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Basic Pathology > Immune System > Flashcards

Immune System Flashcards

1
Q

Innate Immune System
-General facts

A
  • Immediate response.
  • At location of infection.
  • Generalised response.
  • No memory.
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2
Q

Adaptive Immune System

A
  • Delayed response.
  • Involves T & B cells (found away from infection site in secondary lymphoid tissues e.g. Lymph nodes).
  • Specialised response.
  • Memory acquired.
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3
Q

Initial Immune Response

A
  1. Recognition of pathogen by macrophages –> activate innate immune system.
  2. Pathogen antigens picked up by dendritic cells –> travel to T&B cells –> activate adaptive immune system.
  3. Pathogen activates complement via lectin and alternative pathways.
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4
Q

Innate Immune System:
How Macrophages / other innate immune cells recognise Pathogens

A
  • Pathogen Associated Molecular Patterns (PAMPs) on pathogen (e.g. LPS, flagellin, dsRNA).
  • DAMPs from injured / necrotic cells (e.g. uric acid crystals, extracellular ATP, HSP)
  • Recognised by receptors = Pattern Recognition receptors on plasma membrane, in endosome or in cytosol (e.g. TL receptors, NOD, RIG).
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5
Q

Innate Immune System:
Macrophage Role.

A
  1. Phagocytose pathogens.
  2. Release cytokines –> induce inflammation.
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6
Q

Innate Immune System:
Roles of Macrophage Cytokines in Inflammation.

A
  1. Recruit and activate macrophages, monocytes, neutrophils –> phagocytosis of pathogens and release of more cytokines.
  2. Inflammation:
    a. Vasodilation.
    b. Increased vascular permeability.
    c. Mast cell degranulation.
    d. Trigger release of more cytokines from macrophages and neutrophils (acute phase response).
    e. Activate clotting system.
    f. Activate kinin system.
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7
Q

Innate Immune System:
Acute phase response.

A

Release of cytokines (interleukins, TNF) to produce systemic inflammatory response.

  • IL-1 –> brain –> fever / lethargy / decreased appetite.
  • IL-6 –> liver –> acute phase proteins (opsonins).
  • IL-8 –> recruitment and activation of more neutrophils.
  • IL-2, IL-12 –> activates natural killer cells.
  • TNF-a (does all of above).
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8
Q

Innate Immune System:
Opsonins

A
  • Complex molecules.
  • Attach to pathogens.
  • Assist macrophages and neutrophils to recognise pathogen for phagocytosis.
  • E.g. CRP, complement, B cell antibodies.
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9
Q

Complement System

A
  • Proteins: C1 to C9.
  • Initiate complement cascade –> results in MAC complex –> destroys pathogens.
  • C3a, C3b, C4a, C5a, MAC also act as opsonins and trigger inflammation.
  • Triggers:
    • Pathogens –> lectin and alternative pathway.
    • Ab-Ag complexes from adaptive immune system –> classical pathway.
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10
Q

Adaptive Immune System:
How T and B cells recognise pathogen antigens.

A

T cells: T cell receptors.
B cells: Antibodies.

Both are specific for a single cell antigen.

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11
Q

Adaptive Immune System Activation Process.

A
  1. Dendritic cells express pathogen antigens on HLA class II molecules.
  2. Deliver to lymphatic tissues and present to CD4 T cells.
  3. CD4 proliferates into T Helper cells.
  4. T Helper cells:
    a. Present antigens on HLA class I molecules to CD8 T cells.
    b. Release cytokines which assist in proliferation and differentiation of CD8 cells into cytotoxic T cells.
    c. Release cytokines to stimulate B cells to become plasma cells (produce abs) and memory B cells (immune memory).
    d. Travel to infection site –> release cytokines –> activate macrophages –> stimulate inflammation and phagocytosis.
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12
Q

Adaptive Immune System:
Cytotoxic T Cells Role

AKA CD8+ T Cells

A

Kill cells that are infected by pathogens.

