Immune competent mice eject the Strongyloides ratti after one month. Still, S. ratti is a successful parasite, as this limited time span is fully sufficient to reproduce, complete its life cycle and propagate its genes. To ensure survival for this one month, S. ratti, like most helminths, actively suppresses the immune response that is directed towards itself. We have shown that immune evasion is conveyed, among other pathways, by the expansion of Foxp3+ regulatory T lymphocytes (Treg) that antagonize IL-9 production and subsequent IL-9-mediated mast cell activation (Blankenhaus 2014 and 2011). This pathway was dominant in BALB/c mice where Treg depletion accelerated mast cell activation and reduced intestinal parasite burden. Interestingly, additional layers of regulation occurred in C57BL/6 mice that displayed a similar expansion of Treg but remained susceptible for S. ratti after Treg depletion. Next to Tregs that remain the primary regulatory pathway for maintaining peripheral tolerance, a complex network of co-inhibitory receptors acts as a second fine-tuning level of regulation. Infection with S. ratti increased expression of several co-inhibitory receptors on T cells in BALB/c and C57BL/6 mice. Of note, this induction was more pronounced in C57BL/6 mice (Hartmann 2021). Focusing on the co-inhibitory receptor B and T lymphocyte Attenuator (BTLA), we reported that either deficiency for BTLA or its ligand HVEM promoted the mast cell and IL-9-mediated anti-S. ratti immunity in C57BL/6 mice (Breloer 2015). Currently we investigate the impact of the addtional HVEM ligands LIGHT and CD160 in regulating anti-S. ratti immunity.