Genetic regulation of the antibody response to the parasite Ascris spp

Abstract

The nematode Ascaris spp. causes ascariasis in humans and pigs. Ascariasis in humans causes anemia, growth retardation and cognitive deficit, being one of the most prevalent helminthiases around the world. The infection in pigs is an ideal model to study immunological aspects of ascariasis in humans. In both hosts, worm loads are aggregated, with few individuals harboring the highest worm burden which may be attributed to genetic factors. The locus 13q33 has been linked as a QTL for Ascaris susceptibility and total IgE in humans being TNFSF13B (encoding for the cytokine B cell activating factor-BAFF) the major positional candidate gene. A tagSNP in TNFSF13B was associated with the levels of IgG to Ascaris and IgE to ABA-1 in a Colombian population but causal variants remained to be explored. This thesis aimed to analyze the genetic regulation of the antibody response to Ascaris including this genomic region (13q33) and other candidate regions related to type-2 (Th2) immunity, as well as to analyze the relationship between BAFF and the strength of the antibody response to Ascaris, in order to get a better understanding of the role of TNFSF13B/BAFF in the mechanisms of Ascaris susceptibility/resistance using human and pig data under different purposes.