Examination of neonatal immunity in IL-13 receptor alpha 1 deficient mice

Abstract

[ACCESS RESTRICTED TO THE UNIVERSITY OF MISSOURI AT REQUEST OF AUTHOR.] Recent work in our lab has demonstrated a role for interleukin-13 receptor alpha 1 (IL-13R[alpha]1) in the induction of apoptosis of T helper type 1 (Th1) cells in the neonatal immune system. Apoptosis of Th1 cells results in neonatal Th2-bias, which confers susceptibility to both microbial infections and allergic reactions. Unfortunately, there have been few molecular tools developed to study IL-13R[alpha]1 in the mouse despite these findings. Therefore, in order to further examine the role of IL-13R[alpha]1 in neonatal immunity, and also in allergy and asthma, we developed a monoclonal antibody that detects IL-13R[alpha]1 and we have generated mice that deficient in the expression of IL-13R[alpha]1. Using these reagents, IL-13R[alpha]1 was found to influence the primary T helper cell response to antigen, which expands upon it's role, since the role of IL-13R[alpha]1 in apoptosis of neonatal Th1 cells was previously observed upon secondary encounter with antigen. Furthermore, we demonstrate that when IL-13R[alhpa]1 deficient T cells are transferred to wild-type BALB/c mice, neonatal Th2-bias is effectively reversed to yield a Th1-dominated response. These observations strengthen IL-13R[alpha]1's candidacy as a molecular target in neonatal vaccines and also in therapies to prevent the formation of allergies.