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Infection and Immunity > Immune diseases > Flashcards

Immune diseases Flashcards

1
Q

Antigen invades

A

recognised by pattern receptors

activation of complement -> phagocytosed by dendritic cells

carried to lymph nodes

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2
Q

where do B cells mature?

A

bone marrow

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3
Q

B cells MoA

A

Recognise epitope of whole antigen using surface IgD, endocytose and process antigen

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4
Q

where do T cells mature

A

thymus

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5
Q

T cells MoA

A

recognise fragment of antigen presented on class II MHC by dendritic cells

Upregulate CD40 costimulatory molecules and cytokine secretion

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6
Q

what happens once T cells are activated?

A

isotype switch (IgG, A, E) by CD40L on Th2 cells and secrete antibodies

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7
Q

what do Th1 do?

A

activate macrophages

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8
Q

what happens to Tc cells?

A

migrate to tissues

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9
Q

Effector responses

A

Antibodies coat antigen to promote phagocytosis

Macrophages phagocytose opsonised antigens

Cytotoxic T cells and NK cells kill infected cells

T cells in tissues secrete cytokines to recruit and activate neutrophils and macrophages

Antigen is eliminated

Excess cells die by apoptosis

B cells remain as memory cells

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10
Q

types of hypersensitivity reactions

A

I - immediate hypersensitivity (allergy)
II - autoantibodies
III - deposition of immune complexes
IV - T cell mediated tissue injury

II, III + IV = autoimmunity

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11
Q

what do mast cell mediators cause?

A

increased vascular permeability

Vasodilation

Bronchial and smooth muscle contraction

Local inflammation

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12
Q

Type I - immediate hypersensitivity

A

Stimulation of mast cells by crosslinking of FcR bound IgE

Very rapid after exposure to antigen

Mast cells contain lots of granules of histamine -> treat with anti-histamines
-> treat downstream effects -> can’t target mast cells

Allergy or atopy -> strong genetic predisposition

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13
Q

what happens to IgE antibody over time?

A

become more sensitive over time

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14
Q

allergens

A

Requires repeated exposure before substance triggers immune response

By-pass innate response (not pathogenic; no surface molecules to trigger immune system)
Not TH1 or macrophage activation

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15
Q

allergen structure

A

small

glycosylated

high solubility in body fluids

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16
Q

role of IL-4

A

promotes TH2 development and antibody class switching to IgE

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17
Q

Type II - autoantibodies - MECHANISMS

A

[more localised in particular tissues]

  1. Activate complement and stimulate phagocytosis (haemolytic anaemia)
  2. Can recruit neutrophils which cause tissue damage (glomerular nephritis)
  3. Can bind to receptor and stimulate or inhibit function (Graves Disease, myasthenia gravis)
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18
Q

Graves disease

A

antibody agonist (excess thyroid hormones)

treat with thionamides (e.g. carbimazole)

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19
Q

Myasthenia gravis

A

antibody binds to Ach receptors; muscle weakness as Ach doesn’t bind = muscle weakness

treat with anti cholinesterases (e.g. neostigmine)

20
Q

example of a systemic disease

A

Systemic Lupus Erythematosus (SLE)

21
Q

Type III - immune complexes

A

Can occur after multiple injections of antigen (immunisation)

Leads to complement activation and FcR mediated responses

vasculitis, tissue death + organ failure

22
Q

where does Type III - immune complexes usually occur?

A

Usually occurs in small vascular Beds, joints and renal glomeruli

Large cross-linking complexes deposited in small vascular beds

23
Q

vasculitis

A

inflammation of blood vessels

24
Q

Type IV - cell mediated tissue injury

A

Delayed Type Hypersensitivity (DTH) and cytotoxicity

Mediated by TH1 and CD8 cells

Release IFNɣ to activate macrophages and TNF to induce inflammation

Tissue damage caused by hydrolytic enzymes, ROIs and cytokines

prototype disease = type I diabetes (treat with exogeneous insulin)

25
Q

how does autoimmunity arise?

A

from failure/breakdown in mechanisms normally responsible for maintaining self-tolerance

either systemic or organ specific

26
Q

main contributing factors of autoimmunity

A

genetic susceptibility

environmental triggers

27
Q

what can happen once autoimmunity has been initiated?

A

can result in epitope spreading resulting in chronic disease

28
Q

organ specific autoimmune diseases

A

Insulin dependent diabetes mellitus (IDDM)

MS

29
Q

rheumatoid arthritis (RA)

A

inflammation and destruction of joints, antibodies may also be involved

30
Q

inflammatory bowel disease (IBD)

A

chronic inflammation of the gastrointestinal (GI) tract

mainly mediated by cytokines

31
Q

autoimmune disease following chronic infection

A

[tuberculosis]

looks like proteins found in joints

Immune system constantly activated -> hasn’t got rid of pathogenic agent

32
Q

what are autoimmune diseases mainly treated with?

A

anti-inflammatories (naproxen/steroids) and disease modifying agents (methotrexate)

33
Q

what is associated with a lot of autoimmune diseases?

A

LA (HLA-DR4 possible increase in RA)
- Thought to be linked to the way the MHC alleles present the peptides
- Present self-peptides in such a way that they look foreign -> stimulate T cells

HLA-B27 associated with 90-100 fold increased risk of ankylosing spondylitis

34
Q

males vs females - autoimmune diseases

A

increased incidence in females

Possibly linked to hormones -> RA goes whilst woman in breastfeeding

35
Q

transplants

A

Recognition of donor MHC as foreign

Donor tissue killed by CTL(Tc), Th cells and antibodies
- Less likely to get this response if MHC on donor is similar to recipient

Require blood and tissue typing (ABO, HLA systems)

Check for preformed antibodies

36
Q

blood typing

A

ABO system

antigens on surface of RBCs

Produce antibodies against antigens we don’t have
- Group A blood has anti B antibodies
- Group O has anti A and anti B antibodies

Recipient must not have antibodies against donor antigen

37
Q

blood types - universal donor

A

O

38
Q

blood types - universal recipient

A

AB

39
Q

rhesus factor

A

Negative = have antibodies against Rhesus factor

Positive = don’t have antibodies against Rhesus factor

40
Q

tumour immunology

A

most = weakly immunogenic

grow rapidly and overwhelm immune system

tumour specific antigens (oncoproteins) or self-antigens that are usually hidden

Mainly targeted by CTL and NK cells

Therapy - antibodies, vaccines, co-stimulation

41
Q

ADEPT

A

= pro-drug therapy

Antibodies against “overactive” surface protein

Antibodies against immune regulators

42
Q

Immunodeficiency

A

insufficient activation of immune system

43
Q

Congenital

A

X-linked agammaglobulinemia (mutations in genes on X chromosome -> don’t produce antibodies)

Severe combined immunodeficiency (SCID)

44
Q

Acquired

A

As a result of infection, cancer or drug treatment (iatrogenic)

HIV/AIDS

45
Q

HIV

A

Human immunodeficiency virus

46
Q

HIV - MoA

A

Infects dendritic cells and carried to lymph nodes

Activation of CTLs and antibody production results in partial control of infection

Infects T cells via CD4 and chemokine receptors

Gradually causes lymphopenia

Patient dies of opportunistic infections

Infection and Immunity (17 decks)

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