Generation of non-specific and specific B cell responses to the Trypanosoma cruzi B cell Mitogen TcPRAC (129.4)

• Published in: The Journal of immunology (1950) 2009-04, Vol.182 (1_Supplement), p.129-129.4
• Main Authors: Bryan, Marianne A, Norris, Karen A
• Format: Article
• Language: English
• ISSN: 0022-1767; 1550-6606
• DOI: 10.4049/jimmunol.182.Supp.129.4

Acute Trypanosoma cruzi infection results in polyclonal B cell activation and a delay of specific humoral immunity. TcPRAC, a T. cruzi B cell mitogen may contribute to this dysfunction. Stimulation of splenocytes with TcPRAC induced B cell proliferation, secretion of IgM and IL-10, and up-regulation of CD69 and CD86. During experimental infection, TcPRAC specific IgG was undetectable when responses to other T. cruzi antigens developed. Genetic immunization generated TcPRAC specific IgG without apparent B cell dysfunction. TcPRAC immune sera inhibited TcPRAC-induced B cell proliferation in vitro. These results suggest that TcPRAC may contribute to delayed specific antibody development during experimental infection by non-specifically activating B cells and inducing IL-10 and non-specific IgM secretion. In addition, we demonstrated that while TcPRAC was not antigenic during experimental infection, delivery of TcPRAC via genetic immunization elicited specific antibodies. Further experiments will analyze the effect of TcPRAC immunization and neutralization on the generation of T. cruzi specific humoral immunity during early acute phase infection.