The mechanism behind these effects is unknown, and whether there is an immunological basis has yet to be explored. The majority of controlled trials of vaccine efficacy have focused on vaccine specific antibody (Ab) responses to test vaccine efficacy, and few studies have investigated T cell memory induction, despite the fact that it is likely to be critical for long term protection. Indeed, the cellular response to MV seems to be crucial in protecting against severe disease and death, and cellular responses are required to protect against Bordetella pertussis infection. Live vaccines such as bacillus Calmette-Guerin (BCG) and MV have been shown to stimulate Th1 type immune responses. The immune response to DTwP, a killed vaccine, tends to be Th2 biased in early life, despite the fact that the whole cell pertussis component biases towards a Th1 response. DTwP contains an aluminium based adjuvant, aluminium hydroxide, which is excellent at promoting humoral and Th2 responses, but poor at generating good cell mediated immunity and long term T cell memory. This polarisation of cellular reactivity to live and killed vaccines may explain why administering a killed vaccine with a live vaccine abrogates the beneficial effect of the live vaccine. Conversely, administering a live vaccine after DTwP may cause a shift towards protective Th1 type immunity, thus diminishing the harmful effects of DTwP and providing a non-specific survival benefit. Interestingly, aluminium hydroxide has been shown to cause enhanced susceptibility to tuberculosis (TB) in animal models. Thus the aluminium adjuvant in DTwP may play a role in the deleterious effect of DTwP on live vaccines, possibly through an influence on the generation of T cell memory to other infections and vaccines.