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autoimmune diseases Flashcards

1
Q

what does innate immunity comprise in AID?

A

inflammation in target tissues

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2
Q

what does adaptive immunity comprise in AID?

A

learned responses in immune organs

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3
Q

what are the characteristics of innate?

A 
fast response
short duration 
same thing every time
little regulation 
no memory 
pattern recognition against a broad class of antigen 
no amplification 
no learning
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4
Q

what cells does the innate use?

A

macrophages and mast cells, dendritic cells, complement and neutrophils

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5
Q

what are the characteristics of adaptive?

A 
slow response 
highly specific 
long duration 
learning and amplification component 
memory 
many regulatory mechanisms 
only vertebrates have it 
establishes tolerance
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6
Q

what cells are in the adaptive?

A

T and B cells

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7
Q

what is the interaction between innate and adaptive?

A

the innate cells such as neutrophils will recognise foreign antigens. Chemokines attract other immune cells. Dendritic cells will present to a specific T cell. Lymphoid tissue is for communication and memory. Bidirectional feedback system - adaptive can also contribute to inflammation

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8
Q

what is the function of cross talk?

A

between the T cells, DCs and B cells

for immune memory and specific learned responses

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9
Q

what do T cells and B cells activate?

A

cytokines from T cells activate monocytes and macrophages

antibodies from B cells activate the complement

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10
Q

what are the components of the innate immune system?

A

cytokines, chemokines, phagocytic, histamine producing, complement

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11
Q

what are phagocytic cells and what do they do?

A

macrophage: produce chemokines to attract other immune cells
neutrophils - eat and destroy foreign pathogens and coat in toxic chemical
DCs - present to adaptive immune cells

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12
Q

what are HPCs and what do they do?

A

eosinophils, basophils and mast cells
they produce histamine and other chemokines and cytokines
vasodilation and attracting other immune cells
defence against parasites, allergy and anaphylaxis

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13
Q

what does the complement do?

A

it sits in blood all the time and kills cells if sees antigen attached, they directly kill pathogens through the lectin and alternative pathways and may be activated by the adaptive immune system via ABs

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14
Q

what do cyto/chemokines do?

A

cyto - signal between different immune cells

chemo - attract other immune cells to site of inflammation

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15
Q

what is the role of T cells?

A

they cause inflammation through inflammatory cytokines and communication with B cells for ABs

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16
Q

what happens once a T cell is presented with an antigen from a DC?

A

activates Th1 - cytokine production

activates Th2 - to communicate with B cells - produce memory B cells and plasma cells producing ABs

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17
Q

what are autoantibodies?

A

they directly interfere with the physiological function rather than causing inflammation and damage

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18
Q

what is autoimmunity?

A

it is a learned recognition where the adaptive immune system recognises and targets the body’s own molecules cells and tissues instead of infectious agent and malignant cells

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19
Q

what are the main characteristics of autoimmunity?

A

T cells that recognise self antigens
B cells and plasma cells making autoantibodies
inflammation in the target cells - secondary to action of T, B and ABs

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20
Q

what is autoinflammation?

A

it is different to autoimmunity. Seemingly spontaneous attacks of systemic inflammation with no demonstrable source of infection as the precipitating cause. There is the absence of autoantibodies and antigen specific autoreactive T cells with no evidence of auto-antigenic exposure. The B and T cells are not involved - the innate immune system is overreactive without the control of adaptive

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21
Q

what is the main cellular involvement of autoinflammation and autoimmunity?

A

neutrophils and macrophages for autoinflammation

autoimmunity - B and T cells

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22
Q

what is the difference between autoimmunity and autoinflammation in presentation and genetic susceptibility?

A

Aimmunity-continuous progression of breaking of self tolerance, MHCII and adaptive response genes
Ainflamm- recurrent and unprovoked attacks of tissue specific factors and danger signs - cytokine and bacterial sensing pathways as genetics

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23
Q

what is the therapy for Aimmun and Ainflamm?

A

anti-cytokine for Ainflamm and anti T and B cell and Aimmune

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24
Q

what are examples of Ainflamm?

A

polygenic crohns, spondylarthropathies, monogenic hereditary periodic fevers

25
Q

what are examples of Aimmun?

A

monogenic ALPS and IPEX, polygenic RA and SLE

26
Q

what does Aimmunity lead to?

A

inflammation, organ dysfunction and damage

27
Q

what are the mechanisms for Autoimmunity?

A

antigenic factors, genetic predisposition and failure of central tolerance - alone each cannot cause

28
Q

what happens in central tolerance?

A

B cell selection in bone marrow and T in thymus, when they are made they are checked to make sure that they do not react to self antigens and if they do then they are deleted

29
Q

how does genetic predisposition influence autoimmunity?

A

certain HLA/MHC types select for certain self antigens - may make the immune system better at recognising certain antigens and therefore predisposed to a certain disease
other genes that regulate immune functions

30
Q

how do antigenic factors affect autoimmunity?

A

infections may trigger autoimmune response
environmental agents such as smoking
alterations in self proteins that increase that increase their immunogenicity

31
Q

where are T cells originally made?

A

bone marrow and then mature in the thymus

32
Q

what is the process of central tolerance?

A

there is an infinite variety of receptors through random rearrangement. The cells are checked in the thymus against self-antigens. If they recognise they are destroyed, if they only slightly recognise then they are made into regulatory cells and if they do not then they are positively selected for as effector CD4 and CD8 T cells - there is a similiar process in bone marrow for B cells

33
Q

what subtypes of MHC are there?

