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immunology Flashcards

1
Q

describe innate immunity

A
  • natural immunity that is present from birth and is generally non-specific
  • includes physical barriers, inflammatory mediators, complement proteins, acute phase proteins & immune cells
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2
Q

what are the constitutive barriers used to defend the body from pathogens?

A
  • skin
  • mucus
  • commensal bacteria
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3
Q

how does the skin defend the body from pathogens?

A

physical barrier
- composed of tightly packed, high kerantized cells

physiological factors
- low pH 5.5
- low oxygen tension

Sebaceous glands
- secrete hydrophobic oils
- lysosomes
- ammonia

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4
Q

how is mucus used to defend the body from pathogens?

A

mucus membranes line all the bodies cavities that are in contact with the external environment

mucus traps bacteria and contains lysosomes and defensis which directly kill invading pathogens

secretory IgA
- prevents bacteria and viruses attaching to and penetrating epithelial cells

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5
Q

how does commensal bacteria defend the body from pathogens?

A

compete with pathogens for resources and produce fatty acids and bactericides (substance which kills pathogens/bacteria) that stop pathogens growing

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6
Q

what are the key differences between innate immunity and adaptive immunity?

A

INNATE IMMUNITY SYSTEM:
- present continuously
- present from birth
- same generic response occurs to many different microbial species

ADAPTIVE IMMUNITY SYSTEM:
- usually induced by the presence of a ‘foreign’ or non-self materials (not continuous)
- a unique response is generated to each individual pathogen (not the same generic response)

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7
Q

how do macrophages defend the body from pathogens?

A

PHAGOCYTOSE BACTERIA (uses phagocytosis)

  1. PPRs (pattern recognition receptors) on macrophages bind to PAMPs (pathogen associated molecular patterns) on pathogen, which signals the formation of the phagocytic cup
  2. cup extends around the pathogen and pinches off - forming phagosome
  3. phagosome fuses with the lysosome - forming the phagolysosome
  4. pathogen killed and contents degraded
  5. debris released into extracellular fluid
  6. pathogen derived peptides expressed on special cell surface receptors (MHC-II)
  7. pro-inflammatory mediators released - acute inflammation
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8
Q

How do mast cells defend the body from invading pathogens?

A
  • deal with pathogens too large for phagocytosis
  1. When PPRs on mast cells bind to PAMPs on pathogen, the mast cell is stimulated to release pre-formed pro-inflammatory substances such as histamine and try-tease - DEGRANULATION (destroy pathogen)
  2. As this happens, the mast cell also begins to produce pro-inflammatory substances (histamine, TNF, chemokine & leukotrienes)

(TNF - chemical messenger that induces inflammation)

MAST CELLS ARE ASSOCIATED WITH ALLERGY

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9
Q

How to Natural killer cells (NK cells) defend the body from pathogens?

A
  • lymphocytes involved in the rejection of tumours and virally infected cells
  • respond to LOW levels of MHC class I - virally infected and cancerous cells have reduced levels
  • kill virally infected and cancerous cells by degranulation
  • produce IFNy (a cytokine that plays an important role in inducing and modulating an array of immune responses)
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10
Q

How do Neutrophils move to the site of damage or infection in the body?

A

TRANSENDOTHELIAL MIGRATION - recruitment of neutrophils to the site of infection/damage during acute inflammation

  1. loss of intravascular fluid in the presence of inflammation causes slower blood flow, allowing neutrophils to undergo margination
    - neutrophils travels closer to the endothelial cells, instead of centre of organs
  2. Neutrophils can then encounter and bind to adhesion molecules expressed by the endothelial cells
  3. Neutrophils migrate across the endothelium via diapedesis
  4. once in there tissues, the neutrophils travel to the exact site of injury via chemotaxis (movement of an organism due to chemical stimulus)
  5. neutrophils are then activated by PAMPs and pro-inflammatory mediators such an TNF (tif - promotes inflammation by increasing blood neutrophil concentrations)
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11
Q

what are the killing mechanisms of Neutrophils?

A

Phagocytosis:
- phagolysosomal killing (like macrophages) via production of a reaction oxygen species (ROS)

Degranualation:
- release of anti-bacterial granules

NETS:
- release of net-like structures that trap pathogens, leading to PHAGOCYTOSIS

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12
Q

what are the modes of ingestion for neutrophils?

A

receptor mediates ENDOCYTOSIS
- molecules bound to membrane receptors are internalised (important in the generation of an adaptive immunity)

PINOCYTOSIS:
- ingestion of fluid of surrounding cells

PHAGOCYTOSIS:
- bacteria engulfed by cell surface

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13
Q

how do cytokines defend the body from pathogens?

A

Interferons released by virally infected cells signal to neighbouring uninfected cells:

  • Destroy RNA and reduce protein synthesis
  • undergo apoptosis

interferons also active immune cells (e.g. NK cells)

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14
Q

what is adaptive immunity?

