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Immunity pt.1, toxins (h2o2), perforins, granzymes, Doubt - physiological…

- - - - after diff - you get for each
  - - - no reason why you develop it
    - - develop only if exposed to that particular disease
  - - - in association with phagocytosis
    - - plasma cells, b lymphocytes
        
        some antibodies are stored in the form of memory cells
- - - - used to stimulate immune responses artificially
        
        when introduced into body to stimulate response
  - - - toxoids, etc
  - - - by developing
        
        when pathogen multiplies
        
        cells get time to plan out an immune response
      - so vaccines try to mimic this environment
        
        so effectiveness of live vaccine is greater than a dead vaccine
        
        but dosage it less, so effective immune response
        
        antibodies generates
        
        so memory cells are made
  - - - some - immune for life - bcg
      - some - get over after time - covid
        
        these need to be supplemneted with booster vaccine
        
        to ensure secondary response
        
        IgG produced for secondary response
- - - - non-virulant type of pathogens
      - eg bcq, polio
        
        but polio can be sabin/ live and dead/ salk
  - - - rabies vaccine
    - - these can't be introduced even in small conc so they have to be killed
    - - alcohol killed - disinfectatn
        
        phenols
        
        untraviolet light
  - - - eg diptheria bacteria
    - - treated with formaldehyde
        
        partially denatures the toxin
        
        converts it into a toxoid
        
        this might not be able to cause the disease but it will stimulate an immune response to produce antibodies
    - - diptheria, tetanus, etc
  - - - capsule, cell wall
    - - fm polysaccharides fm the surface of capsule of bacteria
        
        coccus bacteria
    - - fm polysaccharides fm cell wall
    - - polysaccharide/ polypeptide fm cell wall
  - - - measles, mumps, rubella
        
        combination of 3 different
    - - tetanus, diptheria, pertussis/ whooping cough
- - - - rbc has presence of specific antigen
        
        O - no antigens
        
        eg
        
        blood of person with B with A - clumping reactions
  - - - if recognised by own cells
  - - - must be foreign body/ antigen
        
        activates b lymphocytes
        
        produce plasma cells
        
        very specific
        
        complementary. to each other
  - - - after 1st exposure, for a brief perios, body suffers
        
        but they don;t get it again because small portion of antibodies are retained - calles memory cells
        
        because antigen characteristics haven't changed
        
        so second time response is quicker, and defeats, even without you realising
- - - - then released to body fluids
    - - mainly by natural killer cells and cytotoxic t cells
- - - - takes time
    - - ready made
  - - - so no drastic
- - - - for everyb pathogen, t cell can recognise it
        
        specific b and t
        
        because receptors are specific to antigen
        
        when t maturea, develops receptors of particulat antigen receptors
        
        to be specific - cna recognise only one kind of antigen - one receptor
  - - - if apc has peptide that matches t cell
        
        t converted into specialised and forms lymphoblast
        
        only if complementary
        
        already clocal selection
        
        now clonal expansion
        
        repeated mititoc division
        
        1 more item...
  - - - once gone to thymus, develop t cell receptors
        
        then can initiate immune response
        
        apcs help it convert to lymphoblast
  - - - Tc - cytotoxic t cells
        
        natural killer cells
        
        t killer cells
        
        tendency to patrol body
        
        lookin for cells infected by pathogens
        
        display peptide frags on cell
        
        first thing to catch is the macrophages
        
        apcs - displayed
        
        1 more item...
      - Tm
        
        memory t cells
        
        when can recognise antigen coz of receptor
        
        they are sensitised
        
        because of presence of antigen
        
        able to retain sensitization for future use
        
        in duture of encounters same antigen, it can produce secondary immune response - very quick and heightened
        
