The Immunological System of the Child: Part I: Development of Immunity in the Child
Open Access
- 1 August 1966
- journal article
- research article
- Published by BMJ in Archives of Disease in Childhood
- Vol. 41 (218) , 358-365
- https://doi.org/10.1136/adc.41.218.358
Abstract
Immunological competence depends upon (a) an intact thymus, certainly during fetal life and perhaps for a certain period in early extrauterine life; an adequate supply of im-munologically competent lymphoid cells, which populate the lymphoid follicles of lymph nodes, gut, and spleen. The immune response to infection consists of 2 important specific phenomena; the development of delayed hypersensitivity to certain chemical constituents of the infectious agent, a phenomenon mediated by small lymphocytes; the formation and secretion of specific antibodies to certain antigens of the infectious agent by cells which become differentiated into cells of the plasma cell series during this process. The primary or initial response to an antigen results in the formation of gammas (19S macroglobulin) antibodies, which have a short half-life, by [periodic acid Schiff] positive plasmacytoid cells, and the subsequent formation, by typical plasma cells, in low titer of intermediate molecular weight antibodies and ultimately of 7S gamma G- globulins with a longer half-life. The primary response is slow and required time for the establishment of delayed hypersensitivity and for the formation of antibodies in relatively low titer. The secondary response usually occurs in an individual with established delayed hypersensitivity, and results in a rapid increase in the number of plasma cells and in the appearance of a high titer of specific gammaG immunoglobulin antibodies in the blood. The fetus can form antibody in utero if infected, but normally does not, and the infant is born with gamma Q-antibodies passively transferred from his mother and a transient deficiency of gamma M- and gammaA-immunoglobulins, which do not normally cross the placenta. After birth, as the level of maternal gamma G-globulin falls by dilution and catabolism, the infant begins to form his own immunoglobulins in response to immunization and contact with micro-organisms in his environment. The newborn infant is peculiarly vulnerable to invasive infections with Gram-negative bacilli during the 1st 2 weeks of neonatal life, possibly because of the transient deficiency of gamma M-globulins. The infant is unusually susceptible to invasive infection with most pyogenic bacteria from about 1-2 months to about 18-24 months of age, because these are primary infections occurring in an infant without previously established delayed hypersensitivity, in whom antibody formation is slow.Keywords
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