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Immunology Flashcards

1
Q

What are the main features of the innate immune system?

A
  • Rapid
  • Non-specific
  • First line of response
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2
Q

List the cellular components of the innate immune system

A
  • Basophils
  • Neutrophils
  • Eosinophils
  • Mast cells
  • Monocytes
  • Macrophages
  • Dendritic cells
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3
Q

Describe the appearance and function of basophils

A
  • Large, blue, very granular, no visible nucleus
  • Low concentration in blood (but only present in blood)
  • Parasites and allergens
  • Spill contents when needed
  • Active in anaphylactic shock
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4
Q

Describe the appearance and function of neutrophils

A
  • Bacteria and fungi
  • HIghly phagocytic
  • produce toxic substances quickly to kill invading cells and knock down infection
  • Can leave blood and enter tissue
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5
Q

Describe the appearance and function of eosinophils

A
  • Similar to neutrophil
  • Phagocytic (less than neutrophil)
  • can eave blood and enter tissue
  • Produce toxic substances
  • Parasites and allergens
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6
Q

Describe the appearance and function of mast cells

A
  • In connective tissue
  • Tissue equiv. of basophils
  • Allergens and parasites
  • Highly active, granular
  • Produce vasodilators
  • Can draw other immune cells closer
  • Only in connective tissue
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7
Q

Describe the appearance and function of monocytes

A
  • Kidney shaped nucleus
  • Very large
  • Clear cytoplasm
  • React to most infections
  • In blood are monocytes, in tissues different
  • Some degree of antigen presenting
  • MHC2 on surface
  • bridge between innate and adaptive immune system
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8
Q

Describe the appearance and function of macrophages

A
  • Tissue resonant cells
  • Come from monocytes
  • In infection increase in number
  • Larger surface area than monocyte
  • Antigen presentation
  • More contact with other cells = more robust response
  • Good at antigen presenting
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9
Q

Describe the appearance and function of dendritic cells

A
  • Lots of “arm” like projections

- Main function is antigen presenting

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10
Q

Describe the main features of the adaptive immune system

A
  • Antigen specific
  • Initially slow
  • Based on memory
  • Tends to produce memory and antibodies
  • ” types - antibody (humoral) response and cell response
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11
Q

What are the cells types in the adaptive immune system?

A
  • B and T

- T-cytotoxic killer and T-helper

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12
Q

What is the role of T helper cells?

A
  • Stimulae innate cells adn B cells to generate more antibodies
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13
Q

What is the role of the innate immune cells in the development of long term (adaptive) immunity?

A
  • Rapid response from immate cells
  • Allows acquiring of antigens that antibodies are based on
  • B-cells precede antibody producing cell
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14
Q

Define antigen

A
  • Any susbstance which activates the immune response, can be pathogenic or non-pathogenic and can be self proteins
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15
Q

Define phagocyte

A

Cells that protect the body by ingesting harmfu foreign particles, bacteria and dead or dying cells

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16
Q

Define opsonin

A

An antibody or other susbtance which binds to foreign microorganisms or cells making them more suscpetible to phagocytosis

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17
Q

Why is it important to have a controlled response to infection?

A

Too much inflammation in response to infection can have harmful effects on the body
- E.g. a fever that is too high can lead to organ damage and protein denaturing

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18
Q

What is a primary lypmhoid organ?

A

The organ in which lymphocytes are generated and may mature

  • Bone marrow for B cells
  • Thymus for T cells
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19
Q

What is a secondary lymphoid organ?

A

The organ in which lymphocytes react to an antigen in an immune response

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20
Q

What is an immunologically naiive animal?

A

One which has not been exposed to that specific antigen before

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21
Q

What is an immunlogically primed animal?

A

One where the immune response is function and can respond to that antigen

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22
Q

What are cytokines?

A

Factors excreted by cells that will have an effect on other cells

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23
Q

What are chemokines?

