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Musculoskeletal Y2 > Pathogenesis of Autoimmune Disease > Flashcards

Pathogenesis of Autoimmune Disease Flashcards

1
Q

Rheumatoid arthritis is basically….

A
  • Chronic joint inflammation that can result in joint damage§
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2
Q

Rheumatoid arthritis site of inflammation?

A
  • Site of inflammation is the synovium (synovitis)
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3
Q

What 2 auto-antibodies are associated with RA?

A

 Rheumatoid factor

 Anti-cyclic citrullinated peptide (CCP) antibodies

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4
Q

What is ANKYLOSING SPONDYLITIS

A
  • Chronic spinal inflammation that can result in spinal fusion and deformity
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5
Q

Site of inflammation in ANKYLOSING SPONDYLITIS?

A

enthesis (where a ligament or tendon joins onto bone) (enthesitis results in calcium deposition and bony fusion)

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6
Q

What antibodies are associated with ANKYLOSING SPONDYLITIS?

A

No autoantibodies (‘seronegative’)

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7
Q

What is SYSTEMIC LUPUS ERYTHEMATOSUS (SLE):

A
  • Chronic tissue inflammation in the presence of antibodies directed against self-antigens
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8
Q

Site of inflammation in SYSTEMIC LUPUS ERYTHEMATOSUS (SLE):

A
  • Multi-site inflammation but particularly the joint, skin and kidney
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9
Q

What antibodies are associated with SYSTEMIC LUPUS ERYTHEMATOSUS (SLE): (2)

A

 Antinuclear antibodies

 Anti-double stranded DNA antibodies

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10
Q

Spondylitis=

A

inflammation of the spine

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11
Q

Describe the pathogenesis of lupus

A
  • Immune complexes (antibody-antigen complexes) can trigger inflammation by interacting with antibody Fc receptors and activating complement.
  • The immune complexes activate complement via the classical pathway leading to inflammation.
  • [Inflammatory cells/ antibodies (such as neutrophils, monocytes, macrophages) have Fc receptors so if you mobilise the autoantibodies onto these immune cells this can trigger inflammation].
  • The formation of immune complexes doesn’t immediately indicate that one particular part of the body is inflamed - as a result, you see very widespread inflammation
  • In lupus, there are excess immune complexes that will have a widespread distribution into tissues and so you get widespread organ inflammation though there are patterns e.g. skin and kidney disease are common in lupus.
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12
Q

where is lupus commonly found (3)

A

joint, skin, kidney

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13
Q

what family of diseases is Lupus a part of

A

CONNECTIVE TISSUE DISEASES.

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14
Q

Examples of CONNECTIVE TISSUE DISEASES (3)

A

Lupus
• Sjogren’s Syndrome
Overlap Syndrome

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15
Q

Sjogren’s Syndrome has autobodies attacking what

A

exocrine glands

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16
Q

Which MHC serotype is RA associated with

A

HLA-DR4

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17
Q

Which MHC serotype is SLE associated with

A

HLA-DR3

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18
Q

Which MHC serotype is ankylosing spondylitis associated with

A

HLA-B27

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19
Q

HLA-DR4 is associated with what disease

A

RA

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20
Q

HLA-DR3 is associated with what disease

A

SLE

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21
Q

HLA-B27 is associated with what disease

A

ankylosing spondylitis

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22
Q

What do MHC regions of genes code for

A

cell surface proteins

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23
Q

HLA-DR is which MHC class

A

II

24
Q

HLA-B is which MHC class

A

I

25
Q

MHC class 1/HLA-B is expressed in which cells

A

All nucleated cells

26
Q

MHC class 2/HLA-DR is expressed in which cells

A

AP cells (B cells, macrophages, dendritic cells)

27
Q

How does an autoimmune disease tend to occur?

A

you get a self antigen binding to the HLA/ MHC molecule and it can trigger an immune reaction/ disease  ’arthritogenic antigen’

28
Q

Pathogenesis of ankylosing spondylitis?

