Cross-talk between apoptosis and cytokines in the regulation of parasitic infection

Apoptosis differentially regulates mesenteric and subcutaneous lymph node immune responses to Trypanosoma cruzi

“…This difference from previous results [17] could be related to the strain of T. cruzi or to the role of caspase-8 in T cell activation, proliferation and IL-2 production [41][42][43]. It has been reported that the blockade of caspase-8 in vivo impairs T cell responses in T. cruzi-infected mice, increasing both parasitemia and type-2 cytokine responses [33,44]. Therefore, it is likely that the blockade of capase-8 may also affect sustained T cell proliferation and regulation of cytokine responses, preventing the recovery of MLN in T. cruzi-infected mice.…”

Decoding caspase signaling in host immunity to the protozoan Trypanosoma cruzi

“…TCR signaling induces caspase-8 activity, which activates the NF-kB pathway, independently of death receptors or their ligands [46] (Figure 2). Therefore, a certain degree of caspase-8 activity is required during the development of immune responses to T. cruzi infection, as discussed elsewhere [50]. Nonetheless, later in the immune response to infection, caspase-8 induces apoptosis following Fas ligation in previously activated T cells.…”

Macrophages and neutrophils cooperate in immune responses to Leishmania infection

“…Onset of apoptosis induces phagocytic clearance of neutrophils that is important for resolution of inflammation and tissue repair [2]. Apoptosis and engulfment of apoptotic cells play immunoregulatory and pathogenic roles in parasitic infections [24]. Engulfment of apoptotic cells induces a biochemical cascade that deactivates macrophages through TGF-b, and drives replication of an intracellular parasite through ornithine decarboxylase activity and production of polyamines [25].…”