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Immunobiology > W8L12-13 - Immune Diseases > Flashcards

W8L12-13 - Immune Diseases Flashcards

1
Q

Inadequate Immune Response

A

Primary immunodeficiency - present at birth (genetic disorder)
Secondary immunodeficiency - acquired (drug or infection)

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2
Q

Examples of Primary Immune Deficiency

A

X-linked agammaglobulinemia (Brutons)
IgA deficiency
DiGeorge syndrome
Severe combined immune deficiency (SCID)

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3
Q

X-linked Agammaglobulinemia (Brutons)

A 
Low number of B cells
Low immunoglobulin levels
No humoral immunity
Mutation in B cell tyrosine kinase gene on X chromosome
- BKT essential for B cell maturation 
- males affected mostly
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4
Q

IgA Deficiency

A

Reduced level of IgA production
Usually asymptomatic
Patients tend to have increased respiratory infections due to reduced sIgA

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5
Q

DiGeorge Syndrome

A

Failure to form T cells due to hypoplasia of thymus (partial or incomplete)
Infants have cleft palate, facial cleft, low ears, absence of parathyroid gland and heart is malformed
Vulnerable to virus and intracellular bacterial infection

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6
Q

Severe Combined Immune Deficiency (SCID)

A

Failure to develop T and B cells
Thymus and lymphoid tissue reduced
Early in life child has recurrent infections
Adenosine deaminase deficiency leads to accumulation of toxic waste in lymphocytes

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7
Q

Examples of Secondary Immune Deficiency

A

Severe malnutrition
Infants first 6 months only maternal Ig
Drug therapy
HIV/AIDS

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8
Q

Whats does HIV and AIDS stand for?

A

HIV - human immunodeficiency virus

AIDS - acquired immune deficiency syndrome

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9
Q

How does HIV/AIDS work?

A

Helper T cells destroyed by HIV
- helper T cells help B cells and cytotoxic T cells
Loss of helper T cell leads to severe immunosuppression
Death due to infection or cancer

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10
Q

Why does HIV enter macrophages 10x better than T lymphocytes?

A

HIV has higher affinity for co receptor CCR5 on macrophages than CXCR4 on T lymphocytes

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11
Q

How can you be immune to HIV?

A

If you are homozygous for mutant allele of CC-CKR5 gene on chromosome 3
This encodes for cell surface protein CCR5 (co-receptor for HIV)
Mutation is a deletion of 32 bp
The resulting protein shortened and loss function
Therefore HIV cant bind

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12
Q

Type 1 Hypersensitivity

A

Immediate hypersensitivity
Anaphylactic shock
Th2 response leading to excessive IgE to antigen
Normal response to worm infection however abnormal for some allergens

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13
Q

Type 2 Hypersensitivity

A 
Circulating antibodies binding to antigen on cell surface or tissue inappropriately 
Causes:
- complement activation
- phagocytosis
- NK cells
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14
Q

Type 3 Hypersensitivity

A 
Soluble antigen reacts with antibody and these complexes deposit into tissues
Often in blood vessel walls
Causes:
- complement activation
- mast cell degranulation
- attracts neutrophils
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15
Q

Type 4 Hypersensitivity

A

Delayed type hypersensitivity
Antigen presenting cells leads to Th1 response
Cytokine response activation cytotoxic T cells

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16
Q

Allergies and Asthma

A

Type 1 reaction (immediate hypersensitivity)
Th2 response
Involves IgE, mast cells and eosinophils
- exposure to allergen leads to activation of Th2 cells producing large amounts of IL-4
- B cells switch to IgE prodcution
- IgE binds to mast cells via Fc receptor
- second exposure to antigen causing crosslinking of IgE on mast cells causing degranulation and attracting eosinophils

17
Q

What are the 2 types of autoimmune disease?

A

Organ specific
- response directed to variety of antigens within organ
- antigens usually molecules expressed on sruface of lving cells
- restricted pattern
Non-organ specific
- reponse to self antigens that are widely distributed
- often intracellular molecules
- multi-system disorders

18
Q

Factors involved in Autoimmune Disease

A

Sequestered antigen
- antigens normally hidden to immune system
- accidental exposure to antigen
Cross reactivity with microbial antigen
- T cell or antibody directed against a microbe antigen also reacts against self antigen
- aka molecular mimicry
Polyclonal activation
- microbial activation of many clones of T or B cells
- non-specific so auto reactive clone may be activated
Non infectious triggers
- drugs, chemicals, hormones

19
Q

What is tolerance?

