Immunity part 3 Flashcards

1
Q

What is active immunity?

A

The specific protection that is acquired through exposure to antigens

This is either achieved by your:
ADAPTIVE IMMUNE RESPONSE (to having caught the disease/ infection etc)
Through IMMUNISATION (aka vaccination) (to that specific disease infection)

The initial exposure to a pathogen can take a few days or weeks to respond to. However, the second time you come across that pathogen, because of memory B cells, your body will remember how to fight off the infection in a few hours.
An acquired immune response can improve on repeated exposures to an injected antigen, or a natural infection

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2
Q

What is passive immunity?

A

Is immunity transferred from another source

An infant receives passive immunity naturally from the transfer of antibodies from the mother in utero (IgG) and through breast milk (IgG & IgA).
Maternal IgG crosses the placenta in the last few weeks of pregnancy and protects the newborn during the first few months of life.
Therefore, infants born prematurely may be deficient
IgA is transferred to the newborn through breastmilk.
Normally an infant has few infectious diseases during the first few months due to protection provided by the mother’s antibodies.
Passive immunity only provides short term protection that lasts weeks to months.

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3
Q

How do we regulate the immune response?

A

Normally, after exposure to a pathogen the immune response is activated.

It is usually self limiting because:
the pathogen has been eliminated

Cytokines & antibodies produced by the immune response have a limited life span & are only secreted briefly for antigen recognition.

A second way we regulate the immune response is through Tolerance

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4
Q

What is tolerance?

A

A term used to define the ability of the immune system to be non-reactive to self-antigens whilst producing immunity to foreign agents.
Tolerance to self antigens protects an individual from harmful autoimmune reactions.
Exposure of an individual to foreign antigens may also leads to tolerance and the inability to respond to potential pathogens that cause infection.

Note – You also get specialized regulation in important organs such as as the brain, testes, ovaries and eyes and so immune damage in these areas can result in serious consequences.

To function properly, the immune system must be able to differentiate foreign antigens from self antigens.
It is the Major Histacompability Complex (MHC) which serve as recognition markers for self and none self

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5
Q

Tell me about Regulation of the Immune Response

A

Self regulation is an essential property of the immune systems.

An inadequate immune response may lead to IMMUNODEFICIENCY

An Inappropriate of excessive reaction can lead to AUTOIMMUNE DISEASES.

(It involves all aspects of the immune response: Antigen, Antibodies, Cytokines, Regulatory T Cells, & Neuroendocrine system)

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6
Q

What are the Tolerance Mechanisms?

A

Central Tolerance
Peripheral Tolerance

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7
Q

What is central tolerance?

A

Eliminate self reactive B-Cells & T- Cells in the central lymphoid organs (Thymus for T- Cells, Bone Marrow for B-Cells)

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8
Q

What is peripheral tolerance?

A

is the deletion or inactivation of autoreactive T- cells or B-cells that escaped elimination in the central lymphoid organs

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9
Q

Tolerance is moderated by?

A

T Regulatory cells

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10
Q

What is tolerance and ageing?

A

As we age, there are changes in immune responsiveness including:
Cell meditated and humeral responses
Elderly people, compared to younger individuals tend to be susceptible to:
infection
have more evidence of autoimmune disorders
Higher prevalence of cancer

Thought may be (in part) due to a biological clock
of T Cell function.

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11
Q

What are disorders of the immune response?

A

Normally, the immune system is a combination of complex defence mechanisms that work together to protect us.
It works to fight infection, heal damaged tissue and prevent disease.
Occasionally, inadequate or inappropriate activation of the immune system can lead to debilitating or life-threatening illnesses which we define as:
Allergies or Hypersensitivity reaction
Transplant rejection
Autoimmune Disorders
Immunodeficient states

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12
Q

Disorders caused by the immune system are collectively called ?

A

Hypersensitivity Reactions

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13
Q

What are the 4 types of Hypersensitivity disorders?