A

Protein signals produced by cells to attract other cells to that region e.g. IL-8, IL-6

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24
Q

Describe MHC I

A
  • On most cells
  • used to present peptides to immune cells
  • In normal cells produced by the cell
  • Recognised by T-cells as being “self” and prevents destruction
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25
Q

Describe the role of MHC I in the immune response

A
  • If cell infected (e.g. viral invasion) then present non-self proteins within MHC I
  • Recognsied as non-self by T-cells
  • Activated cytotixic T cells thorugh binding and chemical signals
  • Leads to desctruction of infected cells
  • T-cells only recognise and are activated by non-self proteins, not stimulated by self proteins expressed by MHC1 normally
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26
Q

Describe the role of MHCII

A
  • Only on APCs (macrophages, dendritic cells)
  • Present non-self antigens to helper T-cells from phagocytosis of pathogens such as bacteria, stimulating its activation
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27
Q

Why can the CNS be describe as immune privileged?

A
  • Do not present MHC complexes

- Remains separate from the immune system because of this

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28
Q

Name the subclasses of antibody (immunoglobulins)

A
  • IgG
  • IgA
  • IgM
  • IgE
  • IgD
    (GAMED)
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29
Q

What are the subsets of lymphocytes?

A
  • T cells
  • B cells
  • Natural killer cells
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30
Q

What are the subsets of T cells?

A
  • Cytotoxic

- Helper

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31
Q

What is the MHC restriction of cytotoxic T cells?

A

MHC1

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32
Q

What is the MHC restriction of T-helper cells?

A

MHC2

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33
Q

What are the 2 routes of antigen processing and their genetic restriction elements for antigen presentation?

A
  • Endogenous (MHC1)

- Exogenous (MHC2)

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34
Q

What cell organelles are involved in exogenous antigen processing?

A

Endosomes, RER, golgi apparatus, cell membrane

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35
Q

What cell organells are involved in endogenous antigen processing?

A
  • Golgi, cytosol proteosome, endoplasmic reticulum
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36
Q

What type of cell recognises the peptide presented on the surface of an APC?

A

T helper cell

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37
Q

In the immunologically naiive animal, where is the immune response started?

A
  • In the lymph nodes draining the site of antigen exposure if peripheral tissue
  • Spleen if blood borne
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38
Q

In the immunologically primed animal, where is the immune reponse started?

A
  • At the local site of antigen exposure

- Lymphoid tissues is involved e.g. GALT or BALT

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39
Q

Describe antigen capture and transport by dendritic cells of naiive animals

A
  • Dendritic clells capture antigen in periphery
  • Transport antigen to LNs
  • Presentation of antigen will take place in cortex of paracoritcal areas
  • Will then exit node via afferent lymphaticsto site where invasion has taken place
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40
Q

Describe antigen capture and transport by dendritic cells of primed animals

A
  • Antigen captured, processed ad presented locally very efficiently
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41
Q

Describe the memory cells present in prime animals

A
  • More sensitive to restimulation by antigen on APC than naiive animals
  • Produce cytokines more quickly
  • Produce more cytokines
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42
Q

What are the routes of entry by antigens into cells

A
  • Phagoctyosis/endocytosis/binding to surface Ig (exogenous)

- Direct to cytosol (endogenous)

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43
Q

Describe the main features exogenous antigen processing

A
  • Phagocytosis/endocytosis/binging to surface Ig
  • MHC II restricted
  • e.g. extracellular pathogens
  • Antigen processed within cell and does not enter proteasome
  • Following phagocytosis/endocytosis into phagosomes/endosomes then to golgi
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44
Q

Describe endogenous antigen processing

A
  • Direct to cytosol
  • MHC I restricted
  • E.g. intracellular pathogens
  • Into cytosol then either to gene transcription in nucleus (and back to cytosol or to ER) or to proteasome
  • From proteasome to ER, then golgi and secretory vesicle
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45
Q

Where is MHC I expressed?

A
  • On all nucleated ells in body except RBCs, platelets and nerve cells
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46
Q

Where is MHC II expressed?

A
  • Only on surface of professional APCs

- In inflamed situations, epithelial cells begin to express MHC II

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47
Q

Describe the structure of MHC I and II and how this assists their function

A
  • Differ slightly in structure at cell membrane

- Both have groove in which foreign peptides sit and are presented to passing lymphocytes

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48
Q

What is meant by genetic restriction when referring to T lymphocytes?

A 
subsets of T cells will only become activated if foreign peptide is presented by their specific class of MHC 
- E.g. helper cells will only recognise an antigen if displayed along with MHCII
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49
Q

What glycoprotein is found on the surface of T-helper cells?