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13
Q

Adaptive Immune System:
How Cytotoxic T Cells Work

A
  1. Infected cell expresses antigen protein on HLA class I molecule.
  2. T cell receptor binds to antigen HLA class 1 complex.
  3. Kill infected cell in 2 ways:
    a. Spray infected cell with enzyme –> destroys cell membrane –> cell lysis and death.
    b. Activate FAS molecule –> instructs infected cell to apoptose.
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14
Q

Adaptive Immune System:
Plasma Cells

A

Differentiated B cells that produce antibodies specific to invading pathogen that triggered its production.

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15
Q

Adaptive Immune System:
Role of Antibodies

A
  1. Attach to and neutralise toxins.
  2. Attach to pathogen receptors and prevent pathogen actions (e.g. prevent virus invasion of cells).
  3. Attach to pathogens and cause agglutination, slowing pathogen down.
  4. Attach to pathogen and act as opsonins.
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16
Q

Hypersensitivity Reactions:
Types

A
  • Type 1.
  • Type 2.
  • Type 3.
  • Type 4.

NB. Mnemonic to remember = ACID.

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17
Q

Hypersensitivity Reaction:
Type 1:
-Mechanism and examples

A

Type 1 = Allergic / Immediate

Mechanism:

  1. Allergens presented to T cells.
  2. Activation of Th2 –> activation and class switching of B cells.
  3. Production of IgE by B cells.
  4. “Cross-linking” between IgE and allergen on Fc receptors.
  5. Mast cell and basophils release vasoactive substances (histamine and leukotrines).
  6. Massive vasodilation.

Examples:

  • Asthma.
  • Allergy.
  • Anaphylaxis.
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18
Q

Hypersensitivity Reaction:
Type 2:
-Mechanism and examples

A

Type 2 = Cytotoxic and Cmooth (linear deposition).

Mechanism:

  1. IgG or IgM bind to cell surface receptor antigens, ECM antigens, or adsorbed exogenous antigens.
  2. Complement +/- Natural Killer cell activation.
  3. Death of “self” cells, inflammation and tissue injury, antibody-mediated cellular dysfunction.

Examples:

  • Goodpasture Syndrome.
  • Myasthenia Gravis.
  • AHA.
  • Grave’s Disease.
  • ABO incompatibility.
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19
Q

Hypersensitivity Reaction:
Type 3:
-Mechanism and examples

A

Type 3 = Immune Complex and Lump-I bump-I deposition.

Mechanism:

  1. IgG or IgM binds to antigen.
  2. Forms Ig-antigen immune complexes.
  3. Complexes ** deposit** in basement membrane of various tissues.
  4. Damage of tissue –> Inflammation.
  5. Complement activated.
  6. Destruction of tissue.

Examples:

  • Post-Strep GN.
  • SLE.
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20
Q

Hypersensitivity Reaction:
Type 4:
-Mechanism and examples

A

Type 4 = Delayed, cell-mediated.

Mechanism:

  1. Antigen (pathogen, self ags, environmental chemicals) sensitises CD8+ or CD4+ (Th1 or Th17) T cells.
  2. T helper cells releases cytokines (IFN-gamma, IL-17), CD8+ directly kills cells.
  3. Cytokines activate macrophages and recruit neutrophils.
  4. Macrophages / neutrophils phagocytose target cell / cause tissue injury.

Examples:

  • Diabetes mellitus.
  • Dermatitis.
  • How Diagnose TB: Type 4 reaction –> granuloma formation.
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21
Q

Enzyme Linked ImmunoSorbent Assay (ELISA)

A

Colourimetric test which uses antibodies and colour change to identify antigens or antibodies.

Gives qualitative and quantitative information (results graphed: absorbance vs concentration).

Types:
* Indirect.
* Sandwich.
* Competitive.

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22
Q

ELISA:
Indirect ELISA.

A

Detects antibody against a known antigen.

