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Locomotor 2 > Immunology of Joint Conditions RA > Flashcards

Immunology of Joint Conditions RA Flashcards

1
Q

what are the natural barriers to prevent infection

A
  • Mechanical
  • chemical
  • microbiological
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2
Q

what are the two types of immune system

A
  • Innate immune system

- adaptive immune system

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3
Q

How does innate immune system recognises patterns

A

common molecular

patterns (PAMPs) by conserved receptors

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4
Q

How does the adaptive immune cells recognise pathogens

A
  • they have antibodies that are produced by B cells

- T. cells have TCR that have foreign antigens that are presented to them by dendritic cells

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5
Q

describe how the variable region on an antbody is made

A
  • random gene recombination

- have Variable (V) Diversity (D) and Joining (J) genes that are randomly placed on the variable region

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6
Q

How is the autoimmunity and cells against are own antigens inhibited from being made

A

by central tolerance and peripheral tolerance

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7
Q

Describe central tolerance

A
  • pro apoptotic and signalling molecules that inhibit it if they are strongly self reactive
  • non or weakly self reactive get through and they are combated by peripheral tolerance
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8
Q

Describe how peripheral tolerance works

A

Growth limiting mechanisms

  • lack of a second degree signal
  • inhibitory signalling
  • Treg cells

Growth overing

  • pro apoptotic signals
  • T reg cells
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9
Q

name some lipid mediators and what they do

A

leukotrienes, PAF and PG

  • increase vascular permeability
  • smooth muscle contraction
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10
Q

name some chemokine and what they do

A
  • IL-8, MCP-1, Fractalkine

- attract and activate phagocytic cells, vascular endothelial cells

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11
Q

name some complements and what they do

A
  • C2a, C3a, C5a

- attract/activate immune cells, vascular permeabiity

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12
Q

what is inflammation critical for

A

1- Inflammation is a critical physiological response that facilitates immunity and tissue repair

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13
Q

What happens when inflammation doesn’t switch of

A

Chronic inflammation results and Chronic inflammation causes pathology: tissue damage in autoimmune diseases and cancer.

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14
Q

name types of chronic inflammatory joint conditions

A

Rheumatoid arthritis

Psoriatic arthritis

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15
Q

What is a Pannus

A
  • hyper proliferation of a synovial membrane
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16
Q

what is RA strongly associated with

A

MHC genes

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17
Q

describe how chronic inflammation happens

A

1- A “trigger(s)” initiates immunity and acute inflammation. These then mediates responses to local self proteins.

2- This starts chronic inflammation by cytokines and other pro-inflammatory mediators.

3- This process persists and protease enzyme are produced that destroy the joint

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18
Q

Why does the immune system attack joints in patients with joint conditions?

A

defects in “immunological tolerance”, failure of regulation, or cross reactivity with “pathogens” could mediate autoimmunity

19
Q

What is central to T cell response and regulation

A

MHC

- determines which peptides are presented to T lymphocytes

20
Q

what does MHC determine

A

Determines T lymphocyte tolerance in the thymus, i.e. what mature T cells we have in the body.

Also determine if and how mature T lymphocytes respond to antigens upon encounter.

21
Q

what can defects in T cell tolerance cause

A

Joint disease

- reducing the strength by which T lymphocyte recognition antigens causes joint disease in mice

22
Q

what cells cause autoimmunity

A
  • CD4+ TH1 cells - lead to IFN gamma and TNF alpha which cause autoimmunity
23
Q

what causes the production of TH1 cells

A
  • IL-12

- IL-23

24
Q

what causes the production of TH2 cells

A
  • IL-4
25
Q

what causes the production of TH17

A

IL-6/IL-21

26
Q

What causes the production of T reg cells

A

TGF beta

27
Q

what do TH2 cells produce

A

IL-5
IL-4
IL-13

  • these case IgE production allergy
28
Q

what do TH17 cells produce

A

IL-17
IL-22
- cause chronic inflammation

29
Q

what do CD4+ T reg cells produce

A
  • TGF beta and IL10
  • IL-10 causes cancer
  • TGF beta - decreases inflammation autoimmunity
30
Q

what three factors predispose individuals to joint diseases

A

1- Genetics

2- Environmental

3- Hormones

31
Q

Describe how genetics can cause joint conditions

A
  • Familial segregation of JDs.

- Higher concordance of JDs in identical than non-identical twins

32
Q

describe hormones and joint conditions related

A
  • females are more susceptible to joint conditions
33
Q

what makes up 50% of susceptibility factors in rheumatoid arthritis

A

genetics

34
Q

What are the environmental factors that contribute to joint conditions

A

Exposure to tobacco (smoking)

Exposure to occupational dust (silica)

Air pollution

High sodium, red meat and iron consumption

Obesity

Low vitamin D intake and levels

35
Q

what is the most common joint condition

A

Rheumatoid arthritis

36
Q

describe Rheumatoid arthritis symptoms

A

mmetrical joints are affected.

Small peripheral joints become inflamed.

Develop morning joint stiffness
of variable durations.

Develop diffuse aching.

Fatigue, malaise and depression may precede other symptomsby weeks or months.

37
Q

What are the symptoms of RA

A

pain in the small joints of the hands and feet, together with symmetric swelling, is the first symptom noticed by patients with RA.

38
Q

what are the antibodies that RA is related to

A

IgG (rheumatoid factors)

citrullinated peptides

39
Q

What T cell response is RA related to

A 
- Strong association with
HLA-DR4. Target self antigen:
Unknown. Possible:
- Collagen type II (?)
 - Heat shock protein 60 (?)
40
Q

describe the joint damage in RA at early, intermediate and late stage

A

Early stage
- Soft tissue swelling

Intermediate stage

  • Mild juxta-articularosteoporosis
  • Narrowing of joint spaceand bone erosions

Late stage
- Large erosions, anatomic deformities

41
Q

How long does RA take to progress

A
  • speed of symptoms is different in patients
  • takes months to years to get initial clinical signs then a short time to joint damage and then months and years to late stage disease
42
Q

what is the molecule that mediates the pathology in RA joints

A

excess TNF alpha

43
Q

what has blockage of TNF alpha lead to

A
  • leads to reduced production of IL-1, IL-8, GM-CSF etc.
44
Q

what can be used to treat TNF alpha

A

an antibody against TNF alpha

- Anti-TNF alpha

Locomotor 2 (30 decks)

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