A

CD4

- Are therefore said to be CD4+

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50
Q

What glycoprotein is found on the surface of T-killer cells

A

CD8

- Are therefore said to be CD8+

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51
Q

Describe the steps of exogenous antigen processing

A
  • Extracellular pathogen take up by APC
  • Processed and presented with MHCII
  • Recognised by CD4+ helper cell
  • T helper cell activated
  • Cytokines produced
  • T helper cell gets bigger, fors lymphoblast, produce more cells and call more cells to area
  • Cytokines act on B-cells
  • Proliferate and differentiate into plasma cells
  • Enhances cellular immune response (development of CTL)
  • more Ig produced
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52
Q

What are the subsets of T helper cells and describe their roles

A
  • Th1 and Th2
  • Difference relates to cytokines the secrete and cells whihc are activated by these cytokines
  • Role of T helper 1 or 2 is to produce cytokines
  • Depending on cytokines produced will enhance proliferation of T cells
53
Q

What is the effect of antigen presentation on lymphocytes?

A
  • Proliferation of lymphocytes so node or spleen enlarges due to increased population of lymphocytes
  • T-lymphocyte circulating, bind to specific APC peptide and lymphocyte activated
  • Forms lymphoblast, divides, clones and forms identical lymphocytes
  • Cytokine synthesis
  • Lymphocyte activation
  • Clonal expansion
  • Differentiation to T or B cells
  • Development of T or B memory cells specific for that antigen
54
Q

What is the importance of GALT in immuntiy to pathogens and also as a potential vehicle for pathogen invasion?

A
  • M cells of GALT can be portals of infection as pathogens collect here
  • M cells needed to concentrate antigen then deliver pulses of it to dentritic cells below
55
Q

Describe the anatomical features of Peyer’s patch M cells

A
  • No villi

- Appears as dents in patches

56
Q

Describe the functions of Peyer’s patch M cells

A
  • Can accumulate pathogens on the surface

- Concentrates antigen and then delivers pulses of that antigen to dendritic cells just below

57
Q

What are the steps in developing acquired immunity to mucosal pathogens?

A
  • Antigen presentation (often dendritic cells)
  • T cell homing in mucosal tissue
  • B cell activation and proliferation
58
Q

Describe the antigen presentation by DCs in the development of acquired immunity to mucosal pathogens

A
  • T cell clones only recognise one antigenic shape = millions of clones exist
  • When DCs present antigen together with MHC, T cells spend longer time sampling DC surface
  • If cognate antigen recognised by T cell, activated by second (co-stimulatory) signal supplied by B7 and CD40
  • DC attached to many T cells recognising antigen (clonal population)
  • T cells disengage and begin to divide
59
Q

Describe T cell homing in the development of acquired immunity to mucosal pathogens

A
  • Following antigen presenting have many T cells which recognise antigen originally presented by DC
  • T cells moving in circulation but infection is intestinal
  • All T cells which have engaged adn divided will express mucosal adhesion receptor (integrin)
  • Integrin recognises vascular cell adhesion molecule 1 (VCAM1)
60
Q

Describe the role of mucosal B cells in the development of acquired immunity to mucosal pathogens

A
  • Following stimulation by T cells, B cells differentiate into antibody producing plasma cells
  • T cell cytokines stimulate plasma cells to change antibody class to produce secretory IgA
61
Q

Why is it important that plasma cells change antibody class in response to mucosal pathogens?

A
  • IgM antibody first produced by plasma cell not appropriate in intestinal infection
  • Will be digested if secreted into intestinal lumen
  • Carry out class switching to produce IgA which will not be digested
62
Q

What are the types of IgA?

A
  • Type 1: non-secretory, in blood

- Type 2: secretory, secreted across surface of mucosa epithelium

63
Q

Describe the structure of IgA

A
  • 2 types
  • both have characteristic joining “J” chain which joins monomeric IgA
  • IgA is therefore dimeric antibody
64
Q

Describe IgA2

A
  • Secretory type
  • The only tyoe to have secretory component
  • Protects it from digestion
  • Especially important in colostrum and milk as neonatal animalshave little immune protection
  • AS lactation progress IgA2 becomes most abudant milk antibody
65
Q

What is the action of cytokine IL-4 produced by Th2 cells and mast cells?

