In current literatures, one of the most documented effector biological mechanisms to helminthes and schistosomes in particular involve the role of Th 1 (cell-mediated), Th 2 (humoral mediated), responses and IgE antibodies. In addition, glutathione S-transferase (GST), is one of the best studied and understood parasitic antigen. Research emanating from the Institute Pasteur by Capron et al. demonstrate that IgE and eosinophils play a protective role in the schistosome infection while T helper cells (Th1) is involved in protection and Th2 is involved in immunopathology. Immune response to parasite infection can shift dramatically especially with the deposition of eggs in certain tissues like the liver. According to Lebens et al., granuloma formation is first mediated by major histocompataability complex (MHC II) CD4+ antigen-specific T-helper cells. First the deposited eggs elicit Th1 dominated response which is marked by the production of pro-inflamatory cytokine including Interleukin (IL)-12, Interferon-gamma (INF-gamma), and Tumor necrosis factor alpha (TNF-alpha). As the disease transforms from the acute state to later chronic stages, the Th2 dominated response mechanism leads to the production of anti-inflamatory cytokine including Interleukin (IL-4, -5, -10, and -13). This is a co-evolving mechanism as the Th1 is more damaging in the short-term but the immunomodulation by Th2 offsets tissue damages which allows for the parasite to survive longer without causing the human host significant damages. Studies in which mice were biased toward the Th1 immune response mechanism following the infection lead to the realization that Th1 is more damaging to the parasite-host relationship. Therefore, the balance between Th1 and Th2 in immunomodulation can be further exploited for vaccine development.