We previously reported that xenografted bovine secondary follicles developed to the antral stage in severe combined immunodeficient (SCID) mice. In the present study, bovine secondary follicles 100–240 μm in diameter were xenografted under the kidney capsules of female SCID mice for 6 and 8 weeks, and we examined the oocytes' fertilization and developmental abilities. Bovine follicles developed with prolongation of grafting and became significantly larger than those before grafting. Injection of equine chorionic gonadotropin (eCG) into host mice made some surviving follicles develop larger than the other follicles. Furthermore, bovine oocytes grew in the follicles, and the mean diameter of the oocytes was 100 μm or more at 6 and 8 weeks of transplantation. Bovine oocytes that had grown in eCG-stimulated SCID mice 8 weeks after grafting were subjected to maturation culture. Some of the oocytes that had grown to 110 μm or more matured to the second metaphase (7% of oocytes 110–119 μm and 44% of those >120 μm). When the oocytes were inseminated with bovine spermatozoa, 15% (6/39) formed a female and a male pronucleus, and 2 days after insemination 24% (18/75) of oocytes cleaved and 2% (2/75) developed to the 5- to 8-cell stage. However, no embryo reached the blastocyst stage. These results indicate that bovine oocytes grown in SCID mice could be fertilized but acquired insufficient competence for embryonic development in the present conditions.

Resistance to the murine intestinal nematode Trichuris muris requires the development of a strong Th2 response. In a reconstituted SCID mouse model, CD4+ Th2 cells can mediate resistance to infection in the absence of antibody (Else & Grencis, 1996). The data presented here address the issue of how CD4+ T cells mediate this protective immunity within the SCID host. These studies demonstrate that timing and cell dose are critical if transfer is to result in resistance, with a minimum of 5 × 106 immune donor cells required to confer immunity. Furthermore, this CD4-mediated protective immunity only operates against the larval stages of the parasite. When the molecules necessary for activated CD4+ T cell migration to the GALT are inhibited with a cocktail of anti-integrin/addressin antibodies (anti-β7, anti-MAdCAM-1 and anti-αE), the resistance conferred by immune donor cells is completely abrogated. This implies that the effector mechanism acts locally at the level of the gut. CD4+ mediated cytotoxicity, directed against the epithelial cells inhabited by the parasite, could represent a novel, locally acting effector mechanism. However, Fas and Fas ligand-deficient mice, which are unable to mount CD4-mediated cytotoxic responses, readily expel T. muris indicating that the mechanism by which CD4+ T cells mediate protective immunity is unlikely to involve killing of infected gut epithelial cells.