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Human Disease > Immunopathology > Flashcards

Immunopathology Flashcards

Acquire immunity Hypersensitivity Auto-immunity Immuno-deficiency

1
Q

What involve in acquired immunity

A

. Specific antigen
. Lymphocytes T (virus) and B (bacteria)
. Memory

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2
Q

Another name for acquired immunity

A

Adaptive immunity

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3
Q

What’s the name for adaptive immune response to extracellular microbe (i.e. bacteria)? What regulated this process?

A

Humoral immunity

B lymphocytes

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4
Q

What’s the name for adaptive immune response to intracellular microbe (i.e. virus)? what regulated this process?

A

Cell-mediated immunity

T lymphocytes

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5
Q

What B cells produce? How do they cause destruction of microbes?

A

Antibody: IgM first then IgG, IgA, IgE in bone marrow

Phagocytosis by PMN and Mø

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6
Q

What T cell produce? How do they cause destruction of microbes?

A

CD4 T helper cell: cytokines (Th1, Th2, Th17, Treg)

Cytokines activate and proliferate CD8 Tcells

CD8 T cytotoxic cell: apoptosis

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7
Q

What are key features of antigens?

A

. bound to aB - immunogen
. high molecular weight (MW>10,000) proteins
. sometimes carbohydrate

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8
Q

What is epitopes?

A

. Smaller fragments of antigens
. recognized by antigen combining site of aB or T cell R
. Comprised 8 AA (linear-T cell) or up to 20 AA (globular-B cell)

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9
Q

Dendritic Cells prime T cells involve in

A
  1. Endocytosis
  2. Toll-like Receptor (TLR) Ligation
  3. Increase expression of MHC-1 co-stimulatory molecules
  4. antigen presentation
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10
Q

Another name for MHC (major histocompatibility complex)

A

Human leukocyte antigen (HLA)

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11
Q

Where does MHC-II/HLA present to?

A

CD4 T helper cells

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12
Q

Where does MHC-I/HLA present to?

A

CD8 T cytotoxic cells

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13
Q

What are the 3 main signals to activate T cell?

A
  1. MHC and peptide on DC present specific antigen : T cell R on T cell
  2. Co-stim signal CD80/CD86 of DC : CD28 of T cell
  3. CD40 on DC : CD40L on T cell
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14
Q

Timeline of generating T cell response

A

4-5d : activate cytokines from Th1, Th2 and Th17
7-10d: activated T cytotoxic cell (with help of Th1)
1-2d : once memorized!

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15
Q

What are the 2 main cytokines that stimulate Cytotoxic T cells?

A

IFN-a and TNF-a by Th1

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16
Q

Primary role of Cytotoxic T cell?

A

Apoptosis

e.g. cancer tumour is a target of T cell killing

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17
Q

What are main signals to activate B cell?

A

MHC-II / peptide / TCR

CD40 on DC : CD40L on activated Th cells

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18
Q

How long does it take to activate B cell, to switch from IgM to IgG for the first time?

A

10 days

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19
Q

How many heavy and light chains in each aB?

A

2 heavy

2 light

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20
Q

Where in the aB determine the Ig isotypes?

A

Constant region of Heavy chain

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21
Q
  1. What aB has the lowest affinity to antigen?

2. What aB has the highest quantity in serum?

A
  1. IgM

2. IgG

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22
Q

What included in adaptive immunity? (important)

A

Humoral immunity (aB)
Cell-mediated immunity (T cell)
Tolerisation (autoimmunity)
Hypersensitivity (second-line exposure of allergen)

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23
Q

What is the primary role of B cell?

A

produce immunoglobulin (aB)

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24
Q

Can innate immunity involve T cell?

A

NO

only mast cell, Mø, NK cells and N˜

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25
Q

What is the main feature of hypersensitivity?

A

Only occurs on the SECOND (subsequent) exposures to antigen

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26
Q

Hypersensitivity rx are induced by allergens. List some examples of Allergen

A 
. small soluble proteins or glycoproteins
. proteases
. dust mite faeces
. food (milk, nut,...)
. insect saliva
. drugs (penicillins, aspirin)
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27
Q

Main features of Type 1 hypersensitivity

A

. IMMEDIATE type
. IgE bound to mast cells (cross linking lead to degranulation)
. IL-4,5 from Th2 mediate IgE production

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28
Q

Predisposing factors to ATOPIC allergy (type 1 hypersensitivity)

A

. High affinity for IgE on mast cells and basophils
. Higher IgE levels (if >1µg)
. Genetic predisposition (Favor Th2- IL-4)
. Environmental pollutants can increase IgE (inhibit Th2 func and inhibit tolerance induction)

note: neonates may develop allergies if exposed to pollutants simultaneously (can train them)

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29
Q

In Type 1 Hyp, what lead to immediate response and what are those responses?

