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18 Cards in this Set
- Front
- Back
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First Line of Defense |
Surface coverage, tries to block anything and everything Skin, sweat, cilia and mucous, stomach acid Mucousal surfaces-projectiles, traps potential pathogens, some have lysozyme Cilia filters Stomach acid traps and kills most pathogens |
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Second Line of Defense |
Non-specific response-attacks anything foreign incl: Leukocytes, antimicrobial proteins, inflam response - Cytokines (messengers) - Interferons: dimmed released upo infection, reg of immune system Tumor Necrosis Factors (TNFs): major mediator of inflam - IL specific signalling molecules for T and B cell activation - Leukocytes, phagocytes, lymphocutes (NK) - Natural Killer cells (non-specific) - Phagocytosis, digests and disposes - Macrophages, Neutophils (1st responders), Eosinophils (attack parasites and responsible for allergiec reactions), basophils (important for inflam response, Mast cells), all are Granulocytes - Antimicrobial proteins help out +inflam response |
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Third Line of response |
- Specific responses, incl T cells (knights, helpr T cells to stimulate T and B to dive and diff, then killer T cells destroy marked antigens) (c-mediated response), B-antibody mediated (effector B cells, antibody production, Memory B cells, recognizes past intrudres) |
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Cell-Mediated Response (3rd line, T-cells) |
1. Helper T activated by recognizing an antigen presented y a macrophage; opsonization, marking an intruder for an IR 2. Activated Helper T stimualte cyto T to divide 3. Cytotoxic T cells search for pathogens 4. Uses performs (swords) to rupture cell membrane of pathogens/infected cells |
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Antibody Mediated Response (3rd, B-cell) |
1. Activated Helper T from CELL rest, stimulates B to grow and divide 2. B cells divide and diff into Memory B and effector B 3. Effector B cells (plasma cells) produce antibodies 4. Antibodies mark antigens for destruction via macrophages |
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Antibodies (relics/strong weapons, 3rd) |
Antibodies=IG, focus on surface of B cells, secreted by plasma - On B cells, Fab (antigen binding fragment), Fc (crystallizable fragment) |
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Antibody Functions (3rd Line) |
- Opsonization for phagocytosis (coat pathogen) - Neutralization (neutralize toxins secreted by pathogens) - activation of complement (classical path start lysing of cell) - Antibody dependent cell mediated cytotoxicity (ADCC) |
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ADCC |
- Most useful tactics - Facilitates parasite phagocytosis, and antibody binds to parasite, and phago recognizes antobody and engulfs parasite - Reactive oxygen intermediates (ROI) released to destroy the pathogen |
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The effects of a successful invasion: pathogenesis of parasitic infections |
- 4 ways that parasites can cause a disease: Trauma, nutrition robbing, toxin production, interactions between host immune/inflam response |
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1. Trauma |
Physical trauma: destruction of cells, tissues, or organs by mechanical or chemical means |
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2. Nutrition robbing |
- diversion of host nutritive substances |
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3. Toxin production |
- Malaria, erythrocysts burst and toxic cellualr wastes in blood, increase in CK, fever |
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4. Interactions between host immnue/inflam |
- Most serious pathogensis |
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How do parasites evade the IS? |
- Plasmodium falciparum - Antiegenic variation/polymorphism - Induction of blocking antibodies - Anergy of T-Cells-immunosupression |
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Entamoeba histolytica Evades IS |
- Cytolytic capacity: damages host cells and tissues - Degradation of antibodies by proteases - Anergy of T-cells immunosuppression - Release of products that inhabit macrophage |
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Fasciola hepatica evades IS |
- Ig-cleabing protease on surface - Brugia malayi: microfilariae secrete antiinflam - Onchocerca volvulus: cystatin on surface, protease inhibitor, blocks antigen processing |
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REconnaissance |
NORMALLY parasites are found, but when that fails, many tests have been developed that take advantage of patients immune system |
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Tests |
1. Skin test: antigen in skin, and many infections produce immediate hypersensitivity reactions 2. Indirect Hemagglutination Test (IHA): RBCs are coated with antigen of parasite and incubated with patient's serum, afflutination of the erythrocytes=psitive 3. Indirect Fluorescent Antibody (IFA): prasites fixes to slide, incubated with patients serum, washed treated with human IG, if anti-ig binds to test serum IG and can be visualized under a fluroresnce microscope 4. Enzyme Linked Immunosorbent Assay (ELISA): test serum added to plates with antigen, remove and rose, anti IG is added, removed and rinsed, anti-ig is enzyme hat catalyzes for colour change, substrate for enzyme added, colour change= + |