How:
1. Antigen coated well.
2. Patient sample added.
3. If antibody present, binds to antigen.
4. Second enzyme linked antibody added.
5. Binds to patient antibody if present.
6. Substrate added.
7. Colour reaction measured.

E.g. HIV antibody which is produced in response to HIV infection.

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23
Q

ELISA:
Sandwich ELISA.

A

Detects antigen of interest.

How:
1. Monoclonal antibody coated well.
2. Patient sample added.
3. If antigen present, binds to antibody.
4. Second enzyme linked monoclonal antibody added.
5. Binds to patient antigen if present.
6. Substrate added.
7. Colour reaction measured.

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24
Q

ELISA:
Competitive ELISA.

A

Detects how much antigen is present.

How:
1. Mix patient sample with antibody.
2. If antigen present, binds with antibody.
3. Add mix to antigen coated well.
4. Any antibody NOT bound to patient antigen will bind to antigen in well.
5. Add second enzyme linked antibody.
6. Binds to antibody bound to well antigen if present.
7. Add substrate.
8. Colour reaction measured.

NB.
Colour change = No or little patient antigen present.
No or some colour change = lots of patient antigen present (test antibody bound to patient antigen so none to bind to well antigen to produce sandwich with second enzyme linked antibody).

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25
Q

Immunologic Tests for Infectious Diseases:
What to do if testing is delayed

A

Refrigerate or freeze sample to prevent bacterial contaminant overgrowth.

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26
Q

Immunologic Tests for Infectious Diseases:
Agglutination tests:
-Examples, advantages and disadvantages

A

Examples:
* Latex agglutination.
* Coaggregation.

Advantages:
* Rapid.
* Can determine serotypes of some bacteria.

Disadvantage:
* Less sensitive than other methods.

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27
Q

Immunologic Tests for Infectious Diseases:
Agglutination tests:
-Method

A
  1. Mix very small particles (latex beads, gelatin particles, bacteria) with reagent antigen or antibody.
  2. Add patient sample.
  3. If target antigen or antibody in patient sample, binds to particle complex –> crosslinking –> agglutination.
  4. Positive agglutination –> sample serially diluted and tested and titer of highest dilution causing agglutination recorded.

NB. Result of 32 = agglutination occured up until 1/32 of starting concentration.

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28
Q

Immunologic Tests for Infectious Diseases:
Complement Fixation:
- Examples, advantages and disadvantages

A

Example:
* Diagnosis of some viral and fungal infections e.g. coccidiodomycosis.

Advantages:
* Measures IgG or IgM antibody titers.
* Accurate.
* Can be modified to detect certain antigens.

Disadvantages:
* Limited applications.
* Labour intensive.
* Requires numerous controls.

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29
Q

Immunologic Tests for Infectious Diseases:
Complement Fixation:
- Method

A
  1. Incubate patient sample (CSF or serum) with known quantities of complement and antigen of target antibody.
  2. Measure degree of complement consumption (amount of complement fixed by target antibody).
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30
Q

Immunologic Tests for Infectious Diseases:
Enzyme Immunoassays:
- Examples, advantages and disadvantages

A

Examples:
* Enzyme immunoassay (EIA).
* Enzyme-linked Immunosorbent assay (ELISA).

Advantages:
* High sensitivity –> good for screening.

Disadvantages:
* Sensitivity varies depending on patient age, microbial serotype, specimen type, stage of disease.

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31
Q

Immunologic Tests for Infectious Diseases:
Enzyme Immunoassays:
- Method

A
  • Use antibodies linked to enzymes.
  • Detects antigens or detects and quantifies antibodies.
  • Titers determined by serial dilution of specimen.
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32
Q

Immunologic Tests for Infectious Diseases:
Precipitation tests:
- Examples, advantages and disadvantages

A

Examples:
* Ouchterlony double diffusion.
* Counterimmunoelectrophoresis.

Disadvantages:
* Limited applications.
* Low sensitivity.

