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Innate immunity lecture
- 1. Innate immunity Prof M.I.N. Matee Department of Microbiology and Immunology School of Medicine
- 2. Immunity: All mechanisms used by the body to protect itself against all things foreign Immunity: innate or acquired
- 5. Host defense mechanisms A. Outer barriers Skin and epithelial linings Skin: keratin sweat (NaCl), sebum (unsat. fatty acids) dead skin cells are shed Mucous membranes: mucus and ciliated epithelium stomach – acid ( pH 2-3) mucus - prevent attachment & entry M cells - endocytose pathogens , aids presentation to B and T lymphocytes Tears & saliva - flushing; lysozyme Saliva - aggregation of bacteria Urinary tract - urinary flow
- 8. B. Phagocytosis cells in blood & lymph active without exposure enhanced by immune system 1. Bacterium binds to ‘arm’ 2. Bacterium engulfed into membrane vesicle; phagosome 3. Vesicle fuses with lysosome 4. Digestive enzymes destroy bacterial cell; peroxide & superoxide also formed 5. Wastes emptied out of cell
- 23. Secreted Pattern Recognition Molecules Acute Phase Proteins Activation of Complement Opsonization of microbial cells Primarily produced by the liver but can be produced by phagocytes
- 26. DURING SOME INFECTIONS CERTAIN COMPONENTS OF INVADING MICROBES PHAGOCYTIC CELL INTERLEUKIN - 1 ACTS AS CHEMICAL MESSENGER WHICH TELLS HYPOTHALAMUS THAT INFECTION IS OCCURRING BODY TEMPERATURE RAISED PRODUCE WHICH
- 33. Activation of C’ System - cont. b C4b + C2b C3b + Bb
- 34. Regulation of Adaptive Response Veterinary Immunology & Immunopathology 91: 1, 2003
Notas do Editor
- Phagocytosis requires 1. Binding to particle / microbe 2. Actin-filament formation under particle. 3. Membrane extension and fusion behind particle 4. Fusion with lysosome (endocytic pathway).
- Hallmarks of an Inflammatory Response Redness Heat Swelling Pain
- Acute-phase proteins are produced by liver cells in response to cytokines released by macrophages in the presence of bacteria. They include serum amyloid protein (SAP) (in mice but not humans), C-reactive protein (CRP), fibrinogen, and mannan- binding lectin (MBL). SAP and CRP are homologous in structure; both are pentraxins, forming five-membered discs, as shown for SAP (photograph on the right). CRP binds phosphorylcholine on certain bacterial and fungal surfaces but does not recognize it in the form in which it is found in host cell membranes. It both acts as an opsonin in its own right and activates the classical complement pathway by binding C1q to augment opsonization. MBL is a member of the collectin family, which includes C1q, which it resembles in its structure. We have already seen how MBL activates complement (see Section 2-7) and how it binds to pathogen surfaces (see Fig. 2.28). Like CRP, MBL can act as an opsonin in its own right, in addition to activating complement. SP-A and SP-D are surfactants A and D, both of which are collectins that coat bacterial surfaces, facilitating their phagocytosis. Photograph courtesy of J. Emsley. Photo from Nature 1994, 367:338-345. © 1994 Macmillan Magazines Limited.
- Fig. 2.8, part 1 of 2. Overview of the main components and effector actions of complement. The early events of all three pathways of complement activation involve a series of cleavage reactions that culminate in the formation of an enzymatic activity called a C3 convertase, which cleaves complement component C3 into C3b and C3a. The production of the C3 convertase is the point at which the three pathways converge and the main effector functions of complement are generated. C3b binds covalently to the bacterial cell membrane and opsonizes the bacteria, enabling phagocytes to internalize them. C3a is a peptide mediator of local inflammation. C5a and C5b are generated by cleavage of C5b by a C5 convertase formed by C3b bound to the C3 convertase (not shown in this simplified diagram). C5a is also a powerful peptide mediator of inflammation. C5b triggers the late events in which the terminal components of complement assemble into a membrane-attack complex that can damage the membrane of certain pathogens. C4a is generated by the cleavage of C4 during the early events of the classical pathway, and not by the action of C3 convertase, hence the *; it is also a peptide mediator of inflammation but its effects are relatively weak. Similarly, C4b, the large cleavage fragment of C4 (not shown), is a weak opsonin. Although the classical complement activation pathway was first discovered as an antibody-triggered pathway, it is now known that C1q can activate this pathway by binding directly to pathogen surfaces, as well as paralleling the MB-lectin activation pathway by binding to antibody that is itself bound to the pathogen surface. In the MB-lectin pathway, MASP stands for mannan-binding lectin-associated serine protease. MBL important in early childhood and essentially act in lieu of antibodies C4 cleavage exposes thioester bond that covalently bonds to nearest surface Alternate pathway does not depend on a pathogen binding protein (spontaneous cleavage of C3)
- Non adaptive recognition receptors called Pathogen Recognition Receptors (PRR). These recognize PAMPs or pathogen associated molecular patterns. This leads to activation of immune response. Receptors can exist on the surface of the cell or intracellular in endocytic compartments. Recognition is based on two principles 1. microbial non-self (PRR/PAMP) 2. Missing self Inhibitory receptors (NK cells) Factor H of Complement In this lecture we will focus on receptors that recognize the pathogen. NK cells will be discussed later and you have already discussed complement. However, we will touch on the receptors of the complement system that the innate immune system uses for recognition. Example: Recognition of a pathogen causes to signals to be released. co-stimulator signals cytokines