We review here the role that sex steroids play in experimental intraperitoneal Taenia crassiceps cysticercosis of male and female BalbC/AnN mice. Briefly, estrogens favour and androgens hinder the reproduction of cysticerci by at least two main mechanisms: 1) through estradiol tilting the TH2/TH1 immune system balance towards parasite-permissive TH2 response,which is IL-6 dependent mediating P450-aromatase over expression, shunting testosterone towards estradiol and thus creating a positive feed-back loop which progressively favours TH2 response, blocking in turns TH1 and furthers parasite growth; and 2) estrogens and androgens acting directly upon the cysticercus reproductive system, favoring or hindering, respectively, its asexual reproduction. Later infection, when parasite loads are for milliars, male mice become estrogenized, deandrogenized and diminish their copulative, aggressive and social behaviors in association with P450-aromatase testis overexpression. Changes in c-fos expression in different areas of the infected mice brain point to the additional connection of the central nervous system with the infection driven events, which senses and perhaps reacts to infection with behavioral changes. This complex immune-neuro-endocrine network management of parasite loads in murine cysticercosis, and its physiological and behavioral consequences upon the host, may be operative in other infections of mammals. Such complexity may also help to explain the often conflicting results, observed between infections with respect to the role of the host sex, and hints to other avenues of research and strategies for their treatment and control.