        1 more item...
      - Ts
        
        suppressor T cells
        
        not seen in B
        
        type which are capable pf inhibiting immune response
        
        suppress activity of b and t lymphocytes (maj types)
        
        if tumour, associated with cancer suppressing genes
      - Th
        
        helper t cells
        
        function - contradicting function of suppressor
        
        when it inhibits, helpers enhance immune response
        
        enhancement of response happens by secretion of signalling moelcules - cytokines
        
        cytokines - signalling molecules - growth or diff of same or diff cells
        
        cytokines have impact on 2 other cells
        
        2 more items...
- - - - as long as there is no receptor - not capable of recognising the antigen
        
        only sensitised by antigen - come into contact with it
        
        remain confined in bone marroe/ thymus
        
        once mature and appropriate receptors - put into blood rapidly circulate bw blood and tissues
        
        coordinate with each other - can come in contact with pathogen
        
        when immature - no specific use for it
  - - - body can compete aith any antigen
        
        each antigen can only be detected and destroyed by one antibody
        
        apc, clonal , differentiation etc is in both b and t cells
  - - - exposure
        
        response of lymphocytes by producing antibodies at initial exposure to pathogens
        
        very ffeeble/ weak
        
        coz after time, it declines rapidly
      - importance
        
        still important
        
        2 reasons
        
        formation of memory cells and specialised cell receptors - sensitised to presence of particular antigen
      - long coz of production of memory cells and receptors
      - over 100 doff strains of viroses
        
        cause common colds
        
        diff srtrains - diff antigens
        
        each time - attacked by diff strain of influenza virus
        
        primary response each and every time
    - - respones of body to subsequent exposure to same pathogen
      - renewed
        
        renewed immune response
      - rapid immune response
      - anamnestic immune response
      - advantage it - response doesn't weaken
        
        might weaken, must doesn't decline as fast
        
        so significant reduction in response levels
        
        already memory cells
        
        faster, lesser amount of decline in secondary
        
        coz already formed in primary
        
        1 more item...
- - - - is blood smear is stained, nucleus is distinct, then you can identify the different cells
        
        apart fm size of cells, nucleus helps to differentiate
    - - in bone marrow
        
        stay there for a while
        
        then transferred elsewhere
        
        scavengers - remove cellular debris
        
        depending on where originted
        
        3 types
        
        3 more items...
      - important in initiating
- - - - diff into everything/ anything fm same family - blood cells
      - come fm layer of cells in yoke sac - mesenchymal cells
        
        but in fetus, multipotent made in lymphoid - spleen, thymus, lymph nodes, liver
        
        but in adults, always produced in bone marrow
        
        sum total of all events by which immature lymphocytes converted into mature lymphocytes - lymphopoiesis
    - - short lifespan
      - related to antibody mediated
      - formed in bone marrow, mature in bone marrow, then transferred to diff lymphoid organs
      - seen in nodules and spleen
        
        tendency to cirdulate bw blood and tissues
        
        present in large number in nodules and spleen
      - initial study, fm bursa of fabricus
        
        lymphoid organ near cloaca - reproductive organ
        
        b for bursa
        
        but formed fm bone marrow too, so it sould be b for bone marrow
      - some analogus structures to cloaca in humans
      - initially when formed, immature
        
        can't recognise presence of antigen
        
        so surface receptors
        
        develop surface receptors when they become mature
        
        antigen binding receptor antibody
        
        recognise presence of antigen and initiate immune response
      - maturing - antigen binding receptor antibody
  - - - unlike b fm bone marrow, stays and matures,
        
        t cells fm bone marrow, but matures in thymus
        
        Thymus - small luymphoid organ behind sternum
        
        chest bone
        
        middle front portion of rib cage
        
        increase in size fm birth till puberty
        
        1 more item...
    - - but when mature, receptors develop
        
        t cell receptors
        
        then can recognise
        
        only then they can respond to antigen
- - - - AMIS - antibody mediated (immune) systems
        
        mech by which attained is by activation of b lymphocytes
        
        humoral - fluid
        
        if antibodies distributed - by blood or lymph
      - role of AMIS
        
        especially active when pathogens have produces toxins and toxins entered into body fluids (blood and. lymph)
        
