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34 Cards in this Set
- Front
- Back
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Immune System |
The cells, molecules and tissues involved in identifying foreign agents, fighting infection and ridding the body of abnormal cells |
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Passive defenses and innate non specific immunity |
Defend against any invader Natural barriers, antimicrobial compounds Phagocytes - neutrophils, polymorphonuclear leukocytes (PMNs), macrophages Complement Natural killer cells |
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Cytokines, chemkines |
Small proteins Coordinate and modulate both kinds of immunity |
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Adaptive specific immunity |
Respond to a specific invader Cell mediated - antigen specific T cells Humoral - antibodies |
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Innate immune defense mechanisms |
Appear to be of ancient origin First line of immune defense Pre-programmed from birth, via evolution Can sense and identify invaders in non specific way in pants vertebrates and invertebrates |
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Adaptive immunity in verebrates |
Much more recent origin |
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Influencing factors, passive defenses, built in barriers include |
Natural host resistance - some organisms are more sensitive to certain pathogens Age - very young and very old Stress - fatigue, exercise, dehydration, climate, stress hormones, inflammation suppression Diet - alterations change normal microbiota Physical, chemical, anatomical barriers Tissue specificity - pathogen must contact |
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Compromised host |
One or more resistance mechanisms inactive Susceptibility increased Suppressed- drug therapy Compromised - AIDS |
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Physical, chemical, anatomical barriers |
Cilia remove particles, mucus helps suspend Lysozyme in tears and secretions Lung mucus prevents colonization Blood and lymph proteins inhibit growth Skin fatty acids Stomach acidity , Rapid gut pH change Normal flora compete with pathogens in gut Flushing of urinary tract |
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Bone marrow stem cell |
Myeloid precursor Lymphoid precursor |
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Lymphoid precursor |
-B cell (bone marrow) -->plasma cell containing antibodies -T cell (thymus) |
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Myleioid precursor |
-Monocyte -->Dendritic cell (phago, APC) -->Macrophage (phago, APC) -Neutrophil (gran, phago) -Mast cell (gran) |
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Primary lymphoid organs |
Thymus Bone marrow |
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Secondary lymphoid organs |
Tonsil Lymph nodes Spleen Peyer's patches of intestine Appendix Lymph vessels |
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Extravascation |
Cells passing in ab out of blood capillary and lymph capillary |
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Phagocytosis |
1. Opsonized microbe binds to phagocyte 2. Cytoplasmic extensions surround and engulf 3. Phagosome forms, acidification 4. Phagosome fuses with lysosomes to form phagolysosome 5. Oxidative burst, lysosomes kill microbe 6. Exocytosis expels debris |
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Lysosomes contain: Lysozyme Proteases Defensins |
hydrolysis of peptidoglycan of cell wall Protein degradation Form pores in bacterial membranes |
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Respiratory oxidative burst |
Oxygen dependent phagocyte killing Increase in O2 uptake, consumption by activated phagocytes |
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Pattern recognition PRR |
Exist on phagocyte membrane (TLR- too like receptors) PRR recognizes a PAMP- pathogen associated molecular pattern ex. TLR4 recognises TLR3 LPS dsRNA TLRs expressed in cells and phagocytes |
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Inflammation |
Characterized by redness, swelling, heat, localized, at site of infection Not an immune response A frequent precursor that facilitates immune responses |
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Systemic inflammation |
aka shock severe edema (swelling), uncontrollable fever, hypotension (low bp) |
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Inflammation Process |
1. Bacteria enter wound 2. Vasodilator molecules released 3. Bacteria multiply and invade 4. Vasodilator concentrations increase 5. Vessel dilates, more blood, increased temp and redness) 6. Vessel more permeable, fluid moves into tissue, swelling, extravasation |
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Inflammation cont. |
7. Antibody and complement factors bind to bacteria 8. Phagocytes engulf and destroy, cytokines released, leukocytes attracted 9. Adhesion molecules on vessel walls facilitate extravasation of immune cells 10. Clotting, then tissue repair |
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Fever |
Systemic response to microbial invasion Results from microbial products, host cell products as a result of pyrogens Good: accelerate phagocyte response and tissue repair Bad: very high benefits pathogen by destroying host tissues >40 |
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Pyrogens |
Endotoxin, interacts with TLR4 on phagocytes Endogenous pyrogens released into circulation Stimulate release of prostaglandins in brain producing fever |
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Complement |
Collective term referring to a group of more than 30 serum proteins |
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Classic complement activation pathway - causes inflammation |
1. C1 binds to antibody surface complex 2. Activated C1 cleaves C4 3. C2 is cleaved, forms C3 convertase 4. C3 is cleaved, forms C5 convertase 5. C5 is cleaved, C5b inserts into membrane 6. C6 binds C5 then C7 7. C8 inserts, polymerized C9, MAC forms 8. Mac forms pore, fluid enters and lyses |
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MAC |
Membrane attack complex |
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Alternative pathway |
LPS/LTA bound C3b binds serum protein factor B, acted on by serum factor D, catalyzes C5-9MAC MAC |
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MBL lectin pathway |
Serum MBL (mannose-binding lectin) protein binds mannose-containing PS unique to bacterial cell surgaces, fixes C4, C2, catalyzes C5-9 MAC Opsonization |
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C3b and MBL |
Soluble PRRs Both are opsonins |
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C3b |
Opsonization Binds with microbial cell surface and C3R receptors on phagocyte surface |
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C3a, C4a, C5a |
Released, diffuse away from focus of infection Stimulate inflammation at site C3a - chemotactic attraction of leukocytes C5b - chemoattraction of neutrophils |
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Complement system goals |
1. Damages invader directly (MAC) 2. Increases efficiency of attack on invader by -enhancing recognition C3b -attracting more neutrophils and leukocytes C5b, C3a |
