Memory and specificity are the hallmarks of the adaptive immune response. The primary immune response is slow to develop and limited, whereas the secondary immune response is generated faster and is more extensive. A fundamental but perhaps more controversial concept is that the character of the second and subsequent immune responses is similar to that of the original primary immune response. This is particularly relevant to the repeated antigenic stimulation of chronic allergic or parasitic disease, where the character of the immune response tends to become "Locked" in a particular way. It is, however, far from clear when decisions are made about the character of immune responses to antigens. Although CD4-positive T cells generate such responses, they only do so when antigen is presented in association with major histocompatability compex (MHC) class II proteins on the surface of an antigen presenting cell. This step alone is, however, insufficient, and a variety of second signals are also recognized as highly relevant to the character of antigen recognition. Accordingly, it is likely that the cellular and cytokine environment during this antigen recognition step will detennine whether such responses develop and how they express themselves with each consecutive antigen challenge. It is reasonable to hypothesize that if
those early antigen presentation events are quantitatively or qualitatively abnormal, then an abnormal or detrimental immune response will develop. Although some data exist on how, when, and what sort of immune responses to aeroallergens develop in normal and atopic children, it is often difficult if not impossible to determine their relation to the exact time and nature of that primary antigen presentation event. Conversely, a study of the secondary immune response as it relates to asthma will only reveal the outcome of those decisions made during the appearance and development of the immune response, and not the forces that came to bear upon those decisions. Nevertheless, advances in our understanding of the molecular and cellular events of antigen presentation per se, and more specifically those events as they apply to the lung, have shed light on some processes likely to be relevant to the asthmatic response. We shall address the question of where, when, and by which cells antigen presentation might occur in the context of the evolution of the asthmatic process, and how such presentation may relate to pathological mechanisms.