The Immune System | BIOL117

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185 Terms

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infectious agents can ________ or ________ a host

damage; kill

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six major categories of infectious agent

  1. bacteria

  2. viruses

  3. fungi

  4. protozoans

  5. multicellular parasites

  6. prions

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virulent

ability of microorganisms to cause serious diseases/side effects

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what are the different shapes of bacteria?

  1. rod (bacilli)

  2. spherical (cocci)

  3. coiled (spirilla)

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virulent bacteria may have __________, __________, or release _________, or ____________

pilli; capsule, toxins; damaging enzymes

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how does prion cause diseases?

prion mess with the structure of protein and make them nonfunctional

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bacteria (prokaryotes/eukaryotes, cell membrane/cell wall, virulence factors, common examples)

  1. prokaryotes

  2. BOTH cell membrane and cell wall

  3. VF: have either pili that allow it to attach to a cell or a capsule to give it extra protection from the body defense, or releases toxins or damaging enzymes

  4. e.g., clostridium tetani, bacillus anthracis, clostridium c difficiles, etc

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virus (prokaryotes/eukaryotes, cell membrane/cell wall, virulence factors, common examples)

  1. no alive (neither prokaryotes/eukaryotes)

  2. no cell wall/cell membrane - have a shell, capsid

  3. VF: insert viral DNA to instruct the nuclei to protein viral RNA

  4. e.g., common cold, influenza, herpes zoster

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fungi (prokaryotes/eukaryotes, cell membrane/cell wall, virulence factors, common examples)

  1. eukaryotes

  2. cell membrane AND cell wall

  3. VF: spores releasing proteolytic enzymes that causes inflammation

  4. examples (three type)

    —> superficial: athletes’s foot, ring worm, onychomycosis

    —> mucosalL yeast infection, thrush

    —> internal: Aspergillosis, candidiasis

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protozoan (prokaryotes/eukaryotes, cell membrane/cell wall, virulence factors, common examples)

  1. eukaryotes

  2. cell membrane (no cell wall)

  3. VF: inherent parasites (can work in or outside of cell)

  4. examples

    —> malara

    —> giardiasis

    —> trichomoniasis

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helminth (prokaryotes/eukaryotes, cell membrane/cell wall, virulence factors, common examples)

  1. eukaryotes

  2. cell membrane (without cell wall)

  3. VF: take nourishment from the host and eating their way through cell

  4. examples:

    —> tapeworm, pinworm, roundworm

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prion (prokaryotes/eukaryotes, cell membrane/cell wall, virulence factors, common examples)

  1. neither eukaryotes or prokaryotes (fragment of infectious protein - misfolded proteins) - all the same amino acids but assembled differently

  2. no cell membrane or cell wall

  3. VF: the misfolded properties cause the protein to act haywire and cause diseases

  4. examples:

    —> Mad Cow Disease

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when does monocytes become macrophages?

when it leave the blood and enter the tissues

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characteristics of innate immunity

  1. prevent entry of any potential harmful substances

  2. responds nonspecifically

  3. two lines of defense (external —> internal)

  4. no memory of the response (generalized and does not remember the pathogens)

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characteristics of adaptive immunity

  1. destroy potential harmful substances

  2. respond specifically (to what the body know) with T & B lymphocytes replication and response

  3. one line of defense (the third line of defense)

  4. keep memory of the response (specific and remember the pathogens)

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what cells in the body release antibody and where does that cell come from?

plasma cells, which come from B-lymphocytes when activated (basically B-lymphocyte differentiate when activated)

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differences between T & B lymphocytes in mediated immunity

  1. T - cell-mediated immunity

  2. B - antibody-mediate immunity

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what is the body first line of defense

skin and mucosal membrane (and their secretion)

<p>skin and mucosal membrane (and their secretion)</p>
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what is the body second line of defense

internal processes: inflammation, fever, and granulocytes (neutrophils, macrophages, dendritic cells, eosinophils, basophils, and NK cells - NOT agranulocyte)

<p>internal processes: inflammation, fever, and granulocytes (neutrophils, macrophages, dendritic cells, eosinophils, basophils, and NK cells - NOT agranulocyte)</p>
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cytokines

small proteins that regulate immune activity through chemotaxis, controlling development and behavior of immune cells, regulating inflammatory response, and destroying cells

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innate immune respond _________ while adaptive immunity __________ to be effect

immediately; takes several days

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differences between autocrine, paracrine, and endocrine cytokines