A
  • induced by the presence of a foreign molecule
  • able to discriminate between ‘self and ‘non self’
  • includes cytokines, antibodies, B&T cells
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15
Q

what is the job of dendritic cells?

A
  • act as a bridge between the innate and adaptive immune systems
  • express antigens on their cell surface and present them to T cells - antigen presenting cells
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16
Q

what is the acute phase response?

A
  • the systematic response involves the change in the plasma concentration of specific proteins in repose to inflammation
  • driven by pro-inflammatory medications released by activated macrophages
  • mediated by liver hepatocytes which produce a variety of acute phase proteins:
  • C3 & MBL (complement system proteins)
  • C reactive protein (CRP)
    primes certain bacteria for destruction by the complement system and phagocytes
  • has a prognostic role (severity, duration of inflammation)
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17
Q

explain the role of the C reactive protein (CRP)

A

A major acute phase protein in humans

used as a marker for inflammation

functions as a Opsonin to ethane bacterial cell phagocytosis

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18
Q

what is the complement system?

A

activated in response to inflammation and creates a cascade of chemical reactions

  1. C3 protein is cleaved into the active C3a and C3b
  2. C3b can then cleave C5 into C5a and C5b
  3. C3b can then amplify the reaction via the alternative pathway, causing more C3 to cleave into C3a and C3b
  4. C5b (along with other factors) produces the membrane attack complex, which inserts into cell walls and destroys the cell by letting salt and water in
  5. C3a and C5a are responsible for acute inflammation (they are anaphylatoxins)
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19
Q

what are acute phase proteins

A

proteins produced by the liver whose plasma concentrations increase or decrease in response to inflammation

C3 > involved in complement

CRP > activates complement via classical pathway
- very rapidly increased during inflammation
- very short half-life = decrease rapidly once well

MBL - activates complement via MBL pathway

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20
Q

how is the immune system enhanced?

A
  • the innate response can be enhanced by antibodies
  • complement system > classical system activated by IgM and IgG
  • IgG acts as opsonis
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21
Q

describe B cells (lymphocyte)

A
  • b cells mature in the bone marrow
  • responsible for humoral immune response
  • important in humoral immune response
  • normally circulate around the body in the primary lymphoid tissue (site of development - bone marrow/thymus) in their inactive form
  • antigen presentation activates the b cells in the secondary lymphoid tissues (e.g. lymph nodes, spleen)
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22
Q

how are B cells activated and produce a high affinity of antibodies?

A
  1. membrane-bound antibodies on the B cells bind to target antigen IgM (or IgD) within the B cell zone of lymph nodes (SECONDARY LYMPHOID TISSUE)
  2. b cells require 2 signals to become fully active and begin proliferation (rapid division) - the antigen and the ‘helper signals’ e.g. from TH cells, PPR and PAMPs or Fromm multiple antigens
  3. once activated, they clonally proliferate and become either a plasma cell (ANTIBODIES) or a memory B cell - germinal centre response
  4. High affinity antibodies are generated:
    -IgM (produced by plasma cells)
    - IgG (produced by B cells responding to certain antigens, assisted by TH cells)
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23
Q

how are lymphocytes transported?

A

lymph and lymphocytes leave lymph node -> medullary sinus -> effect lymphatic vessels -> blood circulation via lymphatic ducts at the subclavian vein

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24
Q

what is the structure of an antibody?

A
  • Y shaped
  • made up of 2 light chains and 2 heavy chains (polypeptides)
  • each has a unique variable region (antigen binding site) which is specific against 1 antigen
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25
Q

what are the 2 types of antibodies?

A

MEMBRANE BOUND ANTIBODY
- located on surface of B cell

SECRETED ANTIBODY
- secreted by plasma cells, present in serum and tissue fluids

26
Q

what is the IgM antibody + its functions?

A
  • FIRST ANTIBODY TO BE MADE IN AN INFECTION
  • monomer when bound to B cell membrane but pentamer when released into plasma

FUNCTIONS:
- B cell activation
- agglutination (immune complex formation - enhances phagocytosis)
- complement system activation through classical pathway

27
Q

what is the IgG antibody + its functions?

A

MOST ABUNDANT ANTIBODY IN THE PLASMA

  • monomer
  • dominant type during secondary antibody response

FUNCTIONS:
- foetal immunity (placental transfer)
- complement activation
- NK cell activation
- neutralisation

28
Q

what is the IgA antibody and its functions?

A

SECOND MOST ABUNDANT ANTIBODY IN THE PLASMA

  • monomer In the serum
  • dimer in secretory fluids (e.g. colostrum)

FUNCTIONS
- helps with neutralisation of pathogens (membrane bound form)
- neonatal defence - protects GI tract of neonates

29
Q

what is the IgD antibody?