        immunity against toxins by pathogens
        
        effective against bacterias - more against polysacch capsule
        
        against viruses
    - - mainly t lymphocytes
        
        mainly by diff types of t cells
        
        immunity against cells affected by pathogens
        
        cellular immunity
        
        unlinke AMIS, CMIS is more effective especially organ transplants - rejection happens because of CMIS and for cancer
- - - - active
        
        definition
        
        types obtained by infection or vaccination
        
        active acquired immunity
        
        development
        
        result of presnce of live pathogen in body
        
        or presence of pathogen in weakened (attenuated) state but has specific antigens on its surface
        
        enables acquirement
        
        when live or weakened or dead, body actively produces antibodies against it
        
        diff ways to develop
        
        by infection
        
        person suffers fm chickenpox, measles, mumps, rubells
        
        slready has pathogens
        
        contract the infection
        
        vaccinations
        
        suspensions of pathogens in
        
        viral and bacterila vaccines
        
        1 more item...
        
        introdiction of antigens
        
        vaccinated and vaccines have antigens
        
        infection is natural active
        
        artificial/ induced active immunity
      - passive acquired immunity
        
        development
        
        condition where ready-made antibodies are introduced to fight infection
        
        role that obdy plays is passive
        
        assumed that body can't produce in short time - so ready made
        
        none of lymphocytes are activated
        
        1 more item...
        
        natural passive
        
        maternal (Ig)
        
        5 types of immunoglobulants (antibodies)
        
        Igg (cross placenta), IGa (in cholestrol), Ige - entire lactation period
        
        ready made directily transferred
        
        artificial /induced passive immunity
        
        introduction of ready made antibodies in the form of serum/. hyper immune sreums
        
        maternal
        
        ready made antibodies
- - - - good because site of infection is peripheral cells
    - - ingest/cut pathogen so that antigen of pathogen
        
        peptide fragments of the antigen are displayed on the apc cells'surface
        
        this phenomenon - antigen presentation
    - - major histo compatibitity complex
        
        activate t cells - divide to form cones of helper t cells
        
        when activates - repeated mitotic division to form a clump
        
        clones then produce cytokine
        
        cytokines - signalling molecules - secreted by cells to influence growth or differentiation of its own cells
        
        this growth or diff cann be for its own or for any other cells
        
        1 more item...
    - - it finds one b cell which surface receptors complementary to peptide fragments on apc
        
        this b cell with complementary apc
        
        called clonal selection
    - - undegoes repeated mitosis
        
        at end - daughter cell genetically identical
        
        clones
        
        because each one has sirface receptor complementary to peptide frags displayed on apc
        
        after clonal selsction, mitotic division
        
        clonal expansion
    - - plasma cells produce antibodies
        
        rate at which plasma produces antibodies
        
        2000 mols per second
        
        rapid
        
        so many because activated b cells, plasma cells are short lived
        
        few days or weeks, plasma cells then die
        
        1 more item...
    - - once infection over, only some memory cells kept
        
        rest destroyed
        
        able to retain memory of previous encounter with pathogen
        
        form the basis of immunolgical memory
        
        so next time body is affected by antigen characteristics
        
        first time, all these steps had to happen , apc, mhc2, clonal etc
        
        1 more item...
- - - - b - amis
      - t - cmis
    - - b - smaller lifespan
      - t - longer life span
    - - b - in bone marrow and matures there
        
        antigen binding receptor antibodies - when its mature
      - t - produced in bone marrow - transferred to thymus to mature
        
        t cell receptors when its mature
    - - b - no memory
        
        but plasma cells have memory
      - t - specialised t cells can retain the memory
        
        memory t cells
    - - b - offer protection for extracellular antigens
        
        viruses, bacterial toxins, fungal parasites
        
        in a tissue
      - t - intracellular antigens
        
        viruses, bacterial toxins, fungal parasites
    - - b - form plasma cells
      - t - form clones of lymphoblast
        
        can diff into cytotoxic, helper, memory, suppressor
    - - b - antibodies
      - t - 4 types of cells
        
