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Infection Science and Clinical Immunology > Autoimmunity > Flashcards

Autoimmunity Flashcards

1
Q

How common is Multiple sclerosis?

A

Relatively common - 1/2000 in Caucasians

Ratio of 3:1 Women to men

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2
Q

What age group are susceptible to Mulitple sclerosis?

A

Age 20-40

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3
Q

What is Multiple sclerosis?

A

Autoimmune condition in which myelin is attakced but only in the CNS

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4
Q

What are the symptoms and signs of Multiple Sclerosis?

A
  • Relasping and remitting disturbances of sensory and motor function
  • Abnormal fatigue and depression
  • Neurologic deficits
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5
Q

What are the CNS Myelin sheath made of?

A

Oligodendrocytes

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6
Q

What are the PNS Myelin sheath made of?

A

Schwann cells

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7
Q

What is a method to check for multiple Sclerosis?

A
  • MRI
  • Neurlogical tests (e.g testing speed of responses in the CNS)
  • Lumbar puncture (testing antibodies in cerebrospinal fluid)
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8
Q

What does Multiple Sclerosis mean?

A

Multiple - multiple body sites and multiple episodes of symptoms
Sclerosis – stiffening of tissue

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9
Q

What is CIS?

A

Clinically isolated syndromes

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10
Q

What does Clincially Isolated syndrome used for?

A

Describing first episode of neurological symptoms that last for at least 24 hours and not caused by anything else (e.g fever or infection)

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11
Q

What is RRMS?

A

Relapsing Remitting Multiple Sclerosis?

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12
Q

What is the Relapsing Remitting Multiple Sclerosis (RRMS) used for?

A

A type of MS that occurs when flare-ups (relapses) of symptoms followed by periods of partial or complete recovery (remission)

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13
Q

What is SPMS?

A

Secondary Progressive Mulitple Sclerosis

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14
Q

What is the term Secondary Progressive Multiple Sclerosis used for?

A

A stage of Mulitple Scerlosis which comes up after relasping remitting Mulitple Sclerosis

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15
Q

What happens to brain volume as over time as it goes through from CIS to RRMS and end on SPMS?

A

Brain volume decreases

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16
Q

What happens to the patient as brain volume decrease?

A

Over time they go from the clincial threshold to disability

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17
Q

Why does remyelination cause MS remission?

A

Myelin is thinner, over time it becomes ineffective

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18
Q

What is linked to causing MS?

A

DRB1 locus of MHC Class II

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19
Q

How is MS caused by autoimmunity?

A

When pathogenic Th17 and Th1 type and Cd8 myelin autoreactive T cells are induced

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20
Q

How is B cells important in MS?

A

In relapsing MS - B Cells act as primary APC driving pathogenic T cells

In progressive MS - B cells enhance the compartmentalised CNS responses through lymphoid follicles and secreted factors

21
Q

How does immune pathogensis have a role in MS?

A

1) Autoreactive CD4+ T Cells are activated
2) CD4+ T cells migrate into the brain and secrete Th1/TH17 type cytokines
3) Local activation by antigen
4) Recruitment of macrophages/CD8+ T cells/B cells

22
Q

What may also cause MS?

A
  • Environmental factors (e.g smoking, obesity)
  • Distance from the equator
  • Priro infection (e.g EBV)
23
Q

What happens froma EBV infection to cause MS?

A

1) Molecular mimicry of the EBV
2) B Cell transform to display LMP1 and LMP2A on its surface
3) CNS tropism - the infected B Cell lives in neural tissue

24
Q

How is MS treated?

A
  • IFN-beta (binds to type I IFN receptor)
  • Natalizumab (Targets CD49d)
  • Alemtuzumab (Targets CD52 on T and B cells)
25
What is the purpose of MS treatment?
- Deplete T or B cells (rituximab/alemtuzumab) - Prevent migration of lymphocytes to the CNS (FTY720)
26
What is Myasthenia Gravis?
Neurological autoimmune disease but antibody mediated - Affects the neuronal muscle junction
27
What is the immunological mechanisms to Myasthenia Gravis?
Antibodies (IgG1) specific for acetylcholine areceptor - Generates MAC
28
What does MG cause?
- Destruction of the membrane - Inability of acetl choline to bin d - Acetyl choline receptor internalisation by IgG cross-linking
29
What number of patients are antibodies for Muscle-specific kinase (MuSK)
10%
30
What does Muscle-Specific Kinase (MuSK) do?
Help Acetyl-choline receptors to cluster - Acetyl choline receptors cannot function in the post synaptic cleft without it
31
What are the diagnosis of MG?
- If breakdown of Ach is inhibited with Edrophonium (an acetyl cholinesterase inhibitor), temporary restoration of muscle function will be seen in MG patients - Circulating antibodies specific for AchR/MuSK - Determining muscle activity using an EMG - CT/MRI of thymus often reveals enlargement
32
What are the signs of MG?
Muscle weakness results in dropping eyelids
33
What makes someone more suspectible to MG
Gender - Often women than men Age - peak in the 20s (women), peak in the 60s (men)
34
What genetics would a MG individual have?
HLA-DRB and HLA-B, TNFRSF11A (RANK) THymic abnormality by having too many/dysregulated T cells
35
What immune treatments are avaliable for Myasthenia Gravis?
- Complement inhibition - B cell depletion - Thymectomy - FcRn inhibitors to reduce levels of antibodies
36
What % of adults does Theumatoid arthritis affect?
1-2%
37
What is Rheumatoid arthritis?
Autoimmun condition of th ejoints caused by immune complexes - Type III hypersensitivity
38
What do RA target?
Post translationally modified proteins (AMPA - Anti-modified protein antibodies) including citrullinated proteins (ACPA - Anti-citrulinated protein antibodies) - Proteins are expressed on osteoclasts And/or: Fc regions on IgM (Rheumatoid factor)
39
What plays as a factor to causing RA?
Gender - often in women than men (2:1) Genetics - HLA-DRB1 and other immune genes (PTPN22) Age - Often 40s or earlier
40
What are unnown external triggers that may cause RA?
- Oral (gum disease?) - Gut (microbial component?) - Lungs (smoking?) causes production of auto-reactive antibodies
41
What is Cytokines role in RAA?
Maintain inflammation alongside chronic antigen
42
What does Macrophages and neutrophiles do in RA?
Remain locally activated producing destructive enzymes
43
What do RANKL and cytokines cause in RA?
Cause macrophages to become osteoclasts and degrade bone
44
What are the cytokines that cause macrophages to become osteoclasts?
Th17, Th1
45
How are T cells and B cells involved in RA?
Rheumatoid synovium contain large number of plasma cells and densely inflitrated with activatd mature T cells (e.g CD4+)
46
What are symptoms of RA?
- Pain in joints - Flareups and fatigue - Low fever and inflammation
47
What can RA cause?
- Higher susceptibility to infection - Increased risk of heart disease - Reduced life expectancy
48
What are treatments for Rheumatoid Arthritis?
DMARDS (Disease-modifying anti-rheumatic drugs e.g methotrexate inhibiting nucleotide synthesis) Biologics (antibodies that target key cells/cytokines e.g infliximab)

Infection Science and Clinical Immunology (8 decks)

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