the immune system Flashcards

1
Q

what is the purpose of the bodys defence system

A

protecting the body against:

  • physical damage: accidental injury
  • extreme conditions: excessive or limiting levels of water, oxygen and temp
  • invasion: of micro-organisms and viruses (pathogens)
  • the body is a pathogen paradise, warm, moist, nutrient rich, means of travel, secure
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2
Q

what is species resistance

A
  • ability to ward off disease through defences
  • opposite = susceptibility (lack of resistance)
  • diseases can be unique to a species
  • tissues don’t provide a suitable environment
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3
Q

how is it complex and imperfect

A
  • individuals protect against a wide variety of foreign molecules and organisms
  • cant predict which invaders will be encountered
  • must know not to attack its own cells and molecules
  • solution = barriers, large array of defences operating at molecular level
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4
Q

what a an overview of the immune response

A

non-specific: defence mechanisms (innate immunity)

  • first line (external barriers)
  • second line (cellular counterattack / internal barriers): phagocytic WBC, antimicrobial proteins, inflammatory response
    specific: defence mechanisms (adaptive immunity), third line defence (‘sentries’)
  • third line (immune system): lymphocytes and antibodies, T cells, B cells, NK cells
  • invading pathogens: confronted in this order with the 2nd and 3rd lines occurring simultaneously
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5
Q

what are mechanical factors involved in 1st line of defence

A
  • skin: impervious barrier, ‘good’ bacteria lives on skin (difficult for pathogens to become established), sebum (kills) and sweat (inhibits growth) and sloughing (removes / inhibits growth)
  • mucous membranes: line bodies cavities (digestive, urinary, reproductive, respiratory), inhibits entry (trapped in mucous), less effective than skin
  • hairs: nose cavity / ears, traps / filters them out
  • cilia: hair like projections, line nasal cavity / trachea, beating of cilia traps particles which are moved / coughed up from lungs
  • epiglottis: control valve, prevents entry of substances into throat
  • urethra: flushing action, inhibits growth
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6
Q

what are chemical factors involved in 1st line of defence

A
  • sebum: sebaceous gland secretion (oil), maintains hair and skin, waterproofing mechanism, kills
  • sweat glands: flush skin, anti-bacterial environment, inhibits growth
  • lysozyme: antimicrobial proteins / enzyme found in secretions (saliva, sweat, tissue fluid, tears), cleansing / flushing action, kills
  • acids: gastric juice (HCl), enzyme, mucous and vaginal secretions (acidic), attack cell wall of pathogens, kill / inhibit
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7
Q

how are phagocytic cells involved in the 2nd line of defence

A
  • chemotaxis: movement, stimuli that allows for a change to occur
  • phagocyte: use chemical receptors to detect pathogens, two main types
    1. neutrophils: move from blood to infected tissue (chemotaxis), engulf / destroy, self destruct when ‘bloated’
    2. macrophages: ‘big eaters’, migrate through body / patrol specific tissues (respiratory tract, connective tissue, epithelial), cellular extensions (feel, grab, latch on, engulf), return to lymph system
    2. 1. eosinophils: deal with large parasites by discharging enzymes
    2. 2. dendritic cells: populate skin and tissues in contact with environment, migrate to lymph nodes if a pathogen is detected
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8
Q

what is innate vs adaptive immunity

A
  • I: all animals, rapid response, 1st and 2nd line defence

- A: vertebrates only, slower response, 3rd line of defence

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9
Q

how are NK cells involved in the 2nd line of defence

A
  • cellular counter attack
  • circulate / roam and attack presenting proteins associated with abnormal and virus infected cells
  • release chemicals that lead to cells death
  • detect cells infected by viruses, cause the loss of semi-selective permeability of membrane (disrupts operation of cell)
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10
Q

how are antimicrobial peptides / proteins involved in the 2nd line of defence

A
  • attack pathogen / impede their reproduction
  • released from cells in response to non-self antigen
  • peptides: similar to NK cells, proliferate membrane
  • interferons (IFN): type of cytokine, secretes by virus infected cells, signals uninfected cells to attack and inhibit viral reproduction
  • 30 proteins in blood plasma = activated by IFN, cascade of events, membrane attack (construction of pore / lysis)
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11
Q

what is the purpose of the inflammatory response in the 2nd line of defence (localised)

