Pam3CSK4 is a synthetic bacterial lipopeptide that binds to and acts as an agonist at toll-like receptor 2 (TLR2).[1] It induces proliferation of isolated mouse spleen cells and activates lymphocytes at a concentration of 50 µg/ml.[2] Pam3CSK4 is a potent immune adjuvant in mice, enhancing the response to antigen, as measured by IgM and IgG levels, when used at a dose of 200 µg/animal. It inhibits Th1 and Th2 responses, suppresses eosinophil infiltration, and induces CD4+ T cell apoptosis in a mouse model of allergic conjunctivitis.[3] Pam3CSK4 (50 µg) decreases lesion size and parasite burden in genetically-resistant and -susceptible mice when administered with L. major to induce leishmaniasis.[4] It also enhances Th1 responses and stimulates IL-17 production in the early phase of infection.
Reference:
[1]. Vasselon, T., Detmers, P.A., Charron, D., et al. TLR2 recognizes a bacterial lipopeptide through direct binding. J. Immunol. 173(12), 7401-7405 (2004).
[2]. Reitermann, A., Metzger, J., Wiesmüller, K.H., et al. Lipopeptide derivatives of bacterial lipoprotein constitute potent immune adjuvants combined with or covalently coupled to antigen or hapten. Biol. Chem. Hoppe Seyler 370(4), 343-352 (1989).
[3]. Fukushima, A., Yamaguchi, T., Ishida, W., et al. TLR2 agonist ameliorates murine experimental allergic conjunctivitis by inducing CD4 positive T-cell apoptosis rather than by affecting the Th1/Th2 balance. Biochem. Biophys. Res. Commun. 339(4), 1048-1055 (2006).
[4]. Huang, L., Hinchman, M., and Mendez, S. Coinjection with TLR2 agonist Pam3CSK4 reduces the pathology of leishmanization in mice. PLoS Negl. Trop. Dis. 9(3), e0003546 (2015).