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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

24
Q

HLA-B is which MHC class

25
MHC class 1/HLA-B is expressed in which cells
All nucleated cells
26
MHC class 2/HLA-DR is expressed in which cells
AP cells (B cells, macrophages, dendritic cells)
27
How does an autoimmune disease tend to occur?
you get a self antigen binding to the HLA/ MHC molecule and it can trigger an immune reaction/ disease  ’arthritogenic antigen’
28
Pathogenesis of ankylosing spondylitis?
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
Why does ankylosing spondylitis not spread everywhere
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
effective treatments for Ankylosing Spondylitis?
IL23 TH17 antibodies
31
Which antibody is SPECIFIC for SLE?
Anti-DS DNA antibodies
32
ANTINUCLEAR ANTIBODIES react to ....
antigens that are within the nucleus
33
If ANA is positive, what happens?
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
SLE patients commonly have X COMPLEMENT LEVELS and Y SERUM ANTI-DS-DNA ANTIBODIES
Low high
35
Pathogenesis of SLE?
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
Dominant cytokine in rheumatology
TNF-alpha
37
TNF alpha is secreted by X and its effect is:
mainly macrophages activates T cells, fever, proinflammatory
38
IL1 is secreted by X and its effect is:
mainly macrophages activates T cells, fever, proinflammatory
39
IL2 is secreted by X and its effect is:
T cells Activates T and B cells
40
IL6 is secreted by X and its effect is:
T cells Activates B cells, acute phase response
41
IFN-gamma is secreted by X and its effect is:
T cells activates macrophages
42
Key treatment for rheumatic diseases?
Anti-TNFalpha antibodies
43
Effects of TNFalpha on an activated macrophage? (9)
``` PGE2 production Hepcidin induction - acute phase response Pro-inflammatory cytokine release Chemokine release Endothelial cell activation Leukocyte accumulation Angiogenesis Chondrocyte activation Osteoclast activation ```
44
What receptor is important in bone distribution of rheumatoid arthritis?
RANKL (receptor activator of nuclear factor kB ligand) is important in bone distribution in rheumatoid arthritis
45
RANKL is Produced by what cells in RA
by T cells and synovial fibroblasts
46
What up regulates RANKL (4)
 IL-1, TNF-alpha  IL-17 – potent action on osteoclastogenesis via RANKL-RANK pathway  PTH-related peptide
47
What antagonises RANKL
decoy receptor (OPG)
48
Main effect of RANKL
decoy receptor (OPG)
49
monoclonal ab against RANKL?
- DENOSUMAB
50
B CELL HYPERACTIVITY IS A KEY FEATURE OF X
SLE
51
What do biological therapies for SLE target
B cells
52
2 examples of B cell targeting biologic therapies
RITUXIMAB | BELIMUMAB
53
What are prostaglandins
Lipid mediators of inflammation that act on platelets, endothelium, uterine tissue and mast cells
54
What pathway produces PG's
COX
55
Sue of NSAIDs in RA?
• 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
What enzyme do glucocorticoids inhibit
Phospholipase A2

Musculoskeletal Y2 (11 decks)

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