        which produce cytokines
    - - b - not motile
        
        antibodies produced don't move to site of infection
        
        act within blood vascular system
      - t - non motile
        
        but certain can move to the site
        
        these can act outside the vascular system
    - - b - amis
        
        humoral - body fluids
        
        immunity only agaisnt pathogens that have entered into body fluids
      - t - against larger pathogens
        
        pathogen infected cells
    - - b - not respond to cancerous cells or organ transplants
      - t - can suppress growth of cancerous/ tumourous cells
        
        cause tissue/ organ rejection
    - - b - can't/ don't inhibit
      - t - can inhibit - because of suppressor t cells
        
        by suppressing b and t cells
- - - - p - initial
      - s - subsequent
        
        each time after first
    - - p - long time
      - s - very rapid adnd quick
    - - p - shorter
        
        after time it declines
      - s - lasts for several years
    - - p - being produced
      - s - already produced memory cells and receptors
    - - p - short-lived
      - s - for longer span of time
        
        several years, or lifetime
- - - - polio
        
        salk/ sabin
      - conventional methods
        
        use the whole microorganism
      - might live, can be killed or inactive, or toxoid
      - won't cause same extent of disease
      - artificial/ induced active immunity
      - whole pathogen
      - stimulates antibody production but doesn't give the disease
    - - hepatitis b
      - prepared by methods in genetic engineering
        
        recombinant dna
      - modify the pathogen by adding/ removing genes
        
        manipulate so it can;t produce toxin but only toxoids
    - - most complex
        
        in most purofied state
        
        most potent
      - chemically synthesised
        
        nowadays some 3rd gen available for diptheria, leukemia - human papillomavirus. hpv
        
        cervical cancer
- - - - in spite of advancements in developing vaccines
        
        not all individuals respond in the same manner
        
        efficiency differes fm individual
      - happen in large popluation
        
        where malnutrition - developing and underdeveloped
        
        starvation. - no food
        
        malnutrition - there is not balanced food
      - most important reason for response
        
        proteinatious food is expensive
        
        not accessible by maj population
        
        not enough protein in diet
        
        less clones
        
        no b cells
        
        1 more item...
      - risk
        
        potential for entire siciety
        
        very susceptible to any disease
        
        can transfer it to other individuals
        
        high risk to society
        
        vectors for diseases
        
        1 more item...
      - problem
        
        vaccinate the person
        
        primary response - produce antobodies
        
        load of antigen should be available for antibody to start
        
        must be multuplid
        
        person doesn't produce enough antibodies but antigens are just multiplies coz pathogens are multiplying too
        
        1 more item...
      - in this situation
        
        high chance that highly infectious diseases to be spread
        
        when begin to spread fm. infected to other normal peopl
        
        transmission cycle
        
        sum total of all events by which infectious/ communicable disease can spread fm infected person to a large proportion of population
        
        outbreak. of infectious
        
        1 more item...
      - herd immunityqcan't immunuse them
        
        immunising large proportion of people, even children of a few months
        
        transmission cycle can be broken
        
        immunuzation program to overcome problem of poor response
        
        whether they show symptoms or not
        
        then those susceptible don't come in contact with the infection
        
        1 more item...
    - - rhino virus
        
        rhinitus/ influenza
        
        common cold
      - in spite of advancements, no vaccine for common cold
        
        coz there are hundred strains for this vaccine
        
        might not be cost effective
        
        coz you can recover fm it easily
      - viruses that are unstable
        
        mutate and produce a new strain
        
        the antigenic proterties are differnet
        
        cant produce
      - primary response
        
        you fall sick
        
        unlikely that you get the same strain again
      - extent to which pathogen can cause variations differe
        
        might be able to mutate, but that antigen is recognised by memory cells
        
        such pathogens mutate, but the antigenic properties don't vary greatly
        
        antigenic drift
        
        such minor shifts that the body can recognise
      - but some mutate and it changes a lot
        
        always primary immune response
        
        variations. are so large that you get primary response again
        
        antigenic shift