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33
Q

Immunologic Tests for Infectious Diseases:
Precipitation tests:
- Methods

A

Measures antigen or antibody in body fluids by degree of visible precipitation of antigen-antibody complexes within a gel or solution.

34
Q

Immunologic Tests for Infectious Diseases:
Western Blot Test:
- Examples, advantages and disadvantages

A

Technically modified Western Blot e.g.’s:
* Line Immunoassay (LIA).
* Recombinant Immunoblot Assay (RIBA).
* Immunochromatographic assays.^

Advantages:
* Good sensitivity (but less sensitive than ELISA).
* Highly specific –> used for confirmation of a positive result from screening.

^Easiest and most commonly used. E.g. of use = Shiga toxin producing microorganisms, Cryptococcus neoformans capsular ag, influenza virus.

35
Q

Immunologic Tests for Infectious Diseases:
Western Blot test:
- Method

A
  1. Target antigens immobilised onto membrane by blotting.
  2. Patient sample added.
  3. If antibody to target antigen present, binds to antigen.
  4. Antibody-antigen complexes detected.
36
Q

Innate Immune System:
Complement System:
-Roles

A
  1. Coating of microbes and induction of phagocytosis.
  2. Pore formation and lysis.
  3. Stimulation for adaptive immune response.
  4. Recruitment of inflammatory cells.
37
Q

Innate Immune System:
Complement System:
-Steps of Classical pathway

A
  1. Antibody binding.
  2. Activation of C1 –> C2 –> C4.
  3. Cleavage of C3.
  4. Activation and formation of MAC complex (C5 - C9).
38
Q

Adaptive Immune System:
Antigen Receptors:
-B cells antigen receptor types and structure

A

Types:

  • Cell surface Ig / B cell receptor.
  • Antibodies.

Structure:

  • 2 heavy chains.
  • 2 light chains.
  • 2 distint regions: Fc (constant region) and Fab (variable region - which binds antigen)
39
Q

Adaptive Immune System:
Antigen Receptors:
-T cells antigen receptor structure

A
  • Total 2 x chains.
  • 1 x Alpha chain.
  • 1 x Beta chain.
  • Constant region on both chains (C alpha, C beta).
  • Variable region on both chains (V alpha, V beta) which bind antigen.
40
Q

How do T lymphocytes recognise pathogens / antigen

A

Through “presentation” of peptide^ bound to MHC molecules on other cells.

^Peptide is result of pathogen / antigen degradation in the cell with MHC molecules.

41
Q

Which MHC class molecules do CD4+ T cells recognise, on which cells are these MHC molecules present, and how do these cells process antigens^ so that they can be expressed on these MHC molecules?

^Antigen processing –> breakdown to peptides.

A

MHC class II molecules.

Present on:

  • Dendritic cells.
  • Macrophages.
  • B cells.

EXTRACELLULAR antigens processed by:

  • Endosomal / lysosomal processing.
42
Q

Which MHC class molecules do CD8+ T cells recognise, on which cells are these MHC molecules present, and how do these cells process antigens^ so that they can be expressed on these MHC molecules?

^Antigen processing –> breakdown into peptides.

A

MHC class I molecules.

Present on:

  • All nucleated cells.
  • Platelets.

INTRACELLULAR antigens processed by:

  • Cytosolic processing in proteosomes.
43
Q

What do B Lymphocytes recognise and bind for activation

A

Free antigens.

44
Q

What are the three processes needed to activate T cells

A
  1. Recognition and binding of antigen peptide-MHC class complex on presenting cells.
  2. Co-stimulation of CD28 from antigen presenting cell which determines which T helper cell a T cell becomes.
  3. Cytokine stimulation (various).
45
Q

What are the main three T helper cells that CD4+ T cells can become

A
  • TH1
  • TH2
  • TH17
46
Q

Roles of activated CD4+ T cells in killing of intracellular pathogens and how this is done.

