In a physiopathological context, asthma is a chronic inflammatory disease of the respiratory airways [
31] and the choice of the study of programmed cell death is particularly due to the fact that these lymphocytes play an irrecusable role in the pathogenesis of asthma [
17,
32,
33]. Despite the plentiful data on asthma, the concept of PCD in the pathogenesis of asthma is and remains misunderstood and controversial [
34,
35]. Increasing interest in this process of PCD [
36] in recent years was fundamental to conduct this present study. During the development of asthma a multitude of Immunogenetic mechanism and cells of immune systems might be involved [
37]. The results of immunological studies suggest a number of changes in the functional state of lymphocytes in patients with asthma. In 1995 Szczeklik et al. [
38] while studying the autoimmune status of patients suffering from Bronchial asthma, found in the blood some antinuclear antibodies, in any case, none of the patients got some antibodies with
NDNA, however, the quantity of autoimmunity of the patients suffering from bronchial pulmonary system reveal the advantage of the synthesis of specific organ antibody, for example
NDNA and/or
DNDNA autoantibodies [
39]. Therefore, the level of IgG anti -
NDNA increased significantly according to the degree of severity of asthma (Figure
2) and given that IgG have the ability to be locked up in the tissues, one could think of a lesion of target tissues in progressive course with the severity degree of the disease. It was revealed in patients with asthma the significant presence of CIC of average size and considered as the most pathogenic of CIC which was formed during a slight plethora of antigens. In relatively healthy donors, a process of enlargement of chronic CIC was observed and this in accordance with a proportional relationship of the level of antigen and antibody corresponding to their elimination. It should be noted that we recorded a direct relationship of dependence between the concentration of CIC and the level of antibodies against DNA and inverse dependence between the concentration of CIC and the concentration of extracellular DNA in the blood (Figure
6). This leads us to suggest the absence of a relation of equivalence between the antibody and the antigen during the progression of the severity degree of asthma. The existence of CIC in the blood is a normal and natural phenomenon of immune reactions. But their high level constitutes a means of diagnosing the pathology. Circulating immune complexes of large size are less soluble and can be easily removed by macrophages unlike CIC of medium and small size. They dissolve easily, making their removal difficult, which explains the CIC concentrations of medium and small size in asthmatics with serious severity. Therefore, the conception of the role played by the immune process in the pathogenesis of asthma is widely acknowledged, however, the importance of indicators of diagnosis and individual prognosis of the immune system remains poorly studied and in particular the accumulation in biological fluids IG antibodies - anti DNA, abzymes with DNAse activities, extracellular DNA, and CIC according to the degree of severity of the disease. The results obtained in this study allow us to suggest that these markers play a vital role in the pathogenesis of autoimmune process during asthma. And it is not excluded that these immunological characteristics stemmed from other natural physiological process. Thus, the observed difference underlined in the mitotic activity and the variation of the level of lymphocytes in culture of clinically healthy donors and asthmatic shows varying degrees of cell survival according to the severity of the disease. From the results of our work we could note that, based on a slowing of cell growth of lymphocytes from asthmatics with severe severity, the lymphocytes of asthmatics with mild severity are characteristic of lymphoproliferous activity in vitro. For the researches on asthma we do not often take into account the severity of asthma. Patients with asthma of mild and severe severity have different backgrounds and do not have the same degree of deficiency of the immune system. Failure to take into account the degree of severity could lead to false reasoning of statistical analysis. We found after our study that PCD of lymphocytes of patients manifested differently based on their degree of severity. Further to the adoption of the concept of PCD of type 1, the death of lymphocytes under the influence of certain doses of glucocorticoids was considered a classic model of apoptosis [
40,
41]. Recently data were published on the sensitivity of subpopulations of lymphocytes of peripheral blood particularly cytotoxic and NK lymphocytes at a high dose of dexamethasone [
42,
43]. The use of systemic glucocorticoids increases systematically the number of lymphocytes in the dipodiploide area. This confirms the hypothesis that the use of corticosteroids inhibit cytokine production (Ile 3, 4, 5) which keeps the high level of Bcl-2 anti apoptotic protein) and consequently leads to an acceleration of apoptosis lymphocytes [
24,
44]. On the other hand, studies showed that the use of dexamethasone leads to a decrease in the number of migrating cells in the lungs after inhalation of specific allergens [
45]. The dexamethasone as inductor of apoptosis is expected to influence the number of proliferating cells especially their reduction [
46,
47]. But according to our data, the lymphocytes of asthmatic patients with mild severity showed resistance to glucocorticoids followed by active proliferation of its cells. There was also a decrease in the number of cells in the late phase of apoptosis. This may be due to a malfunction of the expression of DNase responsible for DNA degradation. It is conceivable in view of these results that there are indeed particularities in the course of apoptosis, in asthmatics and this according to the degree of severity of the disease. However, even if the conditions of the body seem to be met to artificially induce apoptosis, the results obtained could not totally be those of internal conditions. Several parameters can influence the results. Researches on apoptosis still continue nowadays, it may be other unknown physiological parameters which determine the course of this process, of which the absence would influence the results. Asthma can also be linked to a genetic predisposition, and even from a race to another, differences can be observed. Thus, results on the morphology of lymphocytes of asthmatics were obtained. And most of lymphocytes had specific morphological characteristics. Sometimes, cells with characteristics of autophagosomes autophagy were found [
29,
48]. The presence of autophagy could explain the decrease of apoptotic cells in asthmatics with mild severity. And the PCD is universally prevalent in the world of multicellular organisms, and affects all types of tissues. It operates according to the biochemical and morphological parameters strictly defined and do not depend on the causes leading to the initiation of this process. In addition, the study of PCD is very productive to understand a certain number of important processes including immune homeostasis. Finally, according to new data, it has become essential and indispensable to review a certain number of conceptual bases of physiopathology and immunopathology.