Hard science versus phenomenology in reproductive immunology.

It has been suggested that studies of immunological aspects of reproduction have recently changed from the phenomenological (e.g., speculative/descriptive) to hard science (e.g., precise molecular description/ explanation). The significance of this development is explored by analysis of the contribution made by hard science that has led to a number of assertions. Does HLA-G determine maternal tolerance of her semi-allogeneic fetus? Do differences in placentation between humans, rodents, and other species make direct comparisons largely meaningless? Does membrane cofactor protein (CD46) contribute to pregnancy success by protecting sperm and fetal trophoblast from complement-mediated lysis? Does a low frequency in mice of maternal T cells specific for paternal alloantigens occur, and if so, does phenomenon explain specific maternal tolerance in pregnancy? Do placental and decidual macrophage components provide an important immediate antigen-nonspecific host defense to infection? Does the mix of bioactive molecules make the uterus an immunologically privileged site, and does the molecular melange have a pivotal role in promoting growth and development of the placenta and embryo? Does prolactin acting on receptors on lymphocytes suppress function and thereby account for remission of autoimmune disease in pregnant women? Is the efficacy and safety of immunotherapy for recurrent spontaneous abortion a thorny issue that will be resolved by an ongoing funded national trial? What is a scientifically correct timeline of important discoveries and developments in reproductive immunology? It is argued that it is unprofitable to divorce phenomenology from hard science and that the timeline for developments in reproductive immunology begin with Darwin. Irrespective of whether one is dealing with phenomena or hard science data, Hippocrates was correct in his aphorism that "description is infinite and easy; explanation is limited and difficult".