A

Roles:

  1. Macrophage activation –> macrophage killing of ingested pathogens.
  2. Inflammation.

How:

  • Binding of macrophage with ingested pathogen –> cytokine secretion.
47
Q

Most common infection following solid organ transplant, why, and characteristic biopsy findings.

A

CMV.

Why:
Immunosuppressed patient –> common for reactivation of virus or new infection.

Characteristic biopsy findings:
Large eosinophilic intranuclear inclusions.

48
Q

Innate Immune System:
Complement System:
-Steps of Alternate pathway

A
  1. Pathogen binding.
  2. Activate B –> D.
  3. Cleavage of C3.
  4. Activation and formation of MAC (C5 - C9).
49
Q

Innate Immune System:
Complement System:
-Steps of Lectin pathway

A
  1. Binding of Mannose-binding lectin.
  2. Activation of Mannose-binding lectin –> MASP –> C2 –> C4.
  3. Cleavage of C3.
  4. Activation and formation of MAC (C5 - C9).
50
Q

What is the process of B cell activation

A
  1. Free antigen travels to lymphoid organs via lymphatics.
  2. B cell recognition of free antigen.
  3. Binding of free antigen.
  4. Activation and proliferation of B cells into antibody producing plasma cells.
  5. Differentiated plasma cells enter circulation and travels to site of antigen / infection.
51
Q

T Helper 1:
-Which cytokine causes differentiation into Th1 cells
-Which cytokine is secreted by Th1 cells
-What is the target cell for Th1
-Which pathogens do Th1 cells target
-Which diseases do Th1 cells play a role

A

Cytokines inducing Th1 subsets:

  • IFN-gamma.
  • IL-12

Cytokines secreted:

  • IFN-gamma

Target cells:

  • Macrophages - Th1 stimulates “classical” macrophage activation.

Pathogens:

  • Intracellular pathogens.

Diseases:

  • Autoimmunity.
  • Immune mediated chronic inflammation.
52
Q

T Helper 2:
-Which cytokine causes differentiation into Th2 cells
-Which cytokine is secreted by Th2 cells
-What is the target cell for Th2
-Which pathogens do Th2 cells target
-Which diseases do Th2 cells play a role

A

Cytokines inducing Th2 subsets:

  • IL-4.

Cytokines secreted:

  • IL-4.
  • IL-5.
  • IL-13.

Target cells:

  • Eosinophils.
  • Mast cells.
  • B cells - causes class switch to IgE.
  • Macrophages - Th2 stimulates “Alternative” macrophage activation.

Pathogens:

  • Helminths.

Diseases:

  • Allergy.
53
Q

T Helper 17:
-Which cytokine causes differentiation into Th17 cells
-Which cytokine is secreted by Th17 cells
-What is the target cell for Th17
-Which pathogens do Th17 cells target
-Which diseases do Th17 cells play a role

A

Cytokines inducing Th17 subsets:

  • TGF-beta.
  • IL-6.
  • IL-1.
  • IL-23.

Cytokines secreted:

  • IL-17.
  • IL-22.

Target cells:

  • Neutrophils.
  • Monocytes.

Pathogens:

  • Extracellular bacteria and fungi.

Diseases:

  • Autoimmunity.
  • Immune-mediated chronic inflammatory disease.
54
Q

What are the steps in B cell activation and isotype switching

A
  1. Recognition and binding of B cell to antigen.
  2. Secretion of IgM by B cells.
  3. Antigen processed and presented on B cell.
  4. Activated CD4 + T helper cells recognise antigen on B cell.
  5. Binding of T cell CD40L to B cell CD40 receptor.
  6. Secretion of cytokines from T cell.
  7. Stimulation of B cell to isotype switch^.
  8. B cell (now called plasma cell) secretes different antibody depending on switch.

^Involves change in heavy chain of antibody only.