A

Degranulation of mast cells causes release of Histamine, proteases and chemotactic factor

  • vasodilation
  • vascular leakage (to tissues)
  • Smooth m/s spasm
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30
Q

In Type 1 Hyp, skin rx to allergen peaks at __ mins, called __&__

In Type 1 Hyp, systemic manifestation is called __ shock

__ primes __ to migrate in response to chemotactic factors, called __ asthmatics

A

30 mins
wheal and flare (blister and red)

anaphylaxis

IL-5
Eosinophils
extrinsic

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31
Q

List some examples of local anaphylactic Type 1 Hyp

A

Allergic rhinitis - Hay fever
Asthma (smooth m/s)
Atopic eczema or urticaria
Food allergy (GIT)

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32
Q

Type 1 Hyp PATHOLOGICAL processes

A

. Smooth m/s contraction
. Vasodilation - fluid exudates
. Mucus secretion exceeded
. Eosinophil infiltration

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33
Q

Main features of Type 2 Hyp

A

. Cell-bound antigen coated with IgG
. Cells are opsonized by C3b
. Followed by phagocytosis destruction
. Complement cascade forms membrane attack complex (MAC)

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34
Q

Type 2 Hyp: Clinical examples

A 
. Incompatible blood transfusions
. Hyperacute graft rejection
. Myasthenia gravis
. Graves disease
. Acute rheumatic Fever
. Drug hyp
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35
Q

Main features of Type 3 Hyp

A

. immune COMPLEX-MEDIATED
. IgG bound to SOLUBLE antigen
. Arthus rx skin test peaks at 3-8hrs with infiltration of polymorphs
. Complement activation generates anaphyatoxins and attract polymorphs
. ‘Frustrated’ phagocytosis due to C’s mediated inflam

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36
Q

What can Ag:Ab complex (immune complex-mediated hyp) activate?

A
  • Platelet aggregation
  • Complement (anaphylatoxin and polymorphs)
  • Mø
37
Q

Something special about Type 3 Hyp

A

Have 3 phases

  1. formation of immune complex
  2. deposition of immune complex
  3. immune complex mediated inflammation
38
Q

In local vs. systemic rx of Type 3 Hyp
. Excess __ lead to precipitated immune complex. E.g. __
. Excess __ gives soluble immune complexes. E.g. __

A

aB
Pigeon Fanciers Disease

antigen
Serum sickness or deposition of immune complexes in kidney glomerulus

39
Q

Main features of Type 4 Hyp

A

. DELAYED types
. T-cell mediated response (cytokines IFN-g, GM-CSF)
. Skin test - infiltration of mononuclear cells peaking at 24-48hrs (Th recruit Mø)
. Diagnostic for T cell immunodeficiency

40
Q

Type 4 Hyp examples of reaction

A

AIDS
Contact dermatitis (e.g nickel)
TB
chronic granuloma

41
Q

What’s special about Type 4 Hyp in the skin?

A

Staining of CD4 T cell (granuloma)

42
Q

Immediate vs. Delayed Hyp type
. ITH develop in _ mins while DTH develop in _ hrs

. Central appearance is _ for ITH & red induration for DTH

. Peripheral appearance is _ for both ITH & DTH

. __ cells (Ig_) involved in ITH & __ cells involved in DTH

A

30mins
24-48 hrs

blister

red

Mast cells (IgE)
Th cell
43
Q

What is another term for autoimmunity?

A

Tolerisation

44
Q

What is tolerisation

A

. prevents auto-reactivity in the thymus, but:
. auto-reactive cells destroyed by apoptosis
. low affinity auto-reactive T cells may ‘escape’ deletion in the thymus

note: auto-aB and auto-reactive t cells can be found WITHOUT accompanying disease

45
Q

What does NON-self reactive clones of T cell do?

A

enter periphery for normal immune func

46
Q

What are Regulatory T cells and what do they control?