  1. autocrine - act on on the cells that released it (influence one’s own activity)

  2. paracrine - act on local cells (influence local activity)

  3. endocrine - act on distant cells after circulating through the blood (influence elsewhere activity)

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true or false: cytokines is produce by both the innate and adaptive immune system

true

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interferon

a type of cytokines made by virus-infected cell to protect nearby cells from the viruses by basically signalling that it is infected so neighboring cells can response by making antiviral proteins to block virus replication and activate immune cells (e.g., NK cells)

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interferon (IFN) alpha and beta (secreted by, function)

produced by virus infected cell to signal that the cell is infected and for neighboring cells to start producing antiviral proteins to protect themselves

  • also activate NK cells and T-lymphocyte

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interferon (IFN) gamma (secreted by, functions)

produced by T-lymphocutes and natural killer cells to stimulate macrophages to destroy virus-infected cells to phagocytize infected cells)

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complement (secreted by, functions)

a group of inactive protein secreted by the liver until trigger - destroy bacteria and mark pathogens for elimination

  • activated through infection

  • forms the Membrane Attack Complex (MAC) to punch holes (cytolysis) in bacteria cell walls, leading to cell death

  • helps with opsonization (marking pathogens for phagocytosis) and triggering inflammation

  • elimination of immune complexes

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cytolysis

destruction of a cell

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how are proteins in the complement system recognized naming wise?

letter “C”

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(DO NOT NEED) what are the three pathway of complement proteins?

  1. classical pathway - antibody attaches to foreign substance then complement binds to the antibody

  2. alternative pathway - complement binds to PAMPs (pathogen-associated molecular pattern) of bacterial or fungal cell wall

  3. lectin pathway - complement binds to lectins on bacterial or fungal cell wall

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opsonization

a process done by complement proteins to mark pathogens for phagocytosis

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true or false: few microbes can penetrate the intact skin

true

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dermcidin (secreted by, function)

  1. secreted by: sweat glands

  2. functions: antimicrobial peptide that kills bacteria and fungi on the skin surface

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lysozyme (secreted by, function)

  1. secreted by: saliva, tears, mucus, and sweat

  2. functiona: breaks down bacterial cells walls, killing bacteria

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sebum (secreted by, function)

  1. secreted by: sebaceous (oil) gland

  2. function: lubricates the skin and hair and has antimicrobial properties to inhibit bacterial growth

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defensins (secreted by, function)

  1. secreted by: skin, mucous membranes, and neutrophils

  2. function: antimicrobial peptides that poke holes in bacterial cells membranes

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skin releases antimicrobial substances from ________ glands and ________ glands

sweat; sebaceous

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function of mucous membrane as part of the immune system

produce mucus to prevent entry of microbes and release antimicrobial substances (e.g., defensin, lysozymes, IgA)

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IgA (immunoglobin A - location & function)

an antibody that plays a key role in protecting mucosal surfaces (areas exposed to the external environment)

  • located mainly in mucus, saliva, tears, breast milk, and secretion from the respiratory, digestive, and urogenital tracts

  • neutralize pathogens before they can infect cells

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commensal microflora

  1. AKA normal microflora

  2. microorganisms that reside on body surfaces (e.g., GI tract, skin)

  3. nonpathogenic

  4. interfere with attachment of potential pathogenic organisms

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true or false: while the second line of defense include selected immune cell and antimicrobial proteins, they are still nonspecific and does not remember the pathogens that they kills, just kill any potentially harmful substance

true

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function of neutrophils in the immune system

destroy engulfed particles

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functions of dendritic cells and macrophages in the immune system

destroy particles and then present fragments so that the specific immune cells (e.g., T lymphocytes) can learn and kill that pathogens

  • basically the post office that show the FBI most wanted list

<p>destroy particles and then present fragments so that the specific immune cells (e.g., T lymphocytes) can learn and kill that pathogens</p><ul><li><p>basically the post office that show the FBI most wanted list</p></li></ul><p></p>
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functions of basophils and mast cell in the immune system

promote inflammation

  • release granules containing chemicals (histamine, heparin, ecosanoids)

    —> chemicals increase movement of fluid from blood to injured tissue

    —> some induce chemotaxis (attract immune cells)

<p>promote inflammation</p><ul><li><p>release granules containing chemicals (histamine, heparin, ecosanoids)</p><p>—&gt; chemicals increase movement of fluid from blood to injured tissue</p><p>—&gt; some induce chemotaxis (attract immune cells)</p></li></ul><p></p>
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histamine (secreted by, function)