A

class I (all cells) and II (APCs)4

34
Q

where is an antigen on II presented to?

A

CD4 T cells (helper)

35
Q

why may MHC bind better to some antigens than others?

A

MHC variation is finite

36
Q

what mutations can result in severe autoimmunity from birth?

A

mutation in the FoxP3 gene - inability to produce regulatory T cells
mutation in PTPN22 - T cells are activated more easily so in general a stronger immune response

37
Q

which genes encode MHC class I and II?

A

I - HLA-A, B and C

II - HLA-DP, DQ and DR

38
Q

which cells do MHC I present to?

A

CD8 T cells (cytotoxic)

39
Q

what are some causative associations for autoimmunity?

A

sex - women more than men maybe due to hormonal influence - immunity in pregnancy and oestrogen
age - elderly more common
sequestered antigens
environmental triggers

40
Q

how can infection cause autoimmunity?

A

they activate the immune system in general - could be normal and autoimmune. In rheumatic fever there is molecular mimicry - the antibodies against M protein of streptococcus are also reactive against the glycoproteins of the heart and therefore there may need to be a valve replacement, inflammation and defects

41
Q

how can autoantigens trigger autoimmunity?

A

change in the amount or nature can cause autoimmunity

42
Q

what is the basis of a) SLE

b) coeliac disease
c) RA?

A

in SLE there is failure to clear apoptotic debris meaning that there is an increase in sequestered antigens inside the cell. Cell nuclei are not usually recognised by the immune system but if the cell has lysis then they are open to attack

b) tissue transgluatamase can alter gluten meaning it can bind to HLA-DQ
c) citrullination of proteins making them more immumogenic

43
Q

how can smoking cause AI?

A

some AA that are not meant to be encoded in the DNA can incorporate themselves or changed - e.g. arginine to citrulline

44
Q

what is organ specific AI?

A

it is when it affects a single organ. The autoimmunity is directed against autoantibodies of that organ only however it can overlap with other organ specific diseases - autoimmune thyroid disease is common

45
Q

what is systemic AI?

A

when it affects several organs simultaneously as antigens that aren’t restricted to one organ are targeted. Autoimmunity is directed against autoantigens found in most cells of the body. There is overlap with other non-organ specific diseases - connective tissue diseases are common.

46
Q

what are the clinical features of AID?

A 
common for diseases to overlap 
exacerbation and remission 
chronic life long condition 
loss of organ function 
can affect any organ
47
Q

what are the symptoms of hypothyroidism?

A 
weight gain 
change in bowel movements 
inability to maintain temperature 
decline in memory 
tiredness and difficulty concentrating
48
Q

what are the symptoms of hyperthyroidism?

A 
anxiety 
palpitations 
too hot 
weight loss
diarrhoea 
hard to sleep
49
Q

what is hashimotos thyroiditis?

A

destruction of the thyroid follicles by autoimmune process
autoantibodies directed against thyroglobulin and thyroid peroxidase
leads to hypothyroidism

50
Q

what is grave’s disease?

A

the auto-antibody anti-TSH stimulates TSH which stimulates the thyroid so there is inappropriate stimulation - leads to hyperthyroidism

51
Q

what is the basis of myasthenia gravis and what does this result in?

A

autoantibodies bind to the Ach receptor and do not stimulate or cause inflammation they just block - tiredness, weakness, difficult to speak, swallow or keep eyes open that is worse as day progresses

52
Q

what is the basis of pernicious anaemia and what does this cause?

A

autoantibody stops the processing of intrinsic factor meaning that B12 absorption is needed. Therefore RBC are very large, there is a lack of Hb so iron deficiency and cannot make B cells quickly - increasing fatigue

53
Q

what is the biochemical basis of SLE?

A

C3 and C4 are involved and cell nuclei are the main component

54
Q

what are the characteristics of SLE?

A

photosensitive malar rash, alopecia, joint pain (arthralgia), pleural effusions leading to sharp chest pain, and mouth ulcers on hard palate/roof of mouth

55
Q

how would you detect SLE?

A

human cells and serum from patient are added together and dye is added to see where the antibodies are stuck. They stick to many parts of cell nuclei including ssDNA dsDNA ribosomes histones in a positive homogenous pattern

56
Q

what is seen on the skin of patients with SLE and why does this result in AID?

A

on the dermo-epidermal interface there is classic AB deposition and inflammation. UV light damages this so the cells die and lysis occurs. Therefore autoantibodies are exposed to contents in cell nuclei.

57
Q

how can failure to clear apoptotic material result in AID?

A

usually self-antigens are intracellular - sequestered, meaning that they are sheltered from the immune system. When apoptosis occurs the material is cleared but when necrosis occurs it results in a lot of material in the circulation and the antigens may not be cleared - the antigens then trigger the immune system. Some people have genetic defects in clearance of material.

58
Q

what is the clinical result of lupus?

A

activation of the complement system so an accumulation of immune cells in the kidney - this results in loss of blood flow and perfusion so necrosis. There is also inflammation and a leaky glomerulus that results from this resulting in loss of renal function, scarring and irreversible damage.

59
Q

what are examples of connective tissue diseases?

A

SLE, scleroderma, polymyositis, sjogrens syndrome and ubiquitous antigens forming multisystem inflammation

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