Active (Artificially Acquired) Immunity

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Chapter: Pharmaceutical Microbiology : Vaccination And Immunization

Active immunity relates to exposure of the immune system to antigenic materials and the subsequent response.


ACTIVE (ARTIFICIALLY ACQUIRED) IMMUNITY

 

Active immunity relates to exposure of the immune system to antigenic materials and the subsequent response. Such exposure might be related to an infection or to the multiplication of an attenuated vaccine strain, or it might be associated with the direct introduction of non-viable antigenic material into the body e.g. a non-living or inactivated vaccine. The route of exposure to antigen will influence the nature of the subsequent immune response. Thus, injection of antigen will lead primarily to humoral (IgG, IgM) production, while exposure of epithelial tissues (gut, respiratory tract) will lead to the production of secretory antibodies (IgA, IgE) and to the stimulation of humoral antibody production.

The magnitude and specificity of an immune response depends upon the duration of the exposure to antigen and on its time-concentration profile. During a naturally occurring infection (or the administration of a live, attenuated vaccine), the levels of antigen in the host may be low at the onset and localized to the portal of entry to the host. As the amounts of antigen are small, they will react only with a small, highly defined subgroup of small lymphocytes. These may undergo transformation to produce various antibody classes specific to the antigen and undergo clonal expansion. These immune responses and the progress of the infection may progress simultaneously. With time, microorganisms will produce greater amounts of antigenic materials that will, in turn, react with an increasing number of cloned lymphocytes to produce yet more antibodies. Eventually the antibody levels may be sufficient to eliminate the infecting organism from the host. Antibody levels will then decline, with the net result of this encounter being the clonal expansion of particular small lymphocytes relating to a highly specific ‘immunological memory’ of the encounter.

This situation should be contrasted with the injection of a killed or non-living vaccine where the amount of antigen introduced is relatively high when compared with the levels present during the initial stages of an infection. In a non-immune animal, the antigens may react not only with those lymphocytes that are capable of producing antibody of high specificity but also with those of a lower specificity. Antibody of both high and lower specificity may react with and remove the residual antigen. The immune response will cease after this initial (primary) challenge. On a subsequent (secondary) challenge (during a course of vaccinations), the antigen will react with residual preformed antibody relating to the first challenge, together with a more specific subgroup of the original cloned lymphocytes. As the number of challenges is increased, the proportion of stimulated lymphocytes that are specific to the antigen rises. After a sufficient number of consecutive challenges the magnitude and specificity of the immune response matches that which would occur during a natural infection with an organism bearing the antigen. This pattern of exposure brings with it certain problems. Firstly, as the introduced immunogen will react preferentially with preformed antibody rather than lymphocytes then sufficient time must elapse between exposures to allow the natural loss of antibody to occur. Secondly, immunity to infection will only be complete after the final challenge with immunogen. Thirdly, low specificity antibody produced during the early exposures to antigen might be capable of cross-reaction with host tissues to produce an adverse response to the vaccine.


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