  1. basophil and mast cells

  2. increases vasodilation and capillary permeability (triggering inflammation)

<ol><li><p>basophil and mast cells</p></li><li><p>increases vasodilation and capillary permeability (triggering inflammation)</p></li></ol><p></p>
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heparin (secreted by, function)

  1. basophil and mast cells

  2. acts as an anticoagulant

<ol><li><p>basophil and mast cells</p></li><li><p>acts as an anticoagulant</p></li></ol><p></p>
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eicosanoids (secreted by, function)

  1. basophils and mast cells

  2. increases inflammation

<ol><li><p>basophils and mast cells</p></li><li><p>increases inflammation</p></li></ol><p></p>
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how does phagocytosis of neutrophil destroy the pathogen?

respiratory burst - the pathogens will be destroy through reactive oxygen contain molecules - create a burst

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function of natural killer cells

  1. destroy unhealthy/unwanted cells (e.g., virus/bacteria-infected cells, tumor cells, cells of transplanted tissue)

  2. perform immune surveillance (patrol the body, detect unhealthy cells)

  3. release perforin (creating pores on targeted cells)

  4. release granzymes (cause apoptosis of cells)

<ol><li><p>destroy unhealthy/unwanted cells (e.g., virus/bacteria-infected cells, tumor cells, cells of transplanted tissue)</p></li><li><p>perform immune surveillance (patrol the body, detect unhealthy cells)</p></li><li><p>release perforin (creating pores on targeted cells)</p></li><li><p>release granzymes (cause apoptosis of cells)</p></li></ol><p></p>
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perforin (secreted by, function)

  1. natural killer cells (NK cells)

  2. create transmembrane pores in unwanted cells

<ol><li><p>natural killer cells (NK cells)</p></li><li><p>create transmembrane pores in unwanted cells</p></li></ol><p></p>
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granzymes (secreted by, function)

  1. natural killer cells (NK cells)

  2. enter the pore created by perforin and cause apoptosis of cell

<ol><li><p>natural killer cells (NK cells)</p></li><li><p>enter the pore created by perforin and cause apoptosis of cell </p></li></ol><p></p>
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apoptosis

cell death cause by shriveling of cells

<p>cell death cause by shriveling of cells</p>
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how does eosinophils attack multicellular parasites?

release proteins (enzymes and toxic substances) that form transmembrane pores in parasite’s cells

<p>release proteins (enzymes and toxic substances)  that form transmembrane pores in parasite’s cells</p>
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true or false: beside from killing parasites, eosinophil also participate in immune response of allergy, plasma and phagocytosis of antigen-antibody complexes

true

<p>true</p>
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cell of innate immune system recognized microbes as foreign because of _________

receptors (toll-like receptors) - that either recognizes or do not recognizes the pattern on the microbes surface

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steps of inflammations

an immediate response to ward off unwanted substance (local/nonspecific)

  1. release of chemical that initiate immune response

  2. release of chemicals that cause vascular changes (vasodilation, increased capillary permeability, increased endothelial expression of molecules for leukocyte adhesion, CAMs)

  3. recruitment of leukocytes through margination, diapedesis, and chemotaxis

  4. delivery of plasma proteins - form clots, stimulate pain receptors (kinin), increase cpaillary permeability (kinin), increase production of CAMs by capillary cells (kinin)

<p>an immediate response to ward off unwanted substance (local/nonspecific)</p><ol><li><p>release of chemical that initiate immune response</p></li><li><p>release of chemicals that cause vascular changes (vasodilation, increased capillary permeability, increased endothelial expression of molecules for leukocyte adhesion, CAMs)</p></li><li><p>recruitment of leukocytes through margination, diapedesis, and chemotaxis</p></li><li><p>delivery of plasma proteins - form clots, stimulate pain receptors (kinin), increase cpaillary permeability (kinin), increase production of CAMs by capillary cells (kinin)</p></li></ol><p></p>
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kinin (secreted by, function)

  1. liver and other cells (from inactive kininogens)

  2. stimulate pain receptors, increase capillary permeability, increase production of CAMs by repillary cells

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margination of leukocytes

more and more leukocytes adhere to the endothelial membrane of blood vessels through cell adhesion molecules

<p>more and more leukocytes adhere to the endothelial membrane of blood vessels through cell adhesion molecules</p>
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diapedesis of leukocytes

leukocytes squeeze out of the blood vessels wall and into the tissues where the infection site is location

