In cutaneous leishmaniasis, the presence of peripheral lymph nodes (LN) is essential for driving a TH1 response and the absence of all LN in LTβR−/− mice leads to a marked susceptibility to the disease [48], whereas in visceral leishmaniasis, signaling through the LTβR is protective via promoting DC development and maturation [47]. The gene discussed is LTBR; the disease is visceral leishmaniasis.