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BMS292 > Topic One: Dysfunction of the Immune System > Flashcards

Topic One: Dysfunction of the Immune System Flashcards

1
Q

A haematopoietic stem cell transitions into what?

A
  1. Common myeloid progenitor & Common lymphoid progenitor
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2
Q

What does a common myeloid progenitor transition into?

A
  • Erythrocyte
  • Platelets
  • Myeloblast
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3
Q

What does a common lymphoid progenitor transition into?

A

Lymphoblast.

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4
Q

What can a lymphoblast become?

A

T lymphocyte and B lymphocyte

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5
Q

What can a myeloblast transition into?

A
  • Basophil
  • Neutrophil
  • Eosionophil
  • Monocyte
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6
Q

What can a myeloblast transition into?

A
  • Basophil
  • Neutrophil
  • Eosionophil
  • Monocyte
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7
Q

What is the immune system made up of?

A

The innate (non-specific) and adaptive systems.

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8
Q

What is the immune system made up of?

A

The innate (non-specific) and adaptive systems.

This is further subdivided into first and second line defences.

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9
Q

What are first line defences of the innate (non specific) immune system?

A
  • Skin
  • Mucous Membranes
  • Secretions
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10
Q

What is the purpose of first line defences?

A

To prevent organisms from entering the body.

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11
Q

What are the mechanical factors of first line defences??

A

Skin has a strong keratinized epidermis that helps remove bacteria and other infectious agents that have adhered to the epithelial surface.
Via: sweat, oil and low pH

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12
Q

Why is movement significant trait of first line defence?

A

Due to cilia or peristalsis - passages such as airways and GI tract are kept free from microorganisms.

Flushing actions - i.e. tears and saliva = prevention of infection in the eyes and mouth
Trapping effect - mucus lines respiratory and gastrointestinal tract - this helps prevent infection also.

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13
Q

What are the chemical factors of first line defence?

A
  • Fatty acids: These are in the sweat and inhibit bacterial growth.
  • Lysozyme and phospholipase are found in tears, saliva and nasal secretions - these breakdown the cell wall of bacterium.
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14
Q

What are the chemical factors of first line defence?

A
  • Fatty acids: These are in our sweat and inhibit bacterial growth. (sebum)
  • Lysozyme and phospholipase are found in tears, saliva and nasal secretions - these breakdown the cell walls of bacterium.
  • Low pH: sweat and gastric secretions = antimicrobial activity.
  • Definsins are low molecular weight proteins that are also antimicrobial. They are found in the lung and GI tract.
  • Peptides in sweat: these create water channels in certain bacteria - disrupting a transmembrane potential = cell death.
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15
Q

What is an opsonin?

A

A surfactant in the lung - promotes phagocytosis of particles by phagocytic cells.

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16
Q

What are biological factors for first line defences?

A

The normal flora of the skin and in the gastrointestinal tract can prevent the colonization of pathogenic bacteria by secreting toxic substances or by competing with pathogenic bacteria for nutrients or attachment to cell surfaces.

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17
Q

For the innate (non-specific) system of immunity what is the second line of defence?

A
  • Phagocytic cells
  • Antimicrobial proteins
  • The inflammatory response
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18
Q

For the innate (non-specific) system of immunity what is the second line of defence?

A
  • Phagocytic cells
  • Antimicrobial proteins
  • The inflammatory response
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19
Q

What is a complement system?

A

A major non-specific defence mechanism that once activated can lead to increased vascular permeability, the recruitment of phagocytic cells, and lysis and opsonization of bacteria.

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20
Q

What does opsonization refer to?

A

Opsonization refers to the process or molecular mechanism that uses opsonins to make a molecule (e.g. antigen) palatable to the phagocyte. For instance, opsonins (e.g. antibodies) bind to the surface of the bacterial cell.

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21
Q

What is a coagulation system?

A

A coagulation system increases vascular permeability and acts as chemotactic (attractant) for phagocytic cells.

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22
Q

When does the adaptive immune system become active?

A

When the first two lines of defence have been compromised.

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23
Q

What is the adaptive immune system?

A

The third line of defence.

- Lymphocytes and Antibodies.

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24
Q

How does the adaptive immune system respond?

A

It responds specifically to microorganisms and aberrant body cells, and all molecules marked as foreign (antigens)

Specific defensive proteins called antibodies are produced by lymphocytes.

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25
Q

What are the main cells in the adaptive immune system?

A

Cytotoxic T Cell
B Cell
T helper cell

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26
Q

The adaptive immune system is a physiological system that?

A
  • Recognises specific antigens
  • Acts to immobilize, neutralize or destroy foreign substances
  • Amplifies inflammatory response and activates complement.
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27
Q

What is an antigen?

A

An antigen is a substance/molecule that when introduced into the body triggers the production of an antibody by the immune system which in turn kills or neutralises the antigen.

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28
Q

What are examples of complete antigens?

A

Foreign proteins, nucleic acids, some lipids and large polysaccharides

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29
Q

What is a haptens?

A

An incomplete antigen.

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30
Q

Where are haptens found?

A

Poison ivy, halothane (anaesthetic), dander, some detergents and cosmetics.

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31
Q

A hampten is a small molecule that has to bind with what to become antigenic?

A

An endogenous protein.

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32
Q

A hapten is a small molecule that has to bind with what to become antigenic?

A

An endogenous protein.

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33
Q

What is humoral immunity?