<p>leukocytes squeeze out of the blood vessels wall and into the tissues where the infection site is location</p>
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chemotaxis of leukocytes

leukocytes migrate toward chemicals released from damaged dead, or pathogenic cells

<p>leukocytes migrate toward chemicals released from damaged dead, or pathogenic cells</p>
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pyrogens (secreted by, function)

  1. macrophages

  2. fever-inducing

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what are the chemicals involve with inflammation)?

histamine, leukotrienes, prostaglandins, chemotactic factors

<p><span>histamine, leukotrienes, prostaglandins, chemotactic factors</span></p>
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recall the effect of inflammation (how does it happens and what does it cause?)

  1. fluid (exudate) moves from blood to injured or infected area in the tissues

    —> increasing cpaillary permeability

  2. vasodilation brings more blood to the area

  3. loss of plasma proteins to decrease osmotic pressure, thus decreasing fluid reabsorption into the blood (swelling - extra fluid to “wash” infected through lymphatic capillaries) and proteins also help with immune response

  4. macrophages eats bacteria, damaged host cells, and dying neutrophils

  5. tissue repair begins as fibroblast form new CT

<ol><li><p>fluid (exudate) moves from blood to injured or infected area in the tissues </p><p>—&gt; increasing cpaillary permeability</p></li><li><p>vasodilation brings more blood to the area</p></li><li><p>loss of plasma proteins to decrease osmotic pressure, thus decreasing fluid reabsorption into the blood (swelling - extra fluid to “wash” infected through lymphatic capillaries) and proteins also help with immune response</p></li><li><p>macrophages eats bacteria, damaged host cells, and dying neutrophils</p></li><li><p>tissue repair begins as fibroblast form new CT</p></li></ol><p></p>
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4 hallmarks (cardinal signs) of inflammation & its pathology

  1. redness (increased blood flow)

  2. heat (increased blood flow and increased metabolic activity)

  3. swelling (increased in fluid loss from capillaries into the tissue)

  4. pain (stimulation of pain receptors by kinin)

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fever (pyrexia)

abnormal body temperature elevation (1 celcicus or more from normal of 37 celsius) due to release of pyrogens from macrophages or infectious agents

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steps of fever

  1. pyrogen circulate throughout the blood and target hypothalamus

  2. once reached, hypothalamus releases prostaglandin E2

  3. prostaglandin E2 signal the hypothalamus to raise temperature set point leading to fever

  4. hypothalamus stimulate constriction of dermal blood vessels (preventing heat loss) & muscle shivering (generate heat)

  5. bodily metabolic rate increases to promote elimination of harmful substances

  6. liver and spleen bind zinc and iron to slow microbial reproduction

  7. defervescence: body return to normal temperature

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benefits of fever

  1. inhibit reproduction of bacteria & viruses (higher body temp slow down replication)

  2. promotes interferon activity (fever boosts interferon)

  3. increases activity of adaptive immunity (elevated temperature speed up lymphocyte activation & proliferation)

  4. accelerates tissue repair (heat increases metabolic rates)

  5. increases CAMs (Cell Adhesion Molecules) on endothelium of capillaries in lymph nodes

  6. additional immune cells migrating out of blood

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true or false: If either CD4 or CD8 on a T cell matches with MHC Class I or II and binds with moderate strength, the cell survives positive selection because it can recognize self-MHC, which is necessary for proper immune function. However, if the T cell binds too strongly to a self-antigen during negative selection, it undergoes apoptosis to prevent it from attacking the body’s own tissues, helping avoid autoimmunity.

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what is the temperature of low-grade, intermediate grade, and high-grade?

  1. low grade: 100-101 F

  2. intermediate grade: 102 F

  3. high grade: 103-104 F

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risk of intermediate/high fever or long term low -grade fever

  1. changes in metabolic pathways and denaturation of proteins

  2. possible seizures

  3. irreversible brain damage (greater than 106 F)

  4. death (greater than 108 F)

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adaptive immunity involves specific lymphocytes responses to ____________

antigen

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_______________ consist of lymphocytes and their products

immune response

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since it takes days to develop, __________________ is considered the third line of body’s defense

adaptive immunity

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what are the two branches of adaptive immunity and its component?