A

SECOND LEAST ABUNDANT ANTIBODY

monomer
- B cell activation

30
Q

what is the IgE antibody?

A

LEAST ABUNDANT ANTIBODY

monomer
- produced in allergic response

31
Q

What are different types of T cells (lymphocyte)

A
  • T cells mature in the thymus
  • CD4 + Helper T cells: activate B cells and stimulate production of memory B cells
  • CD8 + Killer T cells: kill infected cells via perforin (glycoprotein) /granzymes (cell death inducing prteases) /granulysin
  • Regulatory T cell: lymphocyte suppression
  • Memory T cells: Involved in the adaptive immune response
32
Q

what are T cells responsible for?

A

cellular immune response

33
Q

explain how T cells are activated

A
  1. Dendritic cells recognise and phagocytose antigenic debris
  2. in the presence of pro-inflammatory mediators (e.G. TNF alpha), the dendritic cells ,mature and increase expression of stimulatory molecules on their surface
  3. dendritic cells phagocytose the pathogenic antigens, break the antigens down into short polypeptides and load them onto MHC II molecules
  4. MHC II molecules transported to cell surface - at the same time, the maturing of dendritic cells migrate into the lymph nodes via the afferent lymphatic vessels
  5. co-stimulatory molecules enable T cell to respond to antigen and fully differentiate
34
Q

what is the function of MHC molecules?

A

T cells can only recognise peptide antigens that are presented to their TCR by MHC molecules

TCR - T cell receptor, found on surface of T cells and T lymphoctes

35
Q

what are the 2 classifications of MHC molecules?

A

class I MHC
- expressed on all nucleated cells, present peptide antigens to CD8 + killer T cells

class II MHC
- expressed only on antigen presenting cells (e.g. dendrites, macrophages), present peptide antigens to CD4 + helper T cells

36
Q

what is Agglutination?

A

the action of an antibody when it cross links multiple antigens producing clumps of antigens

  • prevents viruses from binding to and infecting host cells
  • increases the efficacy of pathogen elimination by phagocytic cells
37
Q

explain T cell differentiation in CD4 cells

A

CD4+ T cells -> T helper cells
- antigen-activated CD4 + T cells secrete IL-2 and express IL-2 receptors (T cell growth factor)

CD4 + T cells > T helper cells > effector TH cells:

  • TH1 CELLS: secrete pro-inflammatory cytokines (IL2, IFNy) which stimulates production of ROS (macrophage-mediated)

-TH2 CELLS: secrete mainly IL4, IL5 and IL 6 which promotes B cell proliferation and induces antibody production

  • TFH CELLS: stimulated by presented antigen peptides + MHC II molecules on B cell, then stimulate the B cells to proliferate and differentiate (into plasma + memory cells) by secreting IL4 and IL21
38
Q

explain T cell differentiation in CD8 cells

A

CD8 + T cells -> CTLs (TC cells)

  • IL-2 (provided by TH cells) promotes differentiation and proliferation of antigen activated (via MHC I) CD8+cells into cytotoxic T lymphocytes (CTLs)
  • CTLs migrate out of secondary nodes and enter site of infection (via trans endothelial migration) and then kill virally infected host cells by recognising pathogenic antigens attached to MHC class I
  • also involved in killing cancer cells
39
Q

what are the functions of the immune system?

A
  • to provide robust defence against the wise variety of aggressive external agents (mainly microorganisms)
  • to provide a robust defensive against internal aggressive agents (e.g. cancer)
40
Q

what are consequences of immune recognition?

A
  • intended destruction of the antigen
  • collateral tissue damage
41
Q

what its hypersensitivity?

A
  • an immune response that results in bystander damage to the self
  • usually EXAGGERATION of normal immune mechanisms
42
Q

what are the Gel and Coombs classifications for hypersensitivity reactions?

A

type I = intermediate hypersensitivity

type II = direct cell effects

type III = immune complex mediated

type IV = delayed type hypersensitivity

43
Q

what is the main antibody in hypersensitivity?

A

IgE

44
Q

why is the presence of allergens increasing?

A

hygiene hypothesis: in modern countries, decreased exposure to parasites has left the immune system ‘untrained’

  • children produce more Th2 more likely to develop allergens than children who switch to producing Th 1
45
Q

what are the vasoactive mediators?

A

histamine & tryptase

46
Q

describe type 1 intermediate hypersensitivity

A
  • IgE antibody - ‘IgE mediated hypersensitivity’
  • caused by an allergen = antigen that catalyses reaction
  • first exposure = sensitisation
    subsequent exposure = getting serious
  • MOST ALLERGENIC REACTIONS
  • Th 2 cells release cytokines causing more eosinophils to be produced and for B cells to switch classies produce IgE antibodies
47
Q

describe type I sensitisation

A

person inhales ragweed pollen, they have certain T cells which can bind to pollen, making it an allergen.