55
Q

Functions of B cell antibodies

A
  1. Neutralisation of microbes and toxins.
  2. Opsonisation of microbe –> phagocytosis.
  3. Antibody-dependent cytotoxicity.
  4. Complement activation –> lysis of microbes, complement opsonisation of microbe, and inflammation.
56
Q

What causes autoimmunity and how

A

What:
Genetics

How:
Genetic susceptibility –> failure of self-tolerance –> self-reactive lymphocytes.

57
Q

Autoimmune Disease:
SLE:
-What is it
-What are the autoantibodies
-What are the disease manifestations
-What are the investigations and results

A

What it is:

  • Autoimmune disease involving multiple organs.
  • Caused by failure of self-tolerance mechanisms –> autoabs against self-ags –> formation of immune complexes.
  • Injury to tissues from deposition of immune complexes and binding of abs to various cells and tissues.

Autoantibodies against:

  • dsDNA.^
  • Smith (Sm) antigen.^
  • Ro (SS-A) / La (SS-B) nucleoproteins.
  • Generic ANAs.
  • Phospholipid-protein complexes.

Disease manifestations:
Many and include:

  • Nephritis.
  • Skin lesions.
  • Arthritis.

Investigations:

  • ANA - abnormal titer by immunofluorescence.
  • anti-dsDNA ab - abnormal titer.
  • Anti-Sm ab - presence of ab to Sm nuclear ag
  • Antiphospholipid ab - abnormal serum IgG or IgM anti-cardiolipin abs, positive lupus anticoagulant, OR false positive syphilis serology.
  • C3 / C4 / CH50 - low.

^Specific for SLE

58
Q

Transplantation:
Graft rejection:
-What is graft rejection, what is it mediated by, how do these cells recognise graft antigens, what is the outcome.

A

What it is:

  • Bodies response to foreign cells.

Mediators:

  • T lymphocytes.
  • Antigen presenting cells.

How:

  • Graft allo antigens have different HLA alleles to host.
  • Graft ags presented to host T cells via graft APC or host APC.

Outcome:

  • Activation of CD8+ T cells –> cytotoxicity.
  • Activation of CD4+ Th1 cells –> cytokines.
59
Q

Transplantation:
Graft rejection:
-What is seen in hyperacute rejection

A
  • Complement activation.
  • Endothelial damage.
  • Coagulation activation.
  • Thrombus formation.
  • Ischaemic necrosis of graft.
60
Q

Transplantation:
Graft rejection:
-What is seen in acute rejection

A

Acute cellular rejection:

  • Activation of CD8+ cells –> graft destruction.
  • Activation of CD4+ Th1 cells –> cytokine mediated damage.

Acute Ab mediated rejection:

  • Activation of complement via classical pathway –> inflammation of endothelium.
61
Q

Transplantation:
Graft rejection:
-What is seen in chronic rejection and over how long does this occur

A
  • T cell activation –> cytokine secretion.
  • Allo-antibodies binding to endothelial antigen.
  • Chronic inflammation in vessel wall.
  • Intimal smooth mucle proliferation.
  • Vessel occlusion.

Time:

  • Months or years of progressive loss of graft function.
62
Q

Transplantation:
Graft vs Host disease:
-What is seen in Acute GVHD

A

Epithelial necrosis in liver, skin, gut

63
Q

Transplantation:
Graft vs Host disease:
-What is seen in Chronic GVHD

A
  • Skin lesions.
  • Autoimmune symptoms.
64
Q

List the components of Innate Immune system

A
  • Epithelium.
  • Phagocytic cells - neutrophil, monoctes / macrophages.
  • Antigen presenting cells - dendritic cells.
  • Innate lymphoid cells - NK cells.
  • Complement.
  • Mast cells.
  • Proteins - mannose-binding lectin, CRP.
  • Lung surfactant.
65
Q

Innate Immunity:
Pattern Recognition Receptors:
-Where are Toll-like receptors found

A
  • Plasma membrane.
  • Endosomal membrane.
66
Q

Innate Immunity:
Pattern Recognition Receptors:
-Where are NOD-like receptors found and what do they recognise

A

Location:

  • Cytosol.

