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MSK > Immunology > Flashcards

Immunology Flashcards

1
Q

What is autoimmunity defined as?

A

presence of immune responses against self-tissue/cells

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2
Q

What is the pathogenesis of autoimmune disease?

A

genetic susceptibilty and then there is an initating event and there is breakdown of self tolerance (loss of immune regulation)

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3
Q

Give an exmple of a monogenic autoimmune disease?

A

IPEX syndrome

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4
Q

What does IPEX syndrome stand for?

A

immune dysregulation; polyendocrinopathy; enteropathy and X-linked inheritance

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5
Q

When does IPEX sybdrome present?

A

presents early in childhood

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6
Q

What are the symptoms of IPEX syndrome?

A

severe diarrhoea; eczema; very early onset IDDM; autoimmune manifestations

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7
Q

What is the cure for IPEX syndrome?

A

haematopoeitic stem cell transplantation

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8
Q

What causes IPEX sydnrome?

A

mutation in FOXP3 gene whic his essential for the delevopment of regulatory T-cells-failure of peripheral tolerance

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9
Q

What is the function of regulatory T cells?

A

suppress autoreactive T cells

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10
Q

What gives rise to thte hugely diverse popultation of T cells and B cells

A

random rearragnemnt of Ig heavy and light chain gene segments

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11
Q

What are the tolerance mechanisms required for autoreactive T cells and B cells

A

central tolerance- removal of self-reactive lymphocytes in primary lymphoid tissues: cells in tissue that present self-antigens, if cell recognises the antigen, the cell dies
peripheral tolerance- inactivation os self-reactive lymphocytes that escape central tolerance- regulatory T cells

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12
Q

What is the difference between MHC and HLA?

A

HLA is specific to humans whereas MHC is the name across all species

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13
Q

What type of HLA do all nucleated cell express?

A

class 1: HLA-A; HLA-B;HLA-C

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14
Q

What HLA do specialised APCs also present on their surface?

A

Class 2 MHC

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15
Q

How many variants of each HLA molecule does each individual possess?

A

2

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16
Q

What are the HLA types in class 2?

A

HLA-DP; DLA-DQ; HLA-DR

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17
Q

Why do individual HLA molecules exhibit significant diversity?

A

to maximise the net ability to bind peptides- on a population level, to maximise ability to respond to antigens and disease

18
Q

Why do some HLA molecules protect aginast autoimmune diesase whilst some predispose?

A

some alleles are very able to present self antigen whilst others arent good at it

19
Q

What suggests that there a hormonal infleucne of lymphocytes function?

A

there is an lateration in the course of autoimmune diseases during pregnancy

20
Q

What is molecular mimicry?

A

an antigen from a particular pathogen shares features with self-antigen

21
Q

What is an example of molecular mimicry?

A

acute rheumatic fever after streptococcal infection as strep M5 protein is similar to cardiac tissue proteins

22
Q

What are the potential mechanisms for autoimmune disease?

A

molecular mimicry; unrealted bystander activation; super-antigens; antigen sequestration

23
Q

What is bystander activation?

A

the stimulation of unrelated (heterologous) T cells by cytokines during an Ag-specific T-cell response

24
Q

What is antigen sequestration?

A

when the immune systerm has never seen parts of the body so if during an infection the body sees self-antigens for the first time and it reacts to it

25
Q

What is a superantigen?

A

antigens whic hnon-speciically activate a whole range of T cells and B cells outwith the MHC binding site and fully activate the cell

26
Q

What is hypersensitivity reactions?

A

an immune response that results in bystander damage to the self and whic his usually an exaggeration of noral immune mechanismS

27
Q

What is the hypersenstivity driving SLE?

A

type 3 HS disease

28
Q

What is hypersensitivity driving RA?

A

type 4

29
Q

What type of antibodies are implicated in immune complex mediated reactions?

A

IgG or IgM

30
Q

What happens during type 3 hypersensitivity?

A

system fails to clear the immune complexes whic hthen get trapedf in blood vessels and induce inflammation

31
Q

Who gets SLE

A

females; second and thrid decades

32
Q

What induces the formation of apoptotic bodies>

A

UV radiation; infection (reactive oxygen species production)

33
Q

What happens to the apoptotic bodies in SLE?

A

altered clearance/ increased apoptosis- mutations in complemetn or macrophages

34
Q

What induces production of auto-antibodies in SLE?

A

apoptotic bodies and not removed and they degrade releasing otential auto-antigens whic hcauses the production of AA and immune complex formation

35
Q

What is the SOAP-BRAIN MD mnemonic for the symptoms of SLE?

A

Serositis- pleurisy; pericarditis
Oral ulcers (oral or nasopharyngeal)
Arthritis
Photosensitivity

Blood disorders ( leukopenia; thrombocytopenia; haemolytic anaemia)
Renal involvment- urinalysis(proteinuria or red cell casts)
Antinuclear antibodies
Immunologic phenomena ( dsDNA; Sm; antiphopholipid antibodies)
Neurologic disorder- depression; psychosis; seizures

Malar rash
Discoid rash- erythematous raised rimmed lesions with keratotic scaling, often scarring

36
Q

What is RA characterised by?

A

destruction of joint cartilage and infalmmationg of the synovium

37
Q

What are the initial manifestations of RA?

A

stiffness; pain; swelling; erythema

38
Q

What cytokines have critial roles in the pathogenesis of RA?

A

TNF-alpha and IL-1 and IL6

39
Q

What do TNF-alpha; IL1 and IL6 do in RA?

A

stimulate fibroblasts; osteoclasts and chondrocytes; stimulate release of matric metalloproteinases

40
Q

What is RF?

A

an AA directed against the common Tc region of human IgG

41
Q

What does ACPA stand for?

A

anti-citrullinated peptide antibodies

MSK (39 decks)

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