  1. alleged picked up by immune cells in airways
  2. they migrate to lymph nodes
  3. these are antigen presenting cells
    - dendritic cells
    - macrophages
  4. if person is allergic, antigen presenting cells will express constimulatory molecules (for immune response)
  5. Native T helper cell > binds to antigen > type 2 helper cell (TH2)
    - TH2 release IL4
    - TH2 release IL5 which stimulates production of eosinophils
    - IL-12 activates NK cells
48
Q

describe the second exposure in type 1 hypersensitivity reaction

A
  • mast cell binds to antigen
  • allergen binds to IgE - coated mast cells and basophils
    = this causes degranulation
  • mediator released in allergic reaction = histamine
49
Q

what does histamine cause in early phase reactions (within minutes)?

A
  • bronchi - smooth muscle contraction, difficultly breathing
  • blood vessels - dilation, increased permeability; edema (swelling) & urticaria (hives)

also release proteases + eosinophils

50
Q

what happens in late phase allergic reactions?

A
  • TH2 cells, basophils, eosinophils recruited to site of allergen

Leukotrienes = facilitate communication
> smooth muscle concentration
> attract more immune cells: neutrophils, mast cells, eosinophils (even after allergen is gone)

51
Q

what are the symptoms of type 1 hypersensitivity?

A

mild symptoms:
- asthma
- hayfever
- eczema
- hives

severe symptoms:
- increased vascular permeability
- airway constriction
- can’t supply vital organs
= ANAPHYLATIC SHOCK

52
Q

how can we treat IgE mediated allergic disorders?

A
  • avoidance of allergens
  • anti-histamines
  • block mast cell activation
  • anti-inflammatory agents
  • adrenaline
  • immunotherapy
  • biologics
53
Q

describe type II allergic reactions (direct cell effects)

A
  • antibody mediated
  • generally cytotoxic
  • tissue specific
  • self reactive B cells produce IgG and IgM, these antibodies bind to normal human cells = destroying them
    > IgM & IgG directed towards specific antigens present on cell surfaces
54
Q

describe the sensitisation phase in type II hypersensitivity reactions

A

generation of relevant IgG/IgM antibodies in a classical humoral immune response

55
Q

describe the pathological phase in type II hypersensitivity reactions

A

mediated by normal antibody effector functions, this leads to:

  • destruction of antigen-positive cells (type IIa reactions)
  • stimulation of cell surface antigens (type IIb reactions)
    > too many antibodies could bind to the receptors, leading to an increase in thyroid hormone production
    > antibodies can inhibit the binding of neurotransmitters to receptors at the synapse
56
Q

describe type III hypersensitivity reactions

A

mediated by soluble immune complex: formed when an antibody binds to soluble antigen

  • this antigen-antibody immune complex passes between endothelial cells of the blood vessels and becoming trapped in the surrounding basement membrane = INFLAMMATION
  • B cells go from producing IgM to IgG antibodies
  • commonly occurs in joints
    > arthritis
57
Q

Describe the steps of type III hypersensitivity

A
  1. large quantities of soluble antigen-antibody complexes form in the blood and are not completely removed by macrophages.
  2. these antigen-antibody complexes are lodged in the capillaries between the endothelial cells and the basement membrane
  3. these antigen-antibody complexes activate the classical complement pathway, leading to vasodilation and cell death
  4. the compliment proteins and antigen-antibody complexes attract neutrophils to the area
  5. the neutrophils discharge their killing agents and promote massive INFLAMMATION (this can lead to tissue damage and haemorrhaging)
58
Q

describe type IV hypersensitivity reactions

A

driven by CD4 + T cells

  • activation of CD4+ cells by an antigen > proliferation and differentiation of effector TH1 cells leading to macrophage recruitment and activation
    (CD8+ T cells may also be involved)
59
Q

what are the classical hallmarks of a type IV hypersensitivity reaction?

A
  1. the large number of macrophages at the reaction site
  2. that it takes an average of 24-48 hours for symptoms to manifest after re-exposure to the initiating antigen
  3. granulomas (tiny cluster of white blood cells & other tissue) often form due to infectious pathogens/foreign bodies that cannot be cleared
60
Q

describe the effector phase in type IV hypersensitivity reactions

A
  1. reactivation of TH1 cells by antigen-presenting macrophages
  2. release of pro-inflammatory cytokines by TH1 cells
  3. activation of macrophages (type of white blood cell)
  4. tissue damage and destruction
61
Q

describe the sensitisation phase in type IV hypersensitivity reactions

A

initiating agent > adaptive immune response > generation of CD4 + TH1 cells & CD8 + CTLs (cytotoxic T lymphocytes)

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