Abstract
Immunological competence depends upon (a) an intact thymus, certainly during foetal life and perhaps for a certain period in early extrauterine life; (b) an adequate supply of immunologically competent lymphoid cells, which populate the lymphoid follicles of lymph nodes, gut, and spleen. The immune response to infection consists of two important specific phenomena; (a) the development of delayed hypersensitivity to certain chemical constituents of the infectious agent, a phenomenon mediated by small lymphocytes; (b) theformation 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 yM (19S macroglobulin) antibodies, which have a short half-life, by PAS positive plasmacytoid cells, and the subsequent formation, by typical plasma cells, in low titre of intermediate molecular weight antibodies. and ultimately of 7S yG-globulins with a longer half-life. The primary response is slow and requires time for the establishment of delayed hypersensitivity and for the formation of antibodies in relatively low titre. 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 titre of specific y G-immunoglobulin antibodies in the blood. The foetus can form antibody in utero if infected, but normally does not, and the infant is born with yG-antibodies passively transferred from his mother and a transient deficiency of yM- and yA-immunoglobulins, which do not normally cross the placenta. After birth, as the level of maternal y G-globulin falls by dilution and katabolism, 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 first two weeks of neonatal life, possibly because of the transient deficiency of y 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.
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CITATION STYLE
Janeway, C. A. (1966). The immunological system of the child: Part I: Development of immunity in the child. Archives of Disease in Childhood. BMJ Publishing Group. https://doi.org/10.1136/adc.41.218.358
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