A

Tregs: CD4, CD25, FoxP3+ cells
Control T cell proliferation by production of IL-10 + TGF-b

note: regulatory effect depends on cell-cell contact

47
Q

Features of autoimmune disease (7)

A

. increase mononuclear cells infiltration [lymphocytes, Mø, and p/m cells]
. Loss of tolerance to self
. genetic predispositions HLA
. Classified by 4 Hyp types
. Female bias
. Patient often have multiple autoimmune disease (systemic, local)
. Environmental influences

48
Q

4 SYSTEMIC autoimmune diseases

A

SLE (Systemic Lupus Erythematosus)
Sjögren’s syndrome
Scleroderma
Rheumatoid arthritis

49
Q

How does the immune system recognise self

A

. HLA present unique antigens (Genetic susceptibility)
. Molecular mimicry
. Following infection and tissue damage

50
Q

SYSTEMIC autoimmune disease (1)

SLE

A

. Caused by: lots of auto-aB forming immune complex
. Major auto-aB: at nuclear antigens (ANAs)
. Manifestations: nephritis, skin lesions, arthritis
. Disease remitting and relapsing
. common, esp. 20-30s yrs

51
Q

In SLE, what are inherited susceptibility and environmental triggers

A

. inherited: MHC-II and complement

. environment: UV radiation

52
Q

Diagnosis of SLE

A

. Photosensitivity
. Rashes
. Arthritis (joint pain?)
. Disorder (renal, neurological,…)

note: SLE can affect skin, joints, kidney, etc.

53
Q

SLE associate with what types of Hyp?

A

Type 2 and 3

54
Q

SYSTEMIC autoimmune disease (2)

Systemic sclerosis

A

. Also called scleroderma
. accumulation of fibrous tissue in skin others (=increase collagen production)
. CD4 T cell involved
. female bias (older women)

55
Q

Possible mechanism for sclerosis

A

Cytokines (growth factors) and Ischemia to increase fibrosis/collagen)

56
Q 
SYSTEMIC autoimmune disease (3) 
Rheumatoid arthritis (RA)
A

. Increased TNF cytokines activate B cell, Mø and endothelial cell
. Involve rheumatoid factor and fibroblast
. Pannus formation

treat: have aB bound therapy to clean up TNF cytokines

57
Q

SYSTEMIC autoimmune disease (4)

Sjögren syndrome

A

. Destruction of exocrine glands (lacrimal and salivary glands)
. Symptoms: dry eyes and mouth
. infiltration of CD4-T and B cells
. Female bias (older women)
. Have rheumatoid factor and 50% have ANAs

58
Q

What is rheumatoid factor and ANAs?

A

Rheumatoid factor = aB bind and form immune complex with IgG. Involved in RA and Sjögren syndrome

ANAs = auto-aB directed at nuclear antigens

59
Q

4 LOCAL autoimmune diseases

A 
Multiple sclerosis (neuro)
Hashimoto's Thyroiditis (endocrin)
Type 1 diabetes (endocrin)
Crohn Disease (GIT)
60
Q

LOCAL autoimmune disease (1)

Multiple sclerosis

A 
. Demyelinating disorder
. occur at any age
. female bias
. Caused by: CD4 T cells (specific for antigens from myelin sheath)
. Th1 cells activate Mø
. Relapsing - remitting disease
61
Q

LOCAL autoimmune disease (2)

Hashimoto’s Thyroiditis

A

. HYPOthyroidism (destruction of thyroid)
. thyroid epithelial cells are destroyed by:
- CD8 (direct destruction)
- CD4 (toxic cytokines)
- auto-aB and ADCC

62
Q

What appear in histological feature of Hashimoto’s thyroiditis

A

. Thyroid parenchyma contains a dense lymphocytic infiltrate with germinal centre

63
Q

LOCAL autoimmune disease (3)

Type 1 diabetes

A

. B-islet cells of pancreas attacked by CD8 T cells (also CD4 T)
. pancreas no longer making insulin
. may associate with viral infection
. Have class2 alleles (HLA-DR3,4) in most of Caucasians

64
Q

LOCAL autoimmune disease (4)

Crohn’s disease

A

. Lesions along GIT
. HLA-DR1 association
. NOD2 involvement (inflammasome)
. CD4 T cell activation and granulama formation (site of necrosis)

65
Q

Gross pathology of Crohn’s Disease

A
  • mucosal ulcers and thickened intestinal wall
  • perforation and ass. serositis
  • creeping fats
66
Q

Main types of Immunodeficiency

A

Primary and Secondary Immune Deficiencies

67
Q

What are deficiencies in the INNATE response

A

Defective in:

  • production of polymorphs
  • response to chemotactic stimuli
  • leucocyte adhesion (LFA-1 defect)
  • lysosomes (pyogenic infections)
  • no production of reactive O2 intermediates
68
Q

What infections occur in deficiencies of complement, in innate response?