A

HLA-B27 has a propensity to MISFOLD, which causes cellular stress that triggers IL-23 release and triggers IL-17 production by:
o Adaptive immune cells e.g. CD4+ cells, Th17 cells
o Innate immune cells e.g. CD4- + CD8- (double negative) T cells

29
Q

Why does ankylosing spondylitis not spread everywhere

A

o The cellular stress is more likely to occur in innate immune cells
o These innate cells are present in the entheses and this may explain why enthesopathy occurs in ankylosing spondylitis

30
Q

effective treatments for Ankylosing Spondylitis?

A

IL23 TH17 antibodies

31
Q

Which antibody is SPECIFIC for SLE?

A

Anti-DS DNA antibodies

32
Q

ANTINUCLEAR ANTIBODIES react to ….

A

antigens that are within the nucleus

33
Q

If ANA is positive, what happens?

A

the clinical laboratory will perform further tests to determine which type of ANA it is – typically these include screening for:

  • Anti-Ro
  • Anti-La
  • Anti-centromere
  • Anti-Sm
  • Anti-RNP
  • Anti-ds-DNA antibodies
  • Anti-Scl-70
34
Q

SLE patients commonly have X COMPLEMENT LEVELS and Y SERUM ANTI-DS-DNA ANTIBODIES

A

Low

high

35
Q

Pathogenesis of SLE?

A
  1. Apoptosis leads to translocation of nuclear antigens to membrane surface
  2. Impaired clearance of apoptotic cells results in enhanced presentation of nuclear antigens to immune cells
  3. B cell autoimmunity
  4. Tissue damage by antibody effect mechanisms e.g. complement activation and Fc receptor engagement
36
Q

Dominant cytokine in rheumatology

A

TNF-alpha

37
Q

TNF alpha is secreted by X and its effect is:

A

mainly macrophages

activates T cells, fever, proinflammatory

38
Q

IL1 is secreted by X and its effect is:

A

mainly macrophages

activates T cells, fever, proinflammatory

39
Q

IL2 is secreted by X and its effect is:

A

T cells

Activates T and B cells

40
Q

IL6 is secreted by X and its effect is:

A

T cells

Activates B cells, acute phase response

41
Q

IFN-gamma is secreted by X and its effect is:

A

T cells

activates macrophages

42
Q

Key treatment for rheumatic diseases?

A

Anti-TNFalpha antibodies

43
Q

Effects of TNFalpha on an activated macrophage? (9)

A 
PGE2 production
Hepcidin induction - acute phase response
Pro-inflammatory cytokine release
Chemokine release
Endothelial cell activation
Leukocyte accumulation
Angiogenesis
Chondrocyte activation
Osteoclast activation
44
Q

What receptor is important in bone distribution of rheumatoid arthritis?

A

RANKL (receptor activator of nuclear factor kB ligand) is important in bone distribution in rheumatoid arthritis

45
Q

RANKL is Produced by what cells in RA

A

by T cells and synovial fibroblasts

46
Q

What up regulates RANKL (4)

A

 IL-1, TNF-alpha
 IL-17 – potent action on osteoclastogenesis via RANKL-RANK pathway
 PTH-related peptide

47
Q

What antagonises RANKL

A

decoy receptor (OPG)

48
Q

Main effect of RANKL

A

decoy receptor (OPG)

49
Q

monoclonal ab against RANKL?

A
  • DENOSUMAB
50
Q

B CELL HYPERACTIVITY IS A KEY FEATURE OF X

A

SLE

51
Q

What do biological therapies for SLE target

A

B cells

52
Q

2 examples of B cell targeting biologic therapies

A

RITUXIMAB

BELIMUMAB

53
Q

What are prostaglandins

A

Lipid mediators of inflammation that act on platelets, endothelium, uterine tissue and mast cells

54
Q

What pathway produces PG’s

A

COX

55
Q

Sue of NSAIDs in RA?

A

• Rheumatoid arthritis is a chronic, painful disease and NSAIDs switch off inflammation to a certain degree but they are more important in dealing with pain

56
Q

What enzyme do glucocorticoids inhibit

A

Phospholipase A2

Musculoskeletal Y2 (11 decks)

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