Maternal tolerance is not critically dependent on interleukin‐4

• Published in: Immunology 2001-07, Vol.103 (3), p.382-389
• Main Author: Bonney, Elizabeth A.
• Format: Article
• Language: English
• Subjects: Animals; antigen H-Y; Cytotoxicity, Immunologic; Female; Fertility - immunology; Fetal Death - immunology; Graft Rejection - immunology; H-Y Antigen - immunology; Immune Tolerance; Interleukin-4 - deficiency; Interleukin-4 - immunology; Male; Maternal-Fetal Exchange - immunology; Mice; Mice, Inbred C57BL; Original; Pregnancy; Pregnancy, Animal - immunology; Sex Factors; Skin Transplantation - immunology; Th2 Cells - immunology
• ISSN: 0019-2805; 1365-2567
• DOI: 10.1046/j.1365-2567.2001.01239.x

Summary Pregnant animals can generate and maintain immune responses to fetal antigens. This however, does not usually lead to fetal loss. At least two types of immune response are recognized. T helper type 1 (Th1) responses support the generation of cellular cytotoxicity. In contrast, Th2‐type responses support the production of non‐cytotoxic antibody and suppress the Th1‐type. One attempt to explain why the fetus is not generally rejected has been to suggest that during pregnancy Th2‐type responses are dominant. These responses rely heavily on interleukin‐4 (IL‐4) for both functions. This work focuses on maternal immunity to the male antigen H‐Y, which is expressed in male fetuses. When injected with male spleen cells, female mice of certain strains mount a cytotoxic immune response to H‐Y. However, pregnant females immunized in this way do not deliver litters with fewer males. To help delineate the possible role of IL‐4 in such maternal tolerance, female mice genetically deficient in IL‐4 were studied. The results show that: (1) deficiency in maternal IL‐4 does not affect fertility, (2) deficiency in IL‐4 is not associated with selective loss of male offspring in unimmunized mice, (3) pregnancy does not obliterate anti‐H‐Y reactivity in immunized mice and (4) maternal immunity to H‐Y in the absence of IL‐4 does not result in loss of male offspring. The results suggest that IL‐4‐dependent Th2‐type responses are not critical to maternal tolerance. Other cytokines must be examined for their role in this phenomenon.