WEEK TWO: Autoimmunity & Hypersensitivity (TAE) Slides 43 - 68 Flashcards

1
Q

Autoimmunity

A

when the body recognizes itself as foreign and attacks itself

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2
Q

Autoimmune diseases

A

self tolerance is lost and immune system reacts to self

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3
Q

Generally…what the immune system does when it goes right

A
  • T and B cells are programmed by the THYMUS to identify self as OK
  • Thymus is the organ that helps eliminate ‘self-reactive cells”
  • In autoimmune diseases this doesn’t happen right
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4
Q

Antigens vs antibodies

A
  • An antigen is a foreign substance that enters your body
  • An antibody is a protein produces by immune system
  • Autoantigens, or self-antigens, are made by body to fight own cells and are usually a sign of an illness such as an autoimmune condition
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5
Q

Specific antibodies (immunoglobulins)…what are they?

A
  • Antibodies are also called immunoglobuins or Ig.
  • They are Y-shaped proteins made by immune system’s B lymphocytes or B cells
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6
Q

B-cells and specific antibodies

A
  • B cells attack and eliminate viruses and other toxins outside the cell.
  • They do this by making specific antibodies for a single type of antigen
  • These tailored antibodies lock on to their specific antigens and tag them for attack.
  • Antibodies also block these antigens, keeping them away from healthy cells
  • Ultimately, antibodies kill these antigens, stopping infection
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7
Q

Specific antibodies (immunoglobulins): IgG

A

IgG. These are the most abundant types of antibodies in the plasma. They detoxify harmful substances and provide long-term protection. Small, versatile, short lasting.

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8
Q

Specific antibodies (immunoglobulins): IgM

A

These are the first antibodies made by B cells in response to antigens. Broad spectrum, large, stay in blood.

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9
Q

Specific antibodies (immunoglobulins): IgA

A

Antiviral specific against local infections. Seen in body secretions and other body fluids such as saliva, nasal, respiratory.

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10
Q

Specific antibodies (immunoglobulins): IgE

A

These antibodies trigger allergies and protect against parasites. Small amounts are in your skin, lungs, and mucosal membranes.

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11
Q

Specific antibodies (immunoglobulins): IgD

A
  • These antibodies bind to B cells and signal them to release IgM antibodies. - No specific functions.
  • Each antibody guards against its target antigen, and many types of antibodies are found throughout the body.
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12
Q

A theory of HOW autoimmune disease occur

A
  • Theory of mimicry → parts of our own cells look a lot like foreign cells
  • And/or the “bad” cells have adapted to look like “normal cell” and the immune system is confused
  • Shirley basically said not to study these theories too much.
  • Regardless of cause…autoimmune diseases injure body tissue through hypersensitivity reactions & chronic inflammation
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13
Q

Hypersensitivity - what it is and how many types

A
  • A normal immune response at the wrong time or excessive action
  • Immune reaction that causes inflammation and destruction of healthy tissue
  • 4 types
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14
Q

Hypersensitivity reactions with antibodies and/or cell mediators: Type I

A

IgE → mediated immediate reaciton. Allergen associated. May be mild or severe, 15 - 30 minutes after exposure

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15
Q

Hypersensitivity reactions: type II

A

Reaction to antigens on cells. 15 - 30 minutes. Antibody-mediated reaction (IgG or IgM antibodies)

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16
Q

Hypersensitivity reactions: Type III

A

Immune complex-mediated reaction-persistent inflammation and destruction (SLE)
- Can be chronic and damaging

17
Q

Hypersensitivity reaction: Type IV

A

Cytotoxic, cell mediated, delayed hypersensitivity reaction (T cells instead of antibodies)

18
Q

Hypersensitivity reactions: Immediate vs delayed

A
  • The 1st three types are considered immediate hypersensitivity reactions because they occur within 24 hours
  • The fourth type is considered a delayed hypersensitivity reaction because it usually occurs more than 12 hours after exposure to the allergen, with a maximal reaction time between 48 and 72 hours.
19
Q

IgE hypersensitivity physiology

A

IgE is bound to mast cells via its Fc portion. When an allergen binds to these antibodies, crosslinking of IgE induces degranulation. Destroys the cell.

20
Q

IgG mediated cytotoxic hypersensitivy: physology

A

Cells are destroyed by bound antibody, either by activation of compliment or by a cytotoxic T cell with an Fc receptor for the antibody (ADCC)

21
Q

Immune Complex mediated hypersensitivity: Physiology

A

Antigen-antibody complexes are deposited in tissues, causing activation of compiment, which attracks neutrophils to site. Causes more inflammation + damage. Seen in Lupus + Rheumatoid arthritis.

22
Q

Cell mediated hypersensitivity: physiology

A

Th1 cells secrete cytokines, which activate macrophages and cytotoxic T-Cells and can cause macrophage accumulation at site.

23
Q

Systemic lupus Erythematosus

A
  • Chronic, autoimmune, multi-system, inflammatory disease
  • With unpredictable exacerbations and remissions
  • Not a rare disease
  • Effects mostly women in childbearing years - who then get older
  • Especially effects non-caucasians
24
Q

Etilogy of Lupus

A
  • Unknown exactly
  • Possible triggers → Genetics, gender (hormones), UV light, chemicals, infectious agents and STRESS
25
Q

Pathophysiology of Lupus

A
  • Production of auto-antibodies gainst own cell’s DNA
  • The auto-antibodies get deposited in tissues and make inflammation and destruction
  • Auto-antibodies enter cells and destroy cell DNA
26
Q

S/S of Lupus

A
  1. Arthritis and arthralgias (acute or insidious pain!)
  2. Skin has butterfly rash on face, hair loss, MM ulcers, patchy skin
  3. Blood: anemia, and thrombocytopenia
  4. Plus: Kidney, cardiac and lung damage.
  5. Any cell can be affected
27
Q

Systemic Lupus erythematosus

A

-DX: Hard to diagnose
- S/S: vary so much from person to person
- Basically rule out everything else

28
Q

Treatment of Lupus

A
  • Decrease inflammation so tissue destruction is reduced
  • Malaria drugs are commonly used: they decrease antibody production, pain and inflammation
  • used in combo with corticosteroids which decrease inflammation
29
Q

Treatment of lupus: antimalarials

A
  • Examples: Chloroquine (Aralen) and hydroxychloroquine (Plaquenil) are approved for the treatment of SLE
  • Have been shown to reduce the frequency of disease flares (particularly of Lupus nephritis), Maintain remission, prolong the onset of disease and reduce the risk of complications