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III > WK 10- IMMUNOPATHOLOGY- AUTOIMMUNITY > Flashcards

WK 10- IMMUNOPATHOLOGY- AUTOIMMUNITY Flashcards

1
Q

What is a systemic autoimmune disease

A

Disease attacks connective tissues, and blood vessels due to it targeting DNA/collagen

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2
Q

What types of hypersensitivity are involved in pathology

A

types 2-4, type 1 is typically a general allergy

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3
Q

What triggers autoimmunity

A
  • Certain medications/drugs
  • Trauma
  • Molecular Mimicry
  • Genetics
  • Infection
  • Excessive immune complexes
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4
Q

What is autoimmunity

A

sustained reaction to self T-cells and production of autoantibodies

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5
Q

Why is suppression of reactive lymphocytes and tolerance important in preventing autoimmune disease

A

Strongly reactive lymphocytes are normally suppressed preventing autoimmunity- through central and peripheral tolerance- in autoimmune disease tolerance is broken and highly self-reactive lymphocytes can enter circulation and attack self antigens

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6
Q

What is central tolerance

A

eliminate strongly autoreactive lymphocytes before they reach circulation and also delete weakly reactive cells

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7
Q

What is peripheral tolerance

A

Deletes cells that have made it into the peripheral lymphoid organs that show self-reactivity; done through anergy, suppressing treg cells, deletion due to activation induced cell death, anergy

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8
Q

What is regulatory tolerance

A

Is tolerance induced by regulatory T cells- suppresses self-reactive lymphocytes

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9
Q

How do Treg cells develop

A

Develop in the thymus in response to weak stimulation by self antigens that is not sufficient to cause deletion but is more than required for positive selection

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10
Q

What are the 2 types of Treg cells and what is their function

A

Natural T cells and Induced T cells

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11
Q

What is molecular mimicry- give an example of a disease in which this occurs

A

Occurs when there is a shared similarity between the pathogen and a host cell (ie. have the same epitope)-> due to their molecular similarity the immune system views the host cell also as a foreign target
Eg. RHD
-Group A Strep (GAS) in rheumatoid arthritis mimics the structure of epitopes on connective tissue and on the heart- leads to Ab attacking the heart leading to RHD

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12
Q

What is epitope spreading

A
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13
Q

What is the role of MHC in autoimmune disease

A

Certain MHC have binding clefts specific to autoantigens-> predisposing them to developing an immune response against these Ag- Most common MHC affected is MHC2- this allows for autoimmune disease to run in families as MHC molecules are inherited

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14
Q

What are the 3 major pathogenic mechanisms that lead to autoimmune disease

A
  1. Exposure of hidden (cryptic) epitope
  2. Exposure to infectious agents
  3. Molecular Mimicry
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15
Q

How does exposure of cryptic (hidden) antigens occur and stimulate immune disease

A

Antigens that are in immune privileged sites/or hidden are viewed as foreign and attacked by the immune system-> these antigens can be exposed through;

1) cell walls becoming damaged and leaking intercellular contents/Ag
2) When large immune complexes are formed, new epitopes on the Fc portion of the Ab may be exposed and viewed as foreign-> this created an Ab against a host Ab (rheumatiod factor)
3) If a cell is damaged at the same time as an infection the immune complex picking up/removing the pathogen can also pick up contents of the damaged cell (ie Ag) and present them alongside the pathogen Ag

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16
Q

What 2 diseases are caused by autoAb attacking host cells

A
  1. Autoimmune haemolytic anemia- Anti-erythrocyte Ab bind to erythrocytes and cause intravascular haemolysis (through complement activation), the Ab also tag the erythrocyte for destruction in the spleen (extravascular haemolysis)
  2. Grave’s disease- Ab attack TSH and cause production of thyroid hormone-> the thyroid will act to downregulate TSH but is unable to suppress the exogenous thyroid hormone-> leads to hyperthyroidism
17
Q

What is the pathogenesis of rheumatoid arthritis

A

Modifications of autoantigens of things like fibrin due to things causing citrullination- causes the autoantigen to be viewed as foreign and stimulate APC -> APC will bind Ag and present it to T cells in the lymph node (T cells will be activated and then activate B cells)-> the immune cells will home to the site of the autoAg-> causes infiltration of macrophages (secreting inflammatory cytokines) and fibroblasts ( producing PAMP (causes tissue degredation) and RANK (causes destruction of osteoclasts and upregulation of osteoblasts (causing bone destruction))-> the B cells will also secrete Ab (these will attack the Fc portion of IgG (create rheumatoid factor) and also attack citrulline (Anti-CCP Ab)

18
Q

What are the symptoms of Rheumatoid arthritis

A

Fatigue, anemia, malaise, symmetrical arthritis, cartilage/bone destruction, inflammation, weakness, stiffness in joints, pain

