles and the recruitment of alternatively activated macrophages (AAM&#966;s) to the site of the infection. Unlike wild type mice, TLR2^-/- mice failed to produce significant levels of inflammatory cytokines in either the serum or the spleen during the first two weeks of <i>Taenia</i> infection. TLR2^-/- mice developed a Th2-dominant immune response, whereas TLR2^+/+ mice developed a Th1-dominant immune response after <i>Taenia</i> infection. The insufficient production of inflammatory cytokines at early time points and the lack of Th1-dominant adaptive immunity in TLR2^-/- mice were associated with significantly elevated parasite burdens; in contrast, TLR2^+/+mice were resistant to infection. Furthermore, increased recruitment of AAM&#966;s expressing PD-L1, PD-L2, OX40L and mannose receptor was observed in TLR2^-/- mice. Collectively, these findings indicate that TLR2-dependent signaling pathways are involved in the recognition of <i>T. crassiceps</i> and in the subsequent activation of the innate immune system and production of inflammatory cytokines, which appear to be essential to limit infection during experimental cysticercosis.</p>