These results point towards a major role for the LTβR in an efficient immune response to T. gondii and are in accordance with other studies suggesting that the LTβR acts as an important immune regulator, not only in bacterial infection models for listeriosis or tuberculosis [5, 43, 44] but also in intracellular parasite infection models for malaria [45, 46] or leishmaniasis [47–50]. The gene discussed is LTBR; the disease is malaria.