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].