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Flashcards in Immunology Deck (128):

What are the main features of the innate immune system?

- Rapid
- Non-specific
- First line of response


List the cellular components of the innate immune system

- Basophils
- Neutrophils
- Eosinophils
- Mast cells
- Monocytes
- Macrophages
- Dendritic cells


Describe the appearance and function of basophils

- 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


Describe the appearance and function of neutrophils

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


Describe the appearance and function of eosinophils

- Similar to neutrophil
- Phagocytic (less than neutrophil)
- can eave blood and enter tissue
- Produce toxic substances
- Parasites and allergens


Describe the appearance and function of mast cells

- 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


Describe the appearance and function of monocytes

- 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


Describe the appearance and function of macrophages

- 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


Describe the appearance and function of dendritic cells

- Lots of "arm" like projections
- Main function is antigen presenting


Describe the main features of the adaptive immune system

- Antigen specific
- Initially slow
- Based on memory
- Tends to produce memory and antibodies
- " types - antibody (humoral) response and cell response


What are the cells types in the adaptive immune system?

- B and T
- T-cytotoxic killer and T-helper


What is the role of T helper cells?

- Stimulae innate cells adn B cells to generate more antibodies


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

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


Define antigen

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


Define phagocyte

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


Define opsonin

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


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

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


What is a primary lypmhoid organ?

The organ in which lymphocytes are generated and may mature
- Bone marrow for B cells
- Thymus for T cells


What is a secondary lymphoid organ?

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


What is an immunologically naiive animal?

One which has not been exposed to that specific antigen before


What is an immunlogically primed animal?

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


What are cytokines?

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


What are chemokines?

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


Describe MHC I

- 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


Describe the role of MHC I in the immune response

- 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


Describe the role of MHCII

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


Why can the CNS be describe as immune privileged?

- Do not present MHC complexes
- Remains separate from the immune system because of this


Name the subclasses of antibody (immunoglobulins)

- IgG
- IgA
- IgM
- IgE
- IgD


What are the subsets of lymphocytes?

- T cells
- B cells
- Natural killer cells


What are the subsets of T cells?

- Cytotoxic
- Helper


What is the MHC restriction of cytotoxic T cells?



What is the MHC restriction of T-helper cells?



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

- Endogenous (MHC1)
- Exogenous (MHC2)


What cell organelles are involved in exogenous antigen processing?

Endosomes, RER, golgi apparatus, cell membrane


What cell organells are involved in endogenous antigen processing?

- Golgi, cytosol proteosome, endoplasmic reticulum


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

T helper cell


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

- In the lymph nodes draining the site of antigen exposure if peripheral tissue
- Spleen if blood borne


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

- At the local site of antigen exposure
- Lymphoid tissues is involved e.g. GALT or BALT


Describe antigen capture and transport by dendritic cells of naiive animals

- 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


Describe antigen capture and transport by dendritic cells of primed animals

- Antigen captured, processed ad presented locally very efficiently


Describe the memory cells present in prime animals

- More sensitive to restimulation by antigen on APC than naiive animals
- Produce cytokines more quickly
- Produce more cytokines


What are the routes of entry by antigens into cells

- Phagoctyosis/endocytosis/binding to surface Ig (exogenous)
- Direct to cytosol (endogenous)


Describe the main features exogenous antigen processing

- 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


Describe endogenous antigen processing

- 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


Where is MHC I expressed?

- On all nucleated ells in body except RBCs, platelets and nerve cells


Where is MHC II expressed?

- Only on surface of professional APCs
- In inflamed situations, epithelial cells begin to express MHC II


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

- Differ slightly in structure at cell membrane
- Both have groove in which foreign peptides sit and are presented to passing lymphocytes


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

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


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

- Are therefore said to be CD4+


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

- Are therefore said to be CD8+


Describe the steps of exogenous antigen processing

- 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


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

- 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


What is the effect of antigen presentation on lymphocytes?

- 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


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

- 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


Describe the anatomical features of Peyer's patch M cells

- No villi
- Appears as dents in patches


Describe the functions of Peyer's patch M cells

- Can accumulate pathogens on the surface
- Concentrates antigen and then delivers pulses of that antigen to dendritic cells just below


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

- Antigen presentation (often dendritic cells)
- T cell homing in mucosal tissue
- B cell activation and proliferation


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

- 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


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

- 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)


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

- 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


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

- 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


What are the types of IgA?