A

Type I - Immediate Hypersensitivity Disorders
Type II- Antibody Mediated Disorders
Type III - Immune Complex Mediated Disorders
Type IV - T- Cell Mediated Disorders

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14
Q

What are Type I, Immediate Hypersensitivity Disorders

A

Aka Allergic Reactions
IgE Mediated
Begin rapidly (often within minutes of an antigen presentation)
Antigens referred to as allergens
Examples of allergens include:
house dust mites, animal dander, foods, chemicals (e.g. antibiotic penicillin).

Exposure to an allergen can range from:
Mild / annoying e.g. seasonal rhinitis
Moderate & interfering e.g. asthma
Life threatening e.g. anaphylaxis.

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15
Q

What is the physiology behind Type I, Immediate Hypersensitivity Disorders?

A

An often harmless antigen reacts with a specific IgE antibody located on the membrane receptors on mast cells and blood basophils

This reaction between antigen & antibody causes rapid release of pre formed potent vaso-active and inflammatory mediators- including histamine.

This reaction also causes a rapid production of leukotrienes & prostaglandins which are released into the adjacent tissue.

The effect of all these chemicals (leukotrienes, prostaglandins, histamine) into the tissues cause:

Vasodilation
Smooth muscle Spasm
Increased Permeability of small Blood Vessels
Excessive secretion by epithelial cells

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16
Q

What is the clinical significance of Type I, Immediate Hypersensitivity Disorders?

A

People who are particularly prone to develop Type I hypersensitivity sensitivity are those who produce excessive amounts of IgE

We call this an ATOPIC tendency and can suffer with a variety of manifestations:
Atopic Dermatitis
Allergic Rhinitis
Atopic Conjunctivitis
Extrinsic Allergic Asthma
Food Allergies

17
Q

What is Anaphylaxis?

A

Type I, Immediate Hypersensitivity Disorders
A SEVERE acute IgE mediated reaction to exposure to an antigen (that has previously been sensitized).

Important causative agents:
Insect Stings
Drugs (in particular anti-biotics)
Peanuts

Rapid Onset (after exposure)
Flushing
Palpitations
Odd tingling Sensations
Itching of the skin & larynx
Difficulty Breaching
Due to bronchospasm
If left untreated, will progress to shock with cardiovascular collapse, leading to death

These acute widespread systemic reactions are due to the antigens reaching the blood circulation, causing widespread smooth muscle contraction & vascular contraction.
The mass movement of fluid into the tissues is the cause of shock

18
Q

What are Type II, Antibody Mediated Disorders?

A

IgG or IgM mediated
Circulating antibodies bind specifically to antigens leading to cell death (of those cells with antigens)

There are 2 types of antibody dependent mechanisms in Type II:

Complement mediated Cytotoxicity
Antibody mediated cellular dysfunction (sometimes called Type 5 receptor mediated reaction).

19
Q

There are 2 types of antibody dependent mechanisms in Type II. What are they?

A

Complement mediated Cytotoxicity
Antibody mediated cellular dysfunction (sometimes called Type 5 receptor mediated reaction).

19
Q

What is COMPLEMENT – MEDIATED CYTOTOXICITY?

A

An antibody reacts with a cell surface antigen, and leads to activation of the complement system  which leads to cell lysis (from last weeks lectures- go back & look through slides unsure)

In addition, cells coated in the antibodies become susceptible to phagocytosis (opsonization).
Blood cells are the most commonly damaged by this mechanism

20
Q

What is ANTI-BODY MEDIATED CEULLULAR DYSFUNCTION ?

A

Antibodies which are directed against a cell surface, impair their function without causing cell injury or inflammation.

21
Q

What are some Clinical Examples of Complement Mediated Dysfunction?

A

RBC from an incompatible donor are hemolysed (destroyed) after being coated with antibodies normal present in the recipient.

Systemic Lupus Erythematosus
A person develops antibodies against their own blood cells called autoantibodies.
These autoantibodies may target and damage there own blood cells.

22
Q

What are some Clinical Examples of Anti-body mediated Cellular Dysfunction?

A

Graves Disease
Autoantibodies are directed against thyroid –stimulating hormone (TSH) receptors  this leads to production of thyroxine  which leads to hyperthyroidism.

