MOI: project 12

Lymphotoxin ß receptor (LTβR)-mediated signaling pathways play an important role in both secondary lymphoid organogenesis and the immune response. LTβR-deficient mice (LTβR-/-) show increased susceptibility in various infection models. To further elucidate the role of LTβR, both a classical LTβR-deficient mouse line and cell type-specific LTβR deficient mouse lines are used in a Toxoplasma gondii (T. gondii) infection model. T. gondii is an obligate intracellular parasite that, like the causative agent of malaria, belongs to the Apicomplexa. The role of LTβR in T. gondii infection has been poorly elucidated. Our previous work has shown that LTβR-/- mice exhibit increased mortality, increased parasite burden, and immunopathologies in various organs compared with wild-type mice after Toxoplasma infection, show altered immune cell population composition, and are unable to produce Toxoplasma-specific IgG antibodies. Interestingly, we also observed, particularly in the lung, that expression of interferon-induced GTPases of the 65 kDa family (GBPs) is greatly reduced in LTβR-/- mice after infection. The molecular relationships underlying these changes are the subject of current research.