Recognise:

  • DAMPs (uric acid, ATP).
  • PAMPs (bacterial peptidoglycan).
  • Loss of intracellular K+ ions.
67
Q

Innate Immunity:
Pattern Recognition Receptors:
-Where are RIG-like receptors found and what do they recognise

RIG = Retinoic acid-inducible gene.

A

Location:

  • Cytosol.

Recognise:

  • Viral RNA.
68
Q

Innate Immunity:
Pattern Recognition Receptors:
-Where are C-type lectin receptors found and what do they recognise

A

Location:

  • Plasma membrane of dendritic cells.

Recognise:

  • Fungal glycans.
  • Microbial polysaccharide.
69
Q

Innate Immunity:
Natural Killer Cells:
-Roles

A
  • Recognise and destroy severely stressed or abnormal cells (e.g. virus infected cells or tumour cells).
  • Lyse IgG-coated target cells via binding of CD16 (receptor on NK cell) with IgG Fc tail = Ab-dependent cellular cytotoxicity (ADCC).
  • Secrete cytokines –> activate macrophage to destroy ingested microbes.
70
Q

What are human MHC molecules known as, what Chromosome contains the encoding genes for them, and what are the genes for each class?

MHC = Major Histocompatibility complex

A
  • Human Leukocyte antigens (HLA).
  • Chromosome: 6.

Genes - Class I:

  • HLA-A.
  • HLA-B.
  • HLA-C.

Genes - Class II:

  • HLA-DP.
  • HLA-DQ.
  • HLA-DR.
71
Q

What is immunologic tolerance, what is self-tolerance, and what are the types

A

Immunologic tolerance:
Unresponsiveness to an antigen induced by exposure of lymphocytes to that antigen.

Self-tolerance:
Lack of responsivelness to one’s own antigens. Underlies ability to live in harmony with one’s cells and tissues.

Self-tolerance Types:

  • Central.
  • Peripheral.
72
Q

Self-Tolerance:
-What is Central tolerance
-Where does it occur
-How does it occur

A

What it is:

  • Elimination of immature, self-reactive T and B cells.

Location:

  • Primary (central) lymphoid organs.
  • Thymus - T cells.
  • Bone Marrow - B cells.

How:
Through negative selection (AKA clonal deletion).

T Cells:

  1. APC presents self-ag to immature T cell.
  2. Stimulates apoptosis of T cell OR development of regulatory T cells.

B cells:

  1. Self-antigen recognised by B cell.
  2. Stimulates receptor editing of B cell receptor to no longer recognise that ag OR apoptosis.
73
Q

Self-Tolerance:
-What is Peripheral tolerance
-Where does it occur
-How does it occur

A

What it is:

  • Elimination of self-reactive T and B lymphocytes that have escaped central negative selection.

Location:

  • Peripheral tissues

How:
3 possible mechanisms:

  1. Anergy.
  2. Suppression by regulatory T cells.
  3. Death by apoptosis.
74
Q

Self-Tolerance:
Peripheral Tolerance:
How Anergy eliminates self-reactive cells

A

Anergy = making a cell functionally unresponsive.

How - T cell:

  1. T cell binds self-ag on APC.
  2. No co-stimulatory signal released from APC to activate T cell.
  3. T cell rendered unresponsive.

How - B cell:

  1. B cell binds self-ag.
  2. No Th cell to activate B cell.
  3. B cell rendered unresponsive and eliminated.
75
Q

Self-Tolerance:
Peripheral Tolerance:
How regulatory T cells eliminates self-reactive cells

A

Through regulatory T cells.

  1. Regulatory T cells are formed in the thymus in response to recognition of self-ags OR are induced in peripheral lymphoid tissue.
  2. Regulatory T cells suppress activation of self-reactive T and B cells.

NB. IL-2 and FOXP3 are important for synthesis and maintenance of regulatory T cells.
Mutations in FOXP3 = IPEX autoimmune disease (Immune dysregulation, Polyendocrinopathy, Enteropathy, X-linked).