A

Unresponsiveness to self antigens

20
Q

Mechanisms of Self Tolerance

A

Anergy
- non-responsiveness of cells upon contact with antigen
Receptor editing
- genetic rearrangement of the variable region of BCR and TCR
- BCR and TCR no longer specific for antigen
Clonal deletion
- auto reactive T and B cells eliminated by apoptosis during development
Clonal ignorance
- cells that remain inactivated due to low affinity with self antigen
- low concentration of antigen = low signal
T cell suppressors
- Treg cells regulate/suppress T cells

21
Q

Myasthenia Gravis

A

Antibodies directed to the acetylcholine receptor at neuromuscular junction
Blocks binding of acetylcholine from nerve to receptor on muscle
Receptors also internalised and broken down so fewer available
Weakness and fatigue of voluntary muscles
Occurs in:
40-50% young women
- high levels of anti-AChR antibodies
15-30% older men
Treatment:
- immunosuppressant drugs
- cholinesterase inhibitors

22
Q

Systemic Lupus Erythematosus

A

Erythematosus = reddening of skin
Production of anti nuclear antibodies (ANA)
- positive ANA strongly supports SLE but is not confirmatory
- usually homogenous or speckled pattern
Patients can develop arthritis, skin lesions, kidney disease, pulmonary and neurological damage
SLE 10x more common in women because high oestrogen levels accelerate disease

23
Q

Pathology of SLE

A

Mediated by auto-antibody type 2 and 3 hypersensitivity
- immune complex disease
Tissue damage due to deposition of dsDNA-Ab complexes (kidney)
SLE people may have defective mechanism of clearing DNA after apoptosis, so exposing DNA as antigen
UV light triggers flair up of disease
- UV light induces apoptosis of keratinocytes in skin

24
Q

Rheumatoid Arthritis

A

Inflammation of synovium in joints
Progressive - invades cartilage and bone
Joint destruction

25
Q

RA Pathogenesis

A

Unknown trigger starts inflammation of synovium
- possinby infection
Autoreactive CD4 T lymphocytes activate macrophages
Production of pro-inflammatory cytokines
- IL-1, IL-6, IL-17, TNF-α
- other cells attracted (neutrophils)
Cytokines induce production of metalloproteinases (MMPs) and RANK ligand by surrounding fibroblasts
- MMPs enzymes destroy tissue
- RANK ligand stimulate bone destruction by osteoclasts

26
Q

Antibodies in RA

A 
Rheumatoid Factor (RF)
- anti-IgG (Fc portion)
- usually IgM
- not found in all RA cases
Antibodies to 
- citrullinated peptides (peptides with modified arginine, charge from + to neutral)
- type 2 collagen
- vimentin
27
Q

Sjogrens Syndrome

A

Autoimmune disease involving destruction of exocrine glands
- salivary glands most commonly
- also respiratory and vagina
Prominent feature is sicca (drying) of mouth and eyes
Predominately in women (90%)
Speckled ANA pattern
Pathology not understood
- glands infiltrated with cytokine producing CD4 T cells
- autoantibody response
No specific treatments

28
Q

Scleroderma

A

Hardening of skin, blood vessels, musculoskeletal system
Build up of fibrous tissue in skin causing skin to tighten
4x more frequent in women (45-65 yo)
Anti-nuclear antibodies in 80% of disease
- anti-centromere in 90% limited scleroderma
- anti-nucleolar in 40% scleroderma

29
Q

ANA Patterns

A 
Homogenous
- even staining nucleus
- dense staining mitotic body
Centromere
- fine speckled staining in nucleus
- lining staining in mitotic body
Speckled
- uneven stained nucleus
- unstained mitotic body
Nucleolar
- 2-5 dense staining granules in nucleus
30
Q

Vasculitis

A

Inflammation of blood vessel walls
- caused by infection
- drugs
- maligancy
Autoimmune vasculitis
- neutrophils can release some proteins in extracellular space in resposne to bacterial infection
- anti-neutrophil cytoplasmic antibodies (ANCA)
ANCA
- cytoplasmic granular pattern (C-ANCA) - antigen is proteinase 3
- perinuclear pattern (P-ANCA) - antigen is myeloperoxidase

31
Q

Cryoglobulinemia

A

Cryoglobulins

  • immune complexes
  • can deposit in extremities and form purpura (skin haemorrhage)
  • precipitate in cold conditions

Immunobiology (20 decks)

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