Classes of immunity

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Chapter: Pharmaceutical Microbiology : Vaccination And Immunization

Immunity to infection may be passively acquired through the receipt of preformed, protective antibodies or it may be actively acquired through an immune response following deliberate or accidental exposure to microorganisms or their component parts. Active, acquired immunity might involve either or both of the humoral and cell-mediated responses.


Classes of immunity

 

The theoretical background that underlies immunity to infection has been discussed in detail in Immunity. Immunity to infection may be passively acquired through the receipt of preformed, protective antibodies or it may be actively acquired through an immune response following deliberate or accidental exposure to microorganisms or their component parts. Active, acquired immunity might involve either or both of the humoral and cell-mediated responses.

 

1)  Passive (Artificially Acquired) Immunity

Humoral antibodies of the IgG class are able to cross the placenta from mother to fetus. These antibodies will provide passive protection of the newborn against those diseases which involve humoral immunity and to which the mother is immune. In this manner, most newborn infants in the UK will have passive protection against tetanus, but not against tuberculosis. Protection against the latter relies to a large extent on cell-mediated immunity. Secreted (IgA) antibodies are also passed to the gut of newborn, together with the first deliveries of breast milk (colostrum). Such antibodies provide some passive protection against infections of the gastrointestinal tract. Maternally acquired antibodies will react with antigens associated with an infection but also with antigens introduced to the body as part of an immunization programme. Premature immunization, i.e. before degradation of the maternal antibodies, may reduce the potency of an administered vaccine. This aspect of the timing of a course of vaccinations is discussed later.

Administration of preformed antibodies taken from animals, pooled human serum, or human cell lines is often used to treat existing infections (e.g. tetanus, diphtheria) or condition (e.g. venomous snake bite). Pooled serum may also be administered prophylactically, within a slow-release vehicle, for individuals travelling to parts of the world where diseases such as hepatitis A are endemic. Such administrations confer no long-term immunity and may interfere with concurrent vaccination procedures.

 

2)  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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