A 
Pyogenic infections (immune complex disease)
Neisserial infections
69
Q

Is deficiency in innate response the same with acquired immune response?

A

NO

70
Q

What are indications of T lymphocyte immunodeficiency?

A

. reduce CD3+ T lymphocytes (genetic marker)
. variations of circulating CD4+ and CD8+ lymphocytes (AIDS)
. low response to polyclonal activators (Concanavalin A)
. decreased type Hyp
. changes of T cells area in the lymph node

71
Q

What are indications of B lymphocyte immunodeficiency?

A

. reduced aB (Ig+ve)
. reduce opsonisation
. poor response to polyclonal activators (LPS in vitro)
. poor aB response to vaccination with inactivated vaccines
. increased susceptibility to pyrogenic infections

72
Q

Examples of Primary immunodeficiency Disorder

A 
T+B - Severe Combined Immunodeficiency Disorder (SCID)
T - DiGeorge Syndrome
T+B - Bare Lymphocyte Syndrome
B - X-linked agamma-globulinemia
B - Hyper IgM syndrome
73
Q

Which primary immunodeficiency is classified as stem cell disorder

A

SCID

74
Q

What are the 2 factors causing SCID?

A

ADA deficiency and cytokine signaling mutation

  • ADA: enzyme in purine metab
  • cytokine mutation: result in no growth factors for cell survival
75
Q

What is sad for SCID patient?

A

highly susceptible to infection

‘Bubble’ boy

76
Q

Which primary immunodeficiency disorder has FAILURE of B cell?

A

X-linked Agammaglobulinemia

aka Brutons disease

77
Q

Which primary immunodeficiency disorder has ELEVATED levels of B cell? specific Ig type involved?

A

Hyper IgM Syndrome

- increase IgM and reduce IgG+A

78
Q

What is the cause of Hyper IgM deficiency?

A

deficiency in:

  • CD40L, CD40
  • activation-induced cytidine deaminase (AID)
  • Uracil DNA glycolase (UNG)
79
Q

Which primary immunodeficiency disorders with little/no thymus gland?

A

DiGeorge Syndrome

- so no development of T cell for cell-mediated response

80
Q

Which primary immunodeficiency disorder has lack of MHC-II?

A

Bare Lymphocyte Syndrome

  • so no activation of CD4
  • also reduced IgG, IgA
81
Q

What is one common thing in patient with primary immunodeficiency disorders?

A

very susceptible to infections

82
Q

Secondary immunodeficiency can be seen in patients with:

A 
. autoimmune disease
. neoplasms
. measles, chicken pox, mumps, severe trauma leprosy, Hodgkins disease
. malnutritions
. HIV-AIDS
. Cancer or infection
83
Q

In Secondary immunodeficiency, patient with INFECTION (i.e. measles) have predominance of what?

A

. strong Th1 response but also require Th2 response

84
Q

In Secondary immunodeficiency, patient with NEOPLASMS have predominance of what?

A

. one type of WBC (i.e. B cells in myeloma)

. also absence of WBC due to chemotherapy

85
Q

Does AIDS classified as primary or secondary immunodeficiency?

A

Secondary

86
Q

What is AIDS

A

Acquired immune deficiency syndrome
. gp120 glycoprotein of RNA retrovirus infecting CD4 T cells
. Co-factor required
. associated with Type 4 Hyp

87
Q

What are co-factor required for AIDS

A

members of chemokine receptor family

  • Mø tropic HIV : CCR5
  • lymphotropic HIV: CXCR4
88
Q

In AIDS patient, where has higher CD4 for HIV-RNA retrovirus to bind to?

A

Th cells (compared to Mø and DC)

89
Q

AIDS patient is susceptible to what?

A

Mycobacterium tuberculosis

Human Disease (6 decks)

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