A
  • Activates B cells

- Stimulates B cell differentiation to plasma cells

66
Q

Describe B cell CD40 interaction with Th2 cell CD40

A

Will cause IgA switching in presence of Il-20 (a Th2 cytokine)

67
Q

What is the action of transforming growth factor beta (TGF-beta) on B cells

A
  • Promotes development of IgA+ B cells

- When stimulated with IL-5, IL-6 or IL-10 will differentiate into B blast cells and then IgA secreting plasma cells

68
Q

Describe the anatomical location of Peyer’s patches in different species

A
  • Pigs, ruminants, dogs and horses have 2 distinct patches
  • One large, one smaller
  • Large ileal patch
  • Smaller jejunal patch
69
Q

Describe the large ileal Peyer’s patch

A
  • Extends to/across ileocaecal junction
  • Primary lymphoid tissue in B cell production and maturation
  • In sheep involutes after 6 months, in pigs after 1 year
70
Q

Describe the small jejunal Peyer’s patch

A
  • Maintained throughout life

- Antigen transport and presentation

71
Q

Decribe the histological features of Peyer’s patches

A
  • Dome covered in M cells
  • M cells have no villi - Looks like a dent
  • Number of M cells increases if there is an ongoing infection
72
Q

Describe how the structure of Peyer’s patches aids antigen sampling

A
  • Afferent lymphatic vessles drain intestinal lymphatics into mesenteric lymph nodes
  • Efferent lymphatic drain mesenteric lymph nodes into thoracic duct
  • Aggregated lymphocytes found in follicles which make up Peyer’s patches over which lie antigen sampling follicle associateed epithelium (FAE)
  • FAE consists of M cells and follicular epithelial cells
  • M cells may be further dispersed throughout intestine
  • M cells concentrate particulate luminal antigens and supply pulses of antigens to DCs in sub-epithelial dome
  • FAE enterocytes may be involved in transport of soluble antigens
  • These enterocytes have no digestive function therefore very differnt to normal intestinal enterocyte
73
Q

Describe T cell antigen sampling

A
  • Enter mesenteric lymph nodes via high endothelial vessels
  • Investigate surface of any DC they encounter
  • If do not recognise antigen will return to circulation via efferent lymphatics (thoracic duct and subclavian vessels)
  • Steady state monitoring of DC surface in lymph nodes by T cells
74
Q

Give a basic overview of the interaction of dendritic cells with lymphocytes

A
  • DC in peripheral tissue of intestine (sub-epithelial dome of PPs highly phagocytic, not very immunogenic - immature in this state)
  • Immature DCs express lower levels of MHC and do not express co-stimulatory molecules
  • When phagocytose micro-organisms or lyminal antigens, migrate to T cell areasof dome or draining mesenteric lymph node
  • During migration mature, lose phagocytic capacity, express antigen in conjunction with MHC2
75
Q

Describe the term inflammation

A

Localised condition in which part of the body becomes red, hot, swollen and painful
- May be acute or chronic

76
Q

What are the signs of inflammation?

A
  • redness
  • Heat
  • Swelling
  • Pain
  • Lack of function
77
Q

What is nephritis?

A

Kidney inflammation

78
Q

What is hepatitis?

A

Liver inflammation

79
Q

What is arthritis?

A

Joint inflammation

80
Q

Give examples of acute inflammation

A
  • Infection by microorgansism
  • Hypersensitivity
  • Physical (burns, UV light)
  • Chemical corrosives or irritants
  • Tissue necrosis
81
Q

Give examples of chronic inflammation

A
  • Persistent infection by microorganisms
  • Persistent presence of non-living material
  • Immune mediated diseases (including hypersensitivity)
  • e.g. Johne’s diseases, tuberculosis, rheumatoid arthritis
82
Q