19
Q

What are the major inflamm cells present in RA

A

T cells (majorly), B cells (antibodies), neutrophils, macrophages, fibroblasts

20
Q

What markers in blood would indicate a possible RA diagnosis

-What symptoms are necessary for diagnosis

A
  • Raised ESR, CRP, RF and ACPA

- Weakness, fatigue, bilateral symmetric arthritis, stiffness in joints (occurring within one hour of waking up)

21
Q

What treatments are mainly used in RA

A

Aim is to put patient in remission and suppress disease activity and prevent further destruction
-Methotrexate, Cyclosporine, Ab blockers, TNF-inhibitors (TNF is released from macrophages as an inflamm mediator)

22
Q

What is the pathogenesis of T1D autoimmune

A

Destruction of beta cells due to triggering of T cells by a peptide being released by the beta cell–> causes infiltration of CTL into the cell-> cause destruction by release of perforin and triggering the Fas/FasL pathway to cause apoptosis

23
Q

What is the pathogenesis of multiple sclerosis

A
  1. Naive CD4T cell is activated by an unknown trigger-> 2. Will cross the BBB and encounter Ag on myelin base protein-> 3. Ag is processed and presented by microglial cell -> 4. These cells will secrete cytokines that will causes chemotaxis of more T cells-> 5. will causes infiltration of lymphocytes, plasma cells and macrophages into nervous tissue-> 6. leads to further destruction of myelin sheath and axons
24
Q

What is the pathogenesis of SLE (what does SLE stand for)

A

-System Lupus Erythematosus
Pathogenesis:
1. When the cell undergoes apoptosis cellular contents will be displayed- including nuclear fragments
2. Formation of Ab against nuclear particles (anti-nuclear Ab) will form an immune complex with nuclear Ag
3. These immune complexes attract complement and deposit in the basement membranes/blood vessels (making it a systemic disease) and causing widespread inflammation
4. Ab complex can also attack: RBC (haemolytic anemia), thrombocytes (thrombocytopaenia), ganglion/neurons (CNS defects), glomerulus (glomerulonephritis)
5. Pt who have lupus also are unable to efficiently remove immune complexes meaning that there is a continual build up and progression of inflammation and also a decrease in complement levels

25
Q

What are the theories surrounding the cause of lupus

A
  1. breakdown of neg selection-> creating autoreactive T cells
  2. T cells have defects in their Fas:FasL pathway and can avoid apoptosis
  3. May be linked to some MHC haplotypes
26
Q

What are the symptoms of SLE

A
  • malar rash due to attack of blood vessels (butterfly rash)
  • photosensitivity
  • ulcers (due to attack of mucosa)
  • arthritis (due to attack of joints)- joint deformity
  • renal features (due to attack of basement membrane in kidneys)-> proteinuria, cellular casts, glomerulonephritis
  • neurological features (due to attack of CNS)-> seizures, psychosis
  • haematological features (due to attack of wbc/rbc)-> anaemia, leucopenia, low platelet
27
Q

How is a diagnosis of SLE made

A
  • low complement
  • high presence of anti-nuclear Ab, anti-ribonucleoprotein Ab, ENA (extracted nuclear antigen-allows you to see what Ab are binding to nucleus)
28
Q

What is the pathogenesis of rheumatic heart disease

A
  1. begins as exposure to group A strep that then causes a strep infection (sore throat, infected sore)
  2. 2-3 weeks later, molecular mimicry (resulting from cross reaction to due M protein having similar structure to Ag ) causes rheumatic fever (immune system attacking self Ag)-> polyarthritis (due to attack of Ag in joints), sydenhams chorea (due to attack of Ag on myelin), erythema marginatum (due to Ab attacking Ag on bv), carditis (due to Ab attacking Ag on heart valves)
  3. Constant attacks of RF will lead to chronic inflammation and eventual scar formation of the heart valves-> scar formation causes thickening and can lead to regurgitation and stenosis that can lead to heart failure -> Rheumatic Heart Disease
29
Q

How can RHD be prevented

A

By providing prophylactic penicillin at the beginning of the strep infection you prevent progression into Rheumatic fever and prevent recurrent RF attacks and development of RHD

30
Q

How can molecular mimicry occur in RHD

A

The Ab to cell wall M protein of Group A streptococcus (GAS) may cross react with cardiac myosin

31
Q

How do helminths aid in the treatment of IBD

A

Helminths evade immune destruction through slightly immunosupressing the host, and also act to heal the mucosa where the worm has latched through stimulating macrophages to secrete healing cytokines like TGF-beta

32
Q

How does IBD occur- what cells are involved and what balance is shifted

A
  • healthy person is able to develop Th2/Th17 cells but the Treg cells are able to outweigh their responses and control the inflamm response
  • in an atopic/autoimmune person→ more -Th2/Th17 and less Treg→ meaning the immune response can not be down regulated or controlled

III (13 decks)

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