Introduction
The body’s first line of defence against the environment (innate
immunity) comprises a layer of epithelial cells which line all external
surfaces. Once, this has been breached, the roles of the immune system
and inflammation is to limit the damage, eliminate the foreign substance
and promote repair [1, 2]. Antigens are substances that induce an
immune response, and proteins are the most antigenic material, followed
by carbohydrates and lipids which are weakly antigenic. A large
molecule, such as protein, may have several different sites (epitopes)
to which dissimilar clones of immunologically competent cells respond.
Some foreign proteins possess epitopes similar to those on self-
proteins, accounting for some cases of auto-immunity i.e. the
environmental aetiology of autoimmune disease. Immunological tolerance,
the state of specific unreactivity to the body’s own tissue is thought
to be acquired during fetal life when the immune system has not reached
immunological maturity. Therefore, the body does not mount significant
antibodies against its own tissues. Nevertheless, clones of cells which
can produce ‘autoantibody’ (‘forbidden clones’) are thought to be
produced throughout life and are either suppressed by large amounts of
‘self’ antigen or by antigen-specific T suppressor cells.
‘Autoantibodies’ are produced to a wide variety of antigens in
autoimmune disease. These autoantibodies may be organ- specific, e.g.
intrinsic factor antibodies in pernicious anaemia, thyroid antibodies in
Hashimoto’s disease, or non-organ specific, e.g. antinuclear factor in
systemic lupus erythematosus (SLE). Autoimmune disease states are
thought to arise when this system of mopping up forbidden clones breaks
down [3]. The body can react to an antigen by producing antibody
(humoral immunity) or specific T lymphocytes (cellular immunity).
Antibodies belong to the class of serum proteins known as
immunoglobulins. The T lymphocytes can be directly cytotoxic (T
cytotoxic cells), or may produce cytokines ( T helper cells) which are
short-lived ‘hormones’ that acts on other cells to enhance or suppress
their activity. Interleukins (lymphocyte activating factors) are
specific lymphokines active between cells of the immune system and
affect antibody production . The role of complement- a multi-molecular
activation system of plasma proteins dependent in part on the sequential
activation of a series of proteolytic zymogens is to promote
inflammation, phagocytosis of antigens and immune complexes by
macrophages (opsonization), and, lysis when activation is at or near the
surface of a target cell. Abnormalities of the immune response are seen
in the immunodeficiency diseases and the hypersensitivity reactions.
Immunodeficiency may be inherited or may occur as a result of infection
or drug therapy. It includes defects in antibody production (hypo- or
agammaglobinaemia, selective IgA deficiency), complement fixation(C1 esterase inhibitor(hereditary angioedema), C1q (discoid lupus
erythematosus), C1q, C1r, C4 or C2 (immune complex vasculitis), C3 or
C3b inhibitor ( Kline-felter’s syndrome), C5, C6, C7 or C8 (recurrent
Neisseria ); T lymphocyte function, (Thymic aplasia, purine
nucleoside phosphorylase deficiency, ataxia telangiectasia,
Wiskott-Aldrich syndrome, Bloom’s syndrome, Severe combined
immunodeficiency (SCID)); and phagocyte functioning (Job’s
syndrome, Chronic granulomatous disease (CGD), Chediak-Higashi syndrome,
Myeloperoxidase deficiency ) [5]. Immunological priming can lead, on
further exposure to antigen, to either secondary boosting of the immune
response or to an excessive damaging inflammatory reaction (antibody and
cellular immune response) termed hypersensitivity. The implications of
the immune response in health and the inflammatory (hypersensitivity)
reactions (type I- anaphylactic, type II- cytotoxic, type III- immune
complex mediated, type IV-cell mediated/ delayed, type V- stimulating
antibody, and type VI- antibody-dependent cell mediated cytotoxicity) in
disease are discussed. The proliferation of normal cells is carefully
regulated but tumour cells have undergone mutations which makes them
capable of uncontrolled growth. The immunological mechanisms involved in
cancer growth are highly complex and the understanding of the
relationship between immune function and tumour cells is important
[6].