A
  • purpose: disposal of microbes and their toxins to reduce speed of pathogens
  • destroy them, prevent entry of more pathogens
  • remove damaged tissue / cell debris, repair of damaged tissue
  • signs: redness, swelling, heat and pain
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12
Q

describe the steps of the inflammatory response (localised)

A
  1. skin is broken, non-specific inflammatory response
  2. chemical signals (initiation) released by microbes / injured cells attract mast cells (special cells) which release histamine and heparin and complement proteins
    - histamine: increases BF, dilation of arterioles, constriction of venules (redness / heat), inflate / increase P (swelling), capillaries = more permeable, ‘leak’, helps delivery of antimicrobial proteins / cells
    - heparin: prevents clotting in immediate area, clotting in damaged site (prevents more pathogens from entering)
    - neutrophils and macrophages: release cytokines (signal molecules), promote blood flow, engulf pathogens and products (pain), die and form pus
    - pus: not bad, exploded neutrophils, dead bacteria
  3. histamine and complement proteins signal ‘finished’ and phagocytes are no longer attracted
  4. new cells produced, repair of damaged tissue
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13
Q

what is the purpose of the inflammatory response in 2nd line of defence (systemic)

A
  • cause: severe tissue damage or infection
  • purpose:
    1. increase WBC production, pathogens toxins / pyrogens (signal from WBC)
    2. trigger fever (adjust body’s thermostat)
    3. enhance phagocytosis and accelerate repair, inhibit microbial growth
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14
Q

what substances make up the 3rd line of defence

A
  • adaptive immunity (efficient, selectively targets particular pathogens)
  • features: specificity (targets pathogens), memory (long lived memory cells) and discriminatory (self / non self)
  • humoral: B lymphocytes, secrete antibodies (immunoglobin), ‘tag’ cells for elimination
  • cell mediated: T cells, directly attack pathogens (similar to NK), indiscriminant
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15
Q

what are antigen membrane receptors

A
  • each lymphocyte has a receptor type that recognises a specific antigen of a pathogen
  • large with unique epitopes (sub-region)
  • different arrangement of bonds for each receptor
  • compatible with surface molecules
  • receptors on one cell = same, receptors unique to each B / T cell
  • B cell = Y shaped
  • T cell = V shaped
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16
Q

how do we account for pathogens past present and future

A
  • relies on population of lymphocytes with diverse receptors
  • differentiation of B / T, alternative gene segments are rearranged, different genotypes, different membrane receptors
  • diverse range of antigen receptors (few cells of each)
17
Q

how are B / T cells produced and self tolerance

A
  • lymphocytes originate in bone marrow (stem cells), develop into B or T
  • T: migrate to thymus
  • B: stay in bone marrow
  • cells are tested, lymphocyte with membrane receptors = specific to bodies molecules (show immune response) = non-functional / destroyed
18
Q

what is the relationship between self molecules and MHC

A
  • major histocompatibility complex
  • proteins that mark surface of bodies cells (self)
  • different codes for MHC, large number of alleles
  • class 1: on most body cells
  • class 2: antigen presenting cells, also have this class (dendritic, macrophages, B)
  • MHC causes rejection of organs / tissue grafts
  • foreign MHC = antigen, induce immune response
19
Q

describe the steps in the humoral response (3rd line of defence)

A
  1. b cells bind to antigen
  2. result in activation and proliferation of cells that secrete antibodies, attach to pathogens or ‘free’ antigens
    - note: antibodies don’t directly kill infected cells or pathogens but attract cells
  3. cause aggregation of complement proteins
  4. serve as markers signalling macrophage phagocytosis, both can occur at once
20
Q

describe the process of cell mediated response (3rd line of defence)

A
  • specific t cell: only alerted of pathogen when compatible antigens are presented on surface of cell, infected body cell or via antigen presenting cell
  • antigen presenting cells: APC, leucocytes, engulf and breakdown invaders
  • foreign antigens: on surface of MHC complex (class 2)
  • antigens: also displayed by b cells (MHC2) and infected body cells (MHC1)
21
Q

what are the different stages of an immune response (primary exposure etc)

