Recently, a third type of asthma has been described after tests with bronchial provocation: after immediate or late reactions, individual patients may experience a relapse of asthma, especially at night, over the next few days without repeated contact with the allergen. This picture was described by Gandevia and Milne (1970), who used cedar wood, and Davies et al. (1974) using penicillin derivatives.
It is still unknown whether this phenomenon can be explained by immunological concepts or, more likely, by the appearance of a state of bronchial lability, which then fluctuates under the influence of non-immune circadian rhythms, as is often the case with clinically severe asthma [Soutar et al., 1975]. So far, patients with this recurring asthma have not revealed any immunological features.
Lymphocytes in atopic asthma
There is evidence that the formation of IgE antibodies is controlled and dependent on the normal function of T cells [Ogilvie, Love, 1974]. If this function is severely impaired, the IgE level is low. In patients with atony, in vitro indications of sensitization of lymphocytes were obtained [Richter, Naspitz, 1968; Brostoff, Roitt, 1969; Maini et al., 1971; Malley et al., 1971; Ricci, Romagnani, 1974].
These data do not necessarily contradict the assumption of partial T-cell deficiency in atopy. T-cell deficiency is known to be associated with an antibody response of low affinity, which is thought to play an important role in atopy [Soothill, 1974; Soothill et al., 1976]. Recently, apparently, successfully used extracts of sensitized lymphocytes (transfer factor) with very severe atopic eczema with lymphopepia.
It should also be emphasized that, according to the theory of T-cell deficiency , it temporarily occurs in infancy and, thus, normal T-cell reactivity in adult patients does not refute this hypothesis.
The recognized response of an organism depends on some of the variable factors listed below: 1. Physical and chemical properties of the antigen. 2. Dose, duration of contact and entrance gate of antigen. 3. Immunological reactivity of the body: a) the state of sensitization and immunity of the body in connection with previous contacts; b) the type of antibodies formed (IgE, IgG, IgA, SIgA, IgM) or the degree of sensitization of lymphocytes; c) a quantitative balance between these factors, especially between the reactivity of T and B cells and between local secretory IgA and IgE. 4. The quantitative ratio between antigen and antibodies.
5. The presence of complement.
6. The nature of the tissue, that is, the target organs where the antigen and antibodies interact.
7. The nature and balance of pharmacological mediators released from tissues upon interaction of antigen with antibodies.
8. The effect of drugs that affect the effect of these mediators and regulate it.
9. Sequential events occurring in tissues after the induction of an inflammatory response (for example, swelling of capillary endothelium and platelet aggregation).