Descriibe how acute inflammation at mucosal surfaces is initiated

A
  • Microorganism invades mucosal epithelium
  • Macrophage phagocytoses it
  • Cytokines dilate localised microvasculature, stimulate other resident cells e.g. mast cells
  • Histamine and otehr vasoactive substances increases vascular permeability
  • Chemokines attract neutrophils and monocytes (chemical gradient)
  • Neutrophils and monocytes accumulate in blood vessels in response to chemokines or pathogen products
  • Exudation
  • Receptors for neutrophils and monocytes accumulate on blood vessels in response to cytokines
  • Cell movement slows
  • Stick to endothelium
  • Diapedesis/extravasation
83
Q

Describe how an inflammatory immune reaction proceeds

A
  • Cells entering tissues activated to produce substances which may be toxic to pathogens and host cells
  • Inflammatory cascade takes place
84
Q

Describe the inflammatory cascade

A
  • Inflammatory cell infiltrate produces more cytokines and chemokines
  • More resident cells activated, more cells extravasate (incl. lymphocytes)
  • Amplifies immune response leading to clearance of the antigen
85
Q

Describe how the acute inflammatory response is switched off

A
  • Reduced presenve of antigen reduced cytokine/chemokine production
  • Anti-inflammatory cytokines and inhibitors produced
  • Switch off production and inhibit effect of pro-inflammatory cytokines
  • Healing and return to steady state conditions
86
Q

Define exudate

A

The fluid and small proteins (e.g. fibrin) that leak out of plasma into tissue, causes swelling seen in inflamed tissues

87
Q

Define diapedesis/extravastion

A

The movement of leukocytes out of the vascular system and towards the site of tissue damage or infection

88
Q

What are the major types of hypersensitivity

A
  • Type I, type II, type III, type IV
  • Type I: immediate, mediated by IgE
  • Type II: IgG mediated
  • Type III: IgG/immune complex mediated
  • Type IV: T cell mediated
89
Q

How does hypersensitivity occur?

A

Occurs when animals immune response reacts to normally innocuous environmental antigens

90
Q

Describe Type I hypersensitivity

A
  • Immediate
  • Rapid (within 30 mins)
  • IgE mediated
  • IgE mostly bound to high affinity receptors found on mast cells and basophils
  • Degranulation of cell occurs when bound IgE interacts with antigen
  • Leukocyte stimulate/migration occurs (esp. eosinophils and neutrophils, degranulate in tissues)
91
Q

What is the FAB and immunoglobulins?

A

Fragment antigen binding

92
Q

What is the FC of immunoglobulins?

A

Fragment crystallisable regions

93
Q

What are the effects of type I hypersensitivity and some of the common allergens?

A
  • Anaphylaxis - pollen
  • Asthma - mite faeces
  • Allergic rhinitis - flea saliva
  • Atopic dermatitis - many, often unknown
  • Food allergy - food
94
Q

Describe type II hypersensitivity

A
  • Withinn 5-10 hours
  • Antibody recognises “self” antigen on host cell or tissue (Fab region)
  • Or antibody recognises small molecule attached to cell or tissue (usually binds complement)
  • Cell opsonised and phagocytosed by innate immune cells or innate immune cells engaging antibody produce cell toxins e.g. NK cells
  • Effect of this sometimes called Antibody Dependent Cell mediated Cytotoxicity (ADCC)
  • Can also have drug induced Type II hypersensitivity
95
Q

Give examples of type II hypersensitivity

A
  • Autoimmune haemolytic anaemia/thrombocytopenia (drug bound to surface of erythrocyte recognised by antigen)
  • Myasthenia gravis (antibody recognises ACh receptors)
  • Pemphigus 9antibody recognises proteins of skin and mucous membranes)
96
Q

Describe type III hypersensitivity

A
  • Reaction maximal at ~4-8 hours
  • Immune complex mediated
  • Deposition of small antibody/antigen complexes
  • Escape normal route of clearance
  • Antigen soluble and not attached to organ involved
  • Antigen may be from exogenous source e.g. pathogen, or from endogenous source e.g. “self”
  • Dispersed immune complex may affect many different body systems
  • Localised type II reaction known as Arthus reaction
  • Complexes small and can escape removal from the body
  • Can be deposited almost anywhere
97
Q

Give examples of type III hypersensitivity

A
  • Systemic lupus erythematosus (SLE)
  • Polyarthritis
  • Nephritis
  • Post-infection reactions e.g. inflammatory joint disease followign bacterial infection
98
Q