A

primary immune response: first exposure
- antigen ‘interact’ with complementary B/T cells
- activates clonal selection (proliferation of many identical and antigen-specific cells)
- effector: short-lived, combat antigen
- memory: long-lived, bear receptors for antigen, circulate body / blood
delay response:
- before maximum effector cell response occurs
- illness develops while producing effector B/T cells
- illness diminishes as effector cells destroy antigens
subsequent exposure: to same antigen
- more efficient response
- reaction of memory cells from last exposure
- less delay in generating effector cells, capacity is called immunological memory

22
Q

what are and how do humoral and cell mediated cells work together

A
  • humoral: b cells (chemical attack), effector b cells secrete antibodies into blood and lymph
  • cell-mediated: t cells (direct attack), active destruction by cytotoxic t cells
  • t helper cells: trigger and regulate both types
23
Q

what are helper T cells / how are they stimulated

A
  • (TH): initiating and regulating an immune response, does not carry out a response, receptors bind to antigens presented by MHC2 (roaming macrophages ingest free antigens / pathogens and ‘present’)
  • stimulation of TH:
    1. APC engulf / destroy pathogen, present antigen
    2. when APC and compatible TH interact they release cytokines
    3. interaction stimulates TH cell to proliferate
    4. clones produced, large numbers of effector and memory TH cells
    5. TH release a 2nd cytokine, stimulate cytotoxic t cells and b cells into action
24
Q

what are / how are cytotoxic T cells stimulated

A
  • Tc: cell mediated response, receptors bind to antigens presented by MHC1 (cells infected by virus, cancer)
  • stimulation of Tc: directly kill infected cells
    1. infected body cell display viral antigens on their MHC1
    2. compatible Tc binds to the antigen (MHC1) complex on infected body cell
    3. interaction + cytokinins stimulate Tc cell and proliferate / differentiate into active killer effector (release perforin which leads to lysis)
  • regulation: immune response builds and continues until antigen presentation subsides
25
Q

what are / how are B cells stimulated

A
  • activates compatible b cells to secrete antibodies
    1. b cells internalise antigens and present with MHC2, unlike other APCs, b cells can only print on compatible antigen
    2. binding with and stimulation from a compatible TH (via 2nd cytokine)
    3. activates b cells
    proliferation / differentiation into memory and plasma cells to produce antibodies (important in cell mediated, not separate, complementary / simultaneous)
26
Q

what is active immunity

A
  • dependent on response of immune system
  • contraction: of disease, produces memory cells
  • artificially acquired: immunisation / vaccination
  • contain: inactivated bacterial toxins, killed microbes, parts of microbes or viable but weakened microbes
  • function: doesn’t cause disease, acts as antigens to stimulate primary response (memory cells)
27
Q

what is passive immunity

A
  • transfer: of antibodies between individuals (mother to child), pregnant woman antibodies passed to foetus via placenta
  • artificial: injection of antibodies (immediate immunity)
28
Q

what occurs when one has an abnormal immune function

A
  • exaggerated responses to antigens (allergy)
  • responses to ‘self’ antigens (autoimmunity)
  • diminished immune responses (innate / acquired)
  • allergies (hypersensitivity): exaggerated response to environmental antigens (allergens) on subsequent exposure
  • hay fever: ‘explosive’ release of histamine from mast cells
  • anaphylaxis: antigen introduced systemically (bite)
  • autoimmune diseases: loss of tolerance for ‘self’ molecules, body produces antibodies against own molecules
  • healthy people have lymphocytes capable of reacting against ‘self’ but instances are regulated
  • example: coeliac disease, rheumatoid arthritis, multiple sclerosis, lupus, ankylosing spondylitis
29
Q

what is AIDS HIV

A
  • immunodeficiency disease, escapes immune system, evolves in the host body
  • HIV DNA remains dormant in bodies cells DNA, destroys the immune system
  • transmitted via bodily secretions, manipulates host DNA to produce more HIV
  • HIV destroys TH cells, depressing cellular immunity, although B cells and TC cells initially mount a vigorous response to viral exposure
  • over time a profound deficit of B cell and TC cell function develops
30
Q

what is innate vs adaptive immunity

A
  • I: all animals, rapid response, 1st and 2nd line defence

- A: vertebrates only, slower response, 3rd line of defence