encounters abnormal cells then C3b can progress to the next step because those cells don’t have the inhibitor : C3 (spontaneous hydrolysis) C3i C3ib factor D breaks it into C3ibBb (short lived/ unstable) acts like C3 convertase converts C3 into C3a and C3b enters amplification loop- make more C3b (whole cycle happens again); control amplification by cell membrane (autologous membranes) proteins on surface that prevent further continuation of C3b ex. Protein (DAF- Decay Accelerating Factor) this is on cell surface split B off or degrade C3b prevents C3Bb formation if it is formed it will split it degrade C3b by inducing factor i split into smaller & inactive forms; also using factor H can break down this molecule;; if DAF isn’t present then factor P becomes stable and forms C3b and then C3bBb and then C3b again this acts as a C5 convertase (normal cells have DAF so amplification process doesn’t go anywhere) a.i.1.c. Lectin pathway - involves MBL- mannose (carb, most common substance on bacterial cell surface) binding lectin – produced by liver C4 activated into C4a and C4b C2 into C2a an C2b C3 into C3a and C3b; does not need antigen/antibody complex : MBL + Mannose (pathogen surface) in presence of MASP 1 (mannose associated searing protease) and MASP2activate C4 and C2 (C4a and b and C2a and b) activate C3 into C3a and b C4bC2aC3b (C5 convertase)
- We have 3 different pathways because of different aspects of infection; if infection happens for the first time, your body will not have the antigen for it - d. Lytic Pathway—C5 C5a and C5b C5b activates C6,C7, C8 C5bC6C7C8 complex causes C9 to wedge its way into cell membrane of foreign antigen & forms a big hole/pore and causes cell to disintegrate (cytolysis) MAC- membrane attack complex - * C3a and C5a are responsible for inflammation—release histamine & heparin from basophil & Mast cells - * C3b responsible for opsonization (coats pathogen surfaces, which enhances phagocytosis) - Inflammation Localized tissue response to injury Produces swelling (tumor), redness(rubor), heat (calor) and pain (dolor) ^^ known as cardinal signs of inflammation Stimuli that produces inflammation kills cells, damages connective tissues These changes will change the chemical composition of interstitial fluid. Damaged cells release prostaglandins and proteins The injury may have also released pathogens into the system All these changes will stimulate inflammation Effects of inflammation: o Temp repair and pathogens are prevented from entering the wound o Spread of pathogens is slowed o Facilitates regeneration and permanent repair Mast cells help in inflammation Mast cells release histamine, heparin, etc after mechanical stress or chemical changes Histamine makes caps more permeable so blood flow speeds up to the injured area Local sensory neurons are stimulated which give you the feeling of pain Increased blood flow= increased redness and temperature
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