Describe type IV hypersensitivity

A
  • Within 24-72 hours
  • T cell mediated
  • Dendritic cells and “primed” T cells (e.g. memory T cells)
  • Cells recruit and activate mononuclear cells (e.g. monocytes and tissue macrophages)
  • Inflammation at site of DC/T cell interaction occurs (rather than in draining lymph node)
99
Q

Give examples of type IV hypersensitivity

A
  • Tuberculin reaction in skin
  • Granuloma formation (Johne’s disease in intestine)
  • Allergic contact (also has type I components)
100
Q

Describe how a granuloma is formed

A
  • Occurs when pathogens survive in macrophages
  • Chronically infected macrophages constantly produce TNF-alpha and stimulate T lyphocytes to produce IFN-y
  • These 2 cytokines maintain granuloma in tissue
  • Need to maintain granuloma as dissemination would spread pathogen throughout more of teh tissue and cause more catastrophic infection
101
Q

What is the cellular content of inflammation of the GI tract?

A
  • Intestinal resident cells
  • Macrophages
  • Natural killer cells
  • Some T cells (usually gamma/delta type)
102
Q

Describe how acute inflammation of the GIT occurs

A
  • NK cells and gamma/delta T cells produce IFN-y response to infection by microorganisms
  • NK cells not MHC1 restricted
  • Greatest production of IFN-y when Th1 cells enter intestinal tissue
  • Intestinal epithelial cells detect invading microorganisms (PAMPS) and produce chemokines
  • More cells attracted
103
Q

What chemokines are produced by intestinal epithelial cells when these detect invading microorgansims?

A
  • IL-8
  • IL-6
  • Macrophage chemoattractant protein (MCP)
  • In case of parasites/allergens produce eotaxin (eosinophil chemoattractant)
104
Q

How are PAMPS involved in the inflammatory process?

A
  • Conserved PAMPS e.g. gram -ve LPS or bacterial flagellin recognised by host epithelial cells and innate immune cells
  • Recognition results in cytokine/chemokine production
  • Amplifies immune response at site of infection
105
Q

Explain how NFkappaB is involved in the recognition of PAMPS

A
  • Is translation factor
  • When activated, enters nucleus, binds to genes that express antibacterial proteins
  • NFkB bound to IkB
  • Removed by binding of CD14 to TLR4
  • Allows NFkB to enter nucleus
106
Q

Describe the role of mast cells in intestinal inflammation

A
  • Found only in tissue
  • Increase as result of infection
  • Can degranulate in response to different pathogens
  • Many products
107
Q

What are the products of mast cells?

A
  • Cytokines
  • Granulocyte macrophage colony stimulating factor
  • Stem cell factor
  • Macrophage chemotactic peptide
  • Eotaxin
  • Histamine
  • Heparin
  • Chymase
  • Tryptase
108
Q

What is the action of chymase?

A
  • Serine protease stored in secretory granules

- Induces IL-8 production in epothelial cells and microvascular leakage

109
Q

What triggers mast cells to degranulate?

A
  • IgE (most important)
  • Bacterial fimbriae
  • TLRs and PAMPS
110
Q

What occurs in neutrophil diapedesis?

A
  • Pathogen invades epithelium
  • Mast cells detect this, producce histamine and heparin
  • Affects microvasculature in tissue (more leaky)
  • Vasculature leakier to allow proteins etc to pass through it
  • Epithelial cells producing Il-8 and IL-6
  • Neutrophils in blood, move more freely through vasculature
  • Via chemical gradient move to highest concentration of cytokines IL-6 and IL-8 where invasion is occuring
111
Q

Describe the role of neutrophils in intestinal inflammation

A
  • Called to area by IL-6 and IL-8, produced in response to pathogenic bacteria and fungi
  • Also produced by neutrophils themselves
  • Phagocytose bacteria/fungi
  • Use reactive oxygen species ROS and cytotoxins stored in granules to kill pathogens
112
Q

List the neutrphil cytokines and chemokines

A
  • TNF-alpha
  • IL-1 beta
  • Interferon inducible protein 10 (IP-10)
  • Macrophage inflammatory protein 1 alpha (MIP-1alpha)
  • IL-8, IL-6
113
Q

