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.
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.
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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