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Filarial Parasites Develop Faster and Reproduce Earlier in Response to Host Immune Effectors That Determine Filarial Life Expectancy

Figure 3

Adaptive immunity accelerates early larval development of L. sigmodontis despite impeding its sexual maturation.

(A) Cell recruitment increased significantly over time during infection when filariae were inoculated into rag−/−, il4−/− and double deficient (rag−/−il-4−/−) mice that lack T cells, B cells, and IL-4, but was severely lower overall in rag−/−il-4−/− than in C57BL/6 wild type controls. (B) Filarial larvae in rag−/−il-4−/− mice developed slowest unless rIL-5 was added upon their delivery to the host. (C) However, by D30 p.i. the parasites in rag−/−il-4−/− mice had compensated for their slower development and reached the adult stage earlier than in wild type controls, likely due to the continuous attack by eosinophils and other inflammatory cells in the control mice (see Figure S3A). (D) This resulted in the release of more offspring in rag−/−il-4−/− mice than what is observed in susceptible immunocompetent BALB/c mice. * p<0.05; ** p<0.01, Wilcoxon rank-sum test; n = 5–10 mice per group. Error bars represent s.e.m.

Figure 3