| Themes > Science > Life Sciences > General Biology > Immunology > Immunity to Infection > Early Immune responses (4-96 hrs) |
The immediate defences are available instantly or within an hour or so of invasion. The recognition events set in motion of a second wave of defence primarily triggered by the de novo synthesis of cytokines. The role of macrophages The secondary effects of recognition of microbial pathogens via either the innate carbohydrate receptors or the complement receptors is to active macrophages to synthesise cytokines. In particular TNFalpha, IL12 and IL1 play an important role in the second phase response. TNFalpha is critical in activating local vascular endothelium. This achieves several things
The effect of local vessel clotting is important to prevent spread of the pathogen into the blood stream - antibody neutralisation of TNF allows blood sepsis in experimental bacterial infections. TNFalpha also 'primes' neutrophils, causing them to activate oxygen-dependent intracellular killing mechanisms and making them more effective. In synergy with IL1, TNF stimulates the
acute phase response which triggers massive increases in the serum
concentration of Mannose
Binding Protein (MBP), and C Reactive protein (CRP). These molecules
provide additional means to recognise the invaders. Both bind simple
chemical structures on microbial cells, both have specific receptors on
phagocytes and both are capable of activating the complement system
mimicking C1q and IgM respectively. Natural Killer (NK) cells These lymphocytes lack the clonally variable antigen specific receptors of T and B cells. They are part of the innate immune system and we know they play an important role in viral infections. They are activated by the cytokines IL12 and IFNalpha/beta. Interferon Interferon alpha/beta are produced by a variety of cells in response to viral infection. They have an important role in limiting viral infection in the early phase (before specific immunity is available). They do this both directly and indirectly. They act on a wide variety of cell types to induce the synthesis of a series of proteins which interfere with viral replication both by degrading RNA and by inhibiting protein synthesis. They also potently activate NK cells. |
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