- Type 1: non-secretory, in blood
- Type 2: secretory, secreted across surface of mucosa epithelium


Describe the structure of IgA

- 2 types
- both have characteristic joining "J" chain which joins monomeric IgA
- IgA is therefore dimeric antibody


Describe IgA2

- 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


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

- Activates B cells
- Stimulates B cell differentiation to plasma cells


Describe B cell CD40 interaction with Th2 cell CD40

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


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

- 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


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

- Pigs, ruminants, dogs and horses have 2 distinct patches
- One large, one smaller
- Large ileal patch
- Smaller jejunal patch


Describe the large ileal Peyer's patch

- 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


Describe the small jejunal Peyer's patch

- Maintained throughout life
- Antigen transport and presentation


Decribe the histological features of Peyer's patches

- 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


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

- 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


Describe T cell antigen sampling

- 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


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

- 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


Describe the term inflammation

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


What are the signs of inflammation?

- redness
- Heat
- Swelling
- Pain
- Lack of function


What is nephritis?

Kidney inflammation


What is hepatitis?

Liver inflammation


What is arthritis?

Joint inflammation


Give examples of acute inflammation

- Infection by microorgansism
- Hypersensitivity
- Physical (burns, UV light)
- Chemical corrosives or irritants
- Tissue necrosis


Give examples of chronic inflammation

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


Descriibe how acute inflammation at mucosal surfaces is initiated

- 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


Describe how an inflammatory immune reaction proceeds

- Cells entering tissues activated to produce substances which may be toxic to pathogens and host cells
- Inflammatory cascade takes place


Describe the inflammatory cascade

- 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


Describe how the acute inflammatory response is switched off

- 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


Define exudate

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


Define diapedesis/extravastion

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


What are the major types of hypersensitivity

- 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


How does hypersensitivity occur?

Occurs when animals immune response reacts to normally innocuous environmental antigens


Describe Type I hypersensitivity

- 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)


What is the FAB and immunoglobulins?

Fragment antigen binding


What is the FC of immunoglobulins?

Fragment crystallisable regions


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

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


Describe type II hypersensitivity

- 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


Give examples of type II hypersensitivity

- 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)


Describe type III hypersensitivity

- 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


Give examples of type III hypersensitivity

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


Describe type IV hypersensitivity

- 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)


Give examples of type IV hypersensitivity

- Tuberculin reaction in skin
- Granuloma formation (Johne's disease in intestine)
- Allergic contact (also has type I components)


Describe how a granuloma is formed

- 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


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

- Intestinal resident cells
- Macrophages
- Natural killer cells
- Some T cells (usually gamma/delta type)


Describe how acute inflammation of the GIT occurs

- 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


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

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


How are PAMPS involved in the inflammatory process?

- 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


Explain how NFkappaB is involved in the recognition of PAMPS

- 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


Describe the role of mast cells in intestinal inflammation

- Found only in tissue
- Increase as result of infection
- Can degranulate in response to different pathogens
- Many products


What are the products of mast cells?

- Cytokines
- Granulocyte macrophage colony stimulating factor
- Stem cell factor
- Macrophage chemotactic peptide
- Eotaxin
- Histamine
- Heparin
- Chymase
- Tryptase


What is the action of chymase?

- Serine protease stored in secretory granules
- Induces IL-8 production in epothelial cells and microvascular leakage


What triggers mast cells to degranulate?

- IgE (most important)
- Bacterial fimbriae
- TLRs and PAMPS


What occurs in neutrophil diapedesis?

- 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


Describe the role of neutrophils in intestinal inflammation

- 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


List the neutrphil cytokines and chemokines

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


Describe the role of eosinophils in intestinal indlammation

- 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


Describe the granules of eosinophils

- 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


Describe the cytokines involved with eosinophils

- 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


Outline the steps in eosinophil recruitment in intestinal inflammation

- 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


Describe the role of macrophages in intestinal inflammation

- 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


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

Oxidative burst


What is the importance of macrophages in Salmonellosis?

Ability of pathogen to survive on inside of macrophage determines virulence


Describe the role of Paneth cells in intestinal inflammation

- 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


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

Degranulation not only kills microorganisms but also host tissue cells


Describe the return to a steady state following inflammation

- 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


Describe how a granuloma is formed

- 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


What are the killing pathways utilised by macrophages?

- Peroxidase
- Nitric oxide
- Various toxic substances


What are the effects of a granuloma?

- 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


What are common causes of granulomas?

- Chronic colitis
- Johne's disease


Explain how chronic colitis leads to granuloma formation

- Many different forms
- Not always due to infection
- May be due to food allergy
- May be genetic component


Describe the effects of Johne's disease

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