The innate and adaptive immune response

(Ref. 1-2)

Acute inflammation can be caused by microbial agents such as viruses, bacteria, fungi and parasites, by non-infectious inflammatory stimuli, as in rheumatoid arthritis and graft-versus-host disease, by tissue necrosis as in cancer, and by burns and toxic influences caused by drugs or radiation (Fig. 1).

Fig. 1 Different types of inflammatory stimuli

In all these situations, the inflammatory stimulus will be met by a series of changes in the human body; it will induce production of certain cytokines and hormones which in turn will regulate haematopoiesis, protein synthesis and metabolism.


Most inflammatory stimuli are controlled by a normal immune system. The human immune system is divided into two parts which constantly and closely collaborate - the innate and the adaptive immune system.


The innate system reacts promptly without specificity and memory. Phagocytic cells are important contributors in innate reactivity together with enzymes, complement activation and acute phase proteins. When phagocytic cells are activated, the synthesis of different cytokines is triggered. These cytokines are not only important in regulation of the innate reaction, but also for induction of the adaptive immune system. There, specificity and memory are the two main characteristics. In order to induce a strong adaptive immune response, some lymphocytes must have been educated to recognise the specific antigen on the antigen-presenting cell (APC) in context of self major histocompatibility molecules. The initial recognition will mediate a cellular immune reaction, production of antigen-specific antibodies or a combination of both. Some of the cells which have been educated to recognise a specific antigen will survive for a long time with the memory of the specific antigen intact, rendering the host "immune" to the antigen.


The close collaboration between the innate and acquired immune response is illustrated below (Fig. 2). The APCs produce cytokines, which stimulate the synthesis of acute phase proteins (i.e. CRP) by the hepatocytes. CRP bound to the antigen, increases the phagocytosis of the antigen either by binding to specific CRP receptors on phagocytic cells or via complement receptors when complement is attached to the CRP-antigen complex. APCs process and present antigens in the context of HLA class II for T-cell receptors (TcR) on T-lymphocytes. Cytokines from activated T-cells stimulate B-lymphocytes. Clonal expanasion is induced for both cell types. B-lymphocytes are also activated via antigen binding to B-cell receptors, which are immunoglobulins on the cell surface. Activation of B-lymphocytes induces maturation of B-cells to plasma cells and synthesis of large amounts of soluble antigen-specific immunoglobulins. Free antigens are covered with antibodies. Antibody-covered antigens bind to Fc receptors or complement (C3b) receptors on phagocytic cells. APCs also produce cytokines responsible for stimulation of leukopoiesis, increasing the number of cells available for innate and acquired immune responses.

Fig 2 The Innate and adaptive immune response to inflammatory stimuli. Illustration: Kari C. Toverud, 1998.

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