76
Q

Self-Tolerance:
Peripheral Tolerance:
How Apoptosis eliminates self-reactive cells

A

Through either:

  • BIM (regulated apoptotic initiator) –> triggers apoptosis through Mitochondrial (Intrinsic) pathway.
  • Fas-FasL –> triggers apoptosis through Death Receptor (Extrinsic) pathway.
77
Q

ANA Indirect immunofluorescence:
-Staining patterns, what they indicate, what diseases it is seen in

A

Patterns:

  1. Homogenous or diffuse nuclear staining.
  2. Rim or peripheral staining.
  3. Speckled pattern (uniform or variable sized specks).
  4. Nucleolar pattern (few discrete spots of fluorescence within nucleus).
  5. Centromeric pattern (centromere staining).

Indicates:

  1. Antibodies to chromatin, histones, occasionally dsDNA.
  2. Antibodies to dsDNA, sometimes nuclear envelope proteins.
  3. Antibodies to non-DNA constituents (e.g. Sm antigen, ribonucleoprotein, SS-A / SS-B reactive antigens.
  4. Antibodies to RNA.
  5. Antibodies to centromeres.

Disease:

  1. SLE.
  2. .
  3. Most commonly observed pattern, least specific for disease.
  4. Systemic sclerosis.
  5. Systemic sclerosis, Sjrogren syndrome.
78
Q

What are the autoantibodies against in Rheumatoid arthritis

A
  • CCP (Cyclic citrullinated peptides).
  • Rheumatoid factor (not specific).
79
Q

Autoimmune disease:
Sjogren Syndrome:
-What are the autoantibodies against, what is the consequence, and what are the main clinical features

A

Autoabs against:

  • Ro / SS-A.
  • La / SS-B.

Consequence:

  • Immunologically mediated destruction of lacrimal and salivary glands.

Clinical Features:

  • Dry eyes.
  • Dry mouth.
80
Q

Autoimmune disease:
Systemic Sclerosis (AKA scleroderma):
-What are the autoantibodies against, and what are the main clinical features

A

Autoabs against:

  • DNA topoisomerase I.
  • Centromeric proteins A, B, C.
  • RNA polymerase III.

Main clinical features:

  • Chronic inflammation (as a result of autoimmunity).
  • Widespread damage to small blood vessels.
  • Progressive interstitial and perivascular fibrosis in skin, GI tract, and other organs.
  • Skin - extensive deposition of dense collagen in the dermis AND absence of hair follicles AND foci of inflammation.
  • Claw-like flexion deformity of fingers due to extensive subcutaneous fibrosis.
  • Cutaneous ulcers of fingers due to loss of blood supply.
81
Q

Amyloidosis:
-What is it, what is the pathogenesis, how does it damage tissue, what is the histology, and what diseases can it be seen in

A

What it is:

  • Disorder characterised by extracellular deposits of misfolded proteins that aggregate to form insoluble fibrils.

Proposed pathogenesis:

  • Excessive production of proteins prone to misfolding.
  • Mutations producing misfolded proteins.
  • Defective or incomplete proteolytic degradation of extracellular proteins.

Damages tissue by:

  • Deposits causing pressure on cells and tissues.
  • DOES NOT evoke an inflammatory response.

Histology:

  • Congo red stain of liver - pink-red deposits of amyloid in walls of BVs and along sinusoids.
  • Polarising microscope - yellow-green birefringent deposits.
  • H&E of kidney - glomerular architecture destroyed by massive accumulation of amyloid.

Diseases:

  • Multiple myeloma (deposits of immunoglobulin light chains).
  • RA (amyloid A protein deposits)
  • Alzheimer’s (amyloid beta protein deposits).
  • Familial amylid polyneuropathies (transthyretin accumulation).
  • Associated with dialysis (deposits of beta 2-microglobulin).

Basic Pathology (14 decks)

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