IgG1 and IgG3 are the main antibody components of protein antigens, and their deficiency makes them susceptible to viral infections or infections such as streptococcus and staphylococcus aureus; IgG2 and IgG4 are the main antibody components of podoconjugate antigens, and their deficiency makes them susceptible to infections such as S. influenzae and S. pneumoniae. IgG2 and IgG4 are the main antibody components of podocyte polysaccharide antigens, and once defective, they are prone to infections such as H. influenzae and S. pneumoniae. Some children with recurrent respiratory tract infections have normal or even elevated serum total IgG levels. It is now believed that when a certain IgG subclass is defective or insufficient, other subclasses may have partial compensatory increase, such as IgG1 compensatory increase when IgG is defective, and sometimes IgG4 increase, which can keep the total IgG level normal or increase, while when IgG1 is defective, although there are compensations of other subclasses, but because the proportion is small, so the total IgG level is still significantly decreased, which is manifested as hypo-IgGemia. It is now believed that the majority of IgG subclass defects are not due to gene deletions or mutations but are related to disorders or malfunctions in the regulation between T and B cells. The majority of children with recurrent respiratory infections have significantly abnormal T-cell numbers and subsets, especially CD1+ and severely impaired T-cell proliferation. In support of the view that T-B cells are deregulated, it is speculated that various factors may mainly damage the function of T cells, especially T helper cells, reducing their ability to produce interleukins, weakening the regulatory role of B cell proliferation and differentiation, impairing the IgG and its class conversion process, leading to IgG subclass defects, and causing recurrent respiratory infections. T lymphocytes are a multifunctional cell population, and helper T cells (Th cells) and suppressor T cells (Ts cells) are the main immunoregulatory cells in the T cell population, each with its own function in a certain ratio in normal humans. Th cells assist B lymphocytes in antibody production and cellular immune functions, while Ts cells mainly inhibit B cell product antibody responses and suppress cellular immune effects. Under physiological conditions, the immune balance of the body is maintained, but under pathological conditions this balance is disrupted, resulting in immune dysfunction. In children with recurrent respiratory infections, total T cells (TLC) and Th (CD4) are decreased and Ts (CD8) are increased, leading to a decrease in the Th/Ts ratio. This suggests that the changes in cellular immune function in children with recurrent respiratory infections are mainly manifested by a decrease in the number of T cells and abnormalities in immune regulation. Due to the abnormal immunoregulation, T lymphocytes could not effectively assist/suppress immune effector cells, which may lead to the inability of T killer cells to perform their cell-mediated cytosolic functions, insufficient antibody production by B lymphocytes and poor conversion of immunoglobulins, resulting in acquired immunodeficiency in children with RRTI. The decrease in Th cells may be due to the suppression of T-lymphocyte subsets and T-cell function by certain viral infections, and the decrease in Th(CD4)/Ts(CD8) ratio may be another important cause of recurrent respiratory tract infections, as the decrease in the ratio disturbs the immune environment and causes recurrent respiratory tract infections. The decrease in CD4/Ts(CD8) ratio may be another important cause of recurrent respiratory infections. It has been shown that the T cell subsets CD3+ T lymphocytes, CD4+ T lymphocytes and CD4+ T lymphocytes/CD8+ T lymphocytes ratio (65%/35% of normal) are significantly lower in children with recurrent respiratory infections than in healthy children, indicating that there is a significant abnormality in cellular immune function leading to recurrent respiratory infections. Defective T cells prevent B lymphocytes with IgA on their surface from differentiating into IgA-secreting plasma cells. The presence of a factor IL2 in mitogen-stimulated lymphocyte culture supernatants maintains the long-term survival of stimulated T cells in vitro. This activity is mediated by a factor released by Th Named IL2 by the Second International Conference on Lymphokines in 1979, IL2 is considered to be a key factor in T cell proliferation, and many reports have since been published on a variety of diseases related to IL2 bioactivity. The reduced IL2 activity in children with recurrent respiratory infections may be related to the decrease in Th. The erythrocyte C3b receptor wreath rate was significantly decreased and the immune complex wreath rate was basically normal or increased in children with recurrent respiratory infections, indicating the presence of erythrocyte immune hypofunction in children with recurrent respiratory infections. Due to the reduced number and activity of erythrocyte C3b receptors, they cannot effectively remove microorganisms, antigens and immune complexes from the blood circulation, which also plays a role in the pathogenesis of this disease. The decreased activity of C3b receptors in children with recurrent respiratory infections may also be related to the influence of congenital genetic factors and the decreased activity of secondary receptors due to recurrent infections with pathogens and microorganisms.