Myasthenia Gravis
Autoantibodies to acetylcholine receptors on the neuromuscular endplants either block the action of acetylcholine or mediate destruction of receptors  this leads to decreased neuromuscular function.

23
Q

What is Type III, Immune Complex Mediated?

A

is mediated by antigen- antibody (immune) complexes
these initiate an acute inflammatory reaction in the tissues.

The antigens can be:
Exogenous Antigens- bacteria, viruses or foreign proteins
Endogenous Antigens - DNA (as in SLE) or IgG (as in Rheumatoid Arthritis)

there are 2 patterns of immune complex mediated injury:
The Systemic Pattern
The Local Pattern

24
Q

What are the two patterns of immune complex mediated injury?

A

The Systemic Pattern
The Local Pattern

25
Q

What is The Systemic Immune Complex Pattern?

A

The antigen – antibody complex is formed in the circulation (IgM, IgG and occasionally IgA)
The formed complex is then deposited in the body in various tissues
This deposition therefore initiates:
Inflammatory reaction which results in tissue damage.

Serum Sickness is a type of Type III system immune complex pattern

26
Q

What is a Clinical Example of : The Systemic Immune Complex Pattern?

A

Serum Sickness

is a term coined to describe a collection of symptoms:
rash, lymphadenopathy, arthralgias & occasionally neurological disorders
currently, most common causes of this include:
allergic reaction to antibiotics (especially penicillin)
various foods
Insect venom

27
Q

What is The Local Pattern?

A

often called Arthur’s Reaction
Used to describe a localized area of tissue necrosis as a result of acute immune complex vasculitis.
Can occur after vaccination

An area is injected with the antibody, which causes vasculitis (inflammation of the blood vessels), which eventually leads to tissue necrosis.
triggers the complement cascade which can amplify the immune response.
This can sometimes be seen when a person is repeatedly exposed to antigens from moulds or birds.

28
Q

What is arthur’s reaction?

A

Not very common

Generally very mild symptoms and presentation
S&S occur 24 hours after vaccination
Necrosis is extremely rare

Most of the time treated very effectively with anti- histamines

Difference between Arthur’s Reaction & Serum sickness is
Arthurs > Local reaction
Serum Sickness > systemic reaction

29
Q

What is Type IV, Cell Mediated Hypersensitivity Disorders?

A

These are cell mediated, rather than antibody mediated.
It is the principle mechanism response to a variety of microorganisms such as:
Mycobacterium tuberculosis
viruses
Fungi, protozoa & parasites.

Sensitized T-lymphoctyes contact with a specific antigen and may cause damage by direct toxic effect:

CD4+ T cells release cytokines which influences activities of neutrophils, macrophages

CD8+ T cells kill antigen bearing target cells

30
Q

What are clinical examples of Type IV, Cell Mediated Hypersensitivity Disorders?

A

Allergic Contact Dermatitis
due to an irritant, such as poison ivy, detergents, clothing, rubber etc

31
Q

What are autoimmune conditions?

A

An autoimmune disease is the result of the body producing an immune response against its own tissues.
The autoimmune response can be either:
cell mediated or antibody mediated
This can be helpful with diagnosing it

Autoimmune conditions occur when there is a breakdown in the normal tolerance mechanism
Autoimmune conditions are complex and still not fully understood.

What is known:
Some have a genetic component
Some can be triggered by microbial infection (although the underlying mechanism is still uncertain)

32
Q

What is Type 1 Diabetes?

A

Destruction of insulin secreting cells

33
Q

What is Primary hypothyroidism?

A

damage of thyroid cells

34
Q

What is Addison’s Disease?

A

Damage of adrenal glands

35
Q

What is Myasthenia Gravis?

A

Dysfunction with acetylcholine receptors, type 2 hypersensitivity

36
Q

What is Grave’s Disease?

A

Hyperthyroidism, type 2 hypersensitivity

37
Q

What is Hashimoto’s Disease?

A

Hypothyroidism

38
Q

What is Vitiligo?

A

hypopigmentation – effecting melanocytes