  1. cell-mediated immunity (T-lymphocytes)

  2. antibody-mediated immunity (B-lymphocytes, plasma cells, and antibodies)

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antigens

substance that binds a T-lymphocytes or antibody and can trigger an immune response if foreign to the body

  • have many different type

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what are the barrier that contain viruses as a form?

protein capsid

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true or false: bacteria an fungi have capsid

false: bacteria and fungi have cell wall

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antigen

any substance (e.g., proteins, carbohydrate, or other molecules) that triggers and immune response because it is recognized as foreign y the immune system

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foreign antigen vs. self antigen

  1. Foreign antigen: An antigen from outside the body that usually binds to immune components and triggers an immune response.

  2. Self-antigen: An antigen produced by the body that normally doesn’t bind to immune components, preventing an immune response.

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how does autoimmune disorders work?

when the immune system react to self-antigens and instead of ignoring the self-antigen cell, it starts attacking it

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antigenic determinant

  1. AKA epitope

  2. specific site on antigen recognized by the immune system (determine if foreign or self)

  3. each antigen can have many different epitopes, each with different shapes

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true or false: pathogens tend to have more variety and complexity in their antigenic determinant than human

true; this diversity help them better evade the immune system

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immunogen

antigent that induce an immune response

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immunogenicity

the ability of an antigen to trigger an immune response

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true or false: immunogenicity of an antigen increases with increase in the antigen’s degree of foreignness, size, complexity or quantity

true

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haptens (what it is, function, and an example)

small molecules that can’t trigger an immune response on their own but become immunogenic when attached to a carrier molecules (usually a proteins)

  • can also cause hypersensitivity reactions (allergies)

  • e.g., the toxin in poison ivy becomes immunogenic when it bind to skin proteins

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what happens when the immune system lack tolerance for specific self-antigent?

initiate an immune response as if the cells were foreign

  • cross-reactivity

  • forbidden clones

  • altered self-antigens

  • entering areas of sequestered antigen

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cross reactivity

the immune system mistake self-antigens for foreign antigens because they share similar structures

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forbidden clones

harmful cells that attacks the body own cells despite recognizing self-antigens

  • escaped the elimination process by chance (the body immune response is tasked with destroying all cell like this through negative selection)

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altered self-antigens

mutation or damage altered self-antigens which make them look s unfamiliar to the immune system, promoting it to attack them as if foreign

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receptor complexes (structure of lymphocytes) and the different type

site on T & B lymphocytes that binds one specific antigens

  • TCR (t-cell receptor) antigen receptor of T-lymphocytes

  • BCR (b-cell receptor) antigen receptor of T-lymphocytes

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how do B-lymphocyte and T-lymphocyte interact with antigens?

  1. B-lymphocytes: direct contact with the antigen without the need for processing

  2. T-lymphocytes: don’t make direct contact with antigen - required other cells to process and present the antigen to the coreceptors of the T-cell (helper T-cell require APCs while cototix would require the nucleated cells to have antigen fragments)

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function of helper T-cells (CD4+)

act as coaches to activate other immunes (e.g., NK cells, macrophages)

  • guide the immune response

<p>act as coaches to activate other immunes (e.g., NK cells, macrophages)</p><ul><li><p>guide the immune response</p></li></ul><p></p>
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function of cytotoxic T-cells (CD8+)

act as “assassins” to destroy infected or harmful cells

  • target cells already presenting the antigen

<p>act as “assassins” to destroy infected or harmful cells </p><ul><li><p>target cells already presenting the antigen</p></li></ul><p></p>
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function memory T-cells

remember past invader and respond (e.g., activating an immune response, clal in reinforcement) quickly if the same invader

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function of regulatory T-cells

act as the “calm-down squad”

  • regulate and control the immune response to prevent overraction or autoimmunity

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cluster of differentiation

specific surface markers or proteins found on immune cells - help identify and classify different types of immune cells

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what is the difference between an antigen and a cluster differentiation (CD)?

Antigen:

  • • A foreign substance (e.g., proteins, carbs) that triggers an immune response.

  • • Examples: Bacteria, viruses, pollen.

Cluster of Differentiation (CD):

  • Cell surface markers or proteins found on immune cells.

  • • Help identify and classify immune cells (e.g., CD4 on helper T-cells, CD8 on cytotoxic T-cells).

  • Not foreign substances, but markers on cells involved in the immune system.

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antigen presentation

cells display an antigen on their plasma membrane so T-cells can recognize it and mount an immune response

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how does all nucleated cell of the body present antigen?

use MHC I (major histocompatibility complex) to show “self” antigens