Describe the role of eosinophils in intestinal indlammation

A
  • Migration from blood to tissue in response to parasites and allergens
  • Influenced by cytokines of Th2 type
  • Lysophospholipase activity may reduce cytotoxic lysophosphatides produced during degranulation
114
Q

Describe the granules of eosinophils

A
  • Contain Charcot-Leyden crystal protein
  • Have lysophospholiase activity, may reduce cytotoxic lysophosphatides produced during degranulation
  • Commonly seen in parasitic infections
  • Dark core contains major basic protein
  • Outer matrix contains peroxidase, neurotoxin and cationic protein
  • MBP-classic eosinophil protein, direct killing effect on parasites and bacteria
  • Also stimulates histamine release by mast cells and activated other innate cells
115
Q

Describe the cytokines involved with eosinophils

A
  • IL-4, IL-13 produced by mast cells and Th2 cells, stimulate production of eotaxin from epithelial cells
  • IL-4 stimulates plasma cell differentiation, IL–13 promotes class switching to IgE
  • Eotaxin is eosinophil chemoattractant (chemokine)
  • IL-5 produced by mast cells and Th2 cells activates eosinophils and stimulates degranulation
116
Q

Outline the steps in eosinophil recruitment in intestinal inflammation

A
  • Th2 and mast cells activated
  • Produce IL-4 and IL-13
  • IL-13 stimualtes intestinal epithelial cells to produce eotaxin
  • Mast cell degranulation and histamine release occuring
  • Eosinophils migrate to area of highest eotaxin concentration
117
Q

Describe the role of macrophages in intestinal inflammation

A
  • Some resident, many formed from blood monocytes during infection
  • Migration usually follows first neutrophil or eosinophil migration
  • Marophages phagocytic and utilise same killing pathways as eosinophils and neutrophils
  • Also very competent APCs
118
Q

What is teh killing pathway utilised by eosinophils, neutrophils and macrophages?

A

Oxidative burst

119
Q

What is the importance of macrophages in Salmonellosis?

A

Ability of pathogen to survive on inside of macrophage determines virulence

120
Q

Describe the role of Paneth cells in intestinal inflammation

A
  • Stem cells highly active sinnce enterocyte turnover is high
  • Located at base of crypts
  • Prevent stem cell invasion by secretion of anti-microbial peptides (defensins)
  • Production increased in response to bacteria and parasites
121
Q

Why is it important that the neutrophil response is of very short duration

A

Degranulation not only kills microorganisms but also host tissue cells

122
Q

Describe the return to a steady state following inflammation

A
  • Removal of antigen prevents further stimulation
  • Anti-inflammatory Th2 response down-regulates inflammatory response
  • IL-10 produced by mast cells and Th2 cells inhibit production of inflammatory cytokines (IFN-y, TNF-a, IL-8 etc)
  • Since IL-4 will also be produced by this anti-inflammatory response (by Th2 cell) this phase of immune response drive antibody production
123
Q

Describe how a granuloma is formed

A
  • Macrophage cannot kill micro-oranism becomes chronically infected
  • Macrophage constantly secretes TNF-alpha, stimulates chemokine production
  • Chemokines attract relevant cells seen in granuloma
  • Removing TNF-alpha causes breakdown of granuloma
  • T cells around periphery secrete IFN-y
  • Believed to contribute to chronic reactivity of macrophages
124
Q

What are the killing pathways utilised by macrophages?

A
  • Peroxidase
  • Nitric oxide
  • Various toxic substances
125
Q

What are the effects of a granuloma?

A
  • Severe tissue necrosis
  • Forms focal killing pooint in which micro-orgaisms can eventually be killed
  • Also prevents dissemination since walls off microorganisms
  • Destruction of granuloma can lead to spreading of pathogens
126
Q

What are common causes of granulomas?

A
  • Chronic colitis

- Johne’s disease

127
Q

Explain how chronic colitis leads to granuloma formation

A
  • Many different forms
  • Not always due to infection
  • May be due to food allergy
  • May be genetic component
128
Q

Describe the effects of Johne’s disease

A
  • Severe weight loss

- Young animals infected through milk, clinical signs may not be apparent until 2 or 3 years after infection

GI (31 decks)

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