A

Humoral immunity is mediated by the production of antibodies produced by B lymphocytes (top right) which have been turned into plasma cells.

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34
Q

What is cell-mediated immunity?

A

Cell mediated immunity involves the activation of macrophages, natural killer cells, cytotoxic T-lymphocytes and the release of cytokines in response to an antigen.

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35
Q

What is humoral immunity?

A

Humoral immunity is mediated by the production of antibodies produced by B lymphocytes which have been turned into plasma cells. Plasma cells are antibody producing factories.

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36
Q

Where do B cells mature?

A

B Cells mature in the bone marrow. This occurs over numerous stages and a failure in any of the steps leads to the B cell dying causing apoptosis.

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37
Q

Where do T cells mature?

A

T cells mature in the thymus.
Process takes 2-3days
There are immature lymphocytes which occur rapidly.
Maturing T cells are the only ones able to identify foreign attackers, thus are the only ones allowed to survive.

(Immature lymphocytes usually remain in the bone marrow)

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38
Q

What happens to a naïve immunocompetent B or T cell when it leaves the thymus or bone marrow?

A

They move into the lymph nodes - or other lymphoid tissues “The spleen”
Here they encounter antigens.

The lymphocyte then reacts to a distinct antigen. JUST ONE AND ONLY ONE. They then mature into a fully functional B or T lymphocyte for a particular virus, bacteria.

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39
Q

Although all the details of the maturation process are still being investigated we know that lymphocytes becomes immunocompetent long before meeting the antigens they may later attack. What does this mean?

A

Remarkably, this means it is our genes, not the antigens that determine what specific substances our immune system will be able to recognize and resist.

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40
Q

What is the humoral (antibody-mediated) immune response?

A

This is when a B lymphocyte binds to an antigen - then becoming activated.
It grows and multiplies rapidly to form an army of cell clones identical to itself (bearing the same antigen-specific receptors)

This is called the primary humoral response.

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41
Q

What do most cloned B cells become?

A

They become plasma cells which are antibody producing factories They can produce 2000ABs/second

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42
Q

What is the process for a immunocompetent B Lymphocyte?

A

Immunocompetent B Lymphocyte > Activated B lymphocyte > plasma cell

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43
Q

Antibodies belong to which family of proteins?

A

Immunoglobulins

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44
Q

How is an antibody made up?

A

Each antibody is made up of two identical heavy chains and two identical light chains, shaped to form a Y.

The stem of the Y links the antibody to other participants in the immune defenses. This area is identical in all antibodies of the same class–for instance, all IgEs–and is called the constant region

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45
Q

What is important to know regarding the sections that make up the antibodies arms?

A

The sections that make up the tips of the Y’s arms vary greatly from one antibody to another; this is called the variable region. It is these unique contours in the antigen-binding site that allow the antibody to recognize a matching antigen, much as a lock matches a key.

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46
Q

What is important about the stem of the Y in an antibody?

A

The stem of the Y links the antibody to other participants in the immune defenses. This area is identical in all antibodies of the same class–for instance, all IgEs–and is called the constant region.

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47
Q

What is IgE?

A

IgE is normally present in only trace amounts, but it is responsible for the symptoms of allergy.

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48
Q

Where is IgE found?

A

IgE is normally present in only trace amounts, but it is responsible for the symptoms of allergy.

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49
Q

Where is IgD found?

A

IgD is almost exclusively found inserted into the membrane of B cells, where it somehow regulates the cell’s activation.

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50
Q

Where is IgA found?

A

IgA–a doublet–guards the entrance to the body. It concentrates in body fluids such as tears, saliva, and secretions of the respiratory and gastrointestinal tracts.

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51
Q

Where is IgG found?

A

IgG, the major immunoglobulin in the blood, is also able to enter tissue spaces; it works efficiently to coat microorganisms, speeding their destruction by other cells in the immune system

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52
Q

Where is IgG found, what is it doing??

A

IgG, the major immunoglobulin in the blood, is also able to enter tissue spaces; it works efficiently to coat microorganisms, speeding their destruction by other cells in the immune system

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53
Q

Where is IgM found?

A

IgM usually combines in star-shaped clusters. It tends to remain in the bloodstream, where it is very effective in killing bacteria.

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54
Q

Immunoglobulin M - When does it first appear?

A

IgM:
Following an initial exposure to an antigen - it is the first antibody to appear on the scene
It forms polymers - multiple immunoglobulins are linked together.
It is the largest immunoglobulin and because of this it finds it incredibly difficult to diffuse across barriers.

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55
Q

What is the clinical significance of IgM?

A

IgM presence is highly indicative if a infection has been recent.
Due to it being such a large molecule - unable to diffuse well - it is found in neonates serum and indicates intrauterine infection.

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56
Q

Could you mention some details about IgG?

A
  • Most abundant antibody.
  • Found in plasma (75-85%)
  • Involved in the secondary response

This is the only Ig that passes into the placenta to confer passive immunity foetus before their immune system becomes functional.

IgG though selective - can bind to other kinds of pathogens: protects against agglutination, activates complement and neutralizes toxins.

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57
Q

Could you mention some details regarding IgE?

A
  • Trouble maker of Ig family
  • Present in low conc in the blood
  • Related exclusively to allergy exposure.
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58
Q

How does IgA exist?

A

as a monomer and dimer.

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59
Q

Describe the IgA monomer. (Plasma)

A

It is a small component (Y) - it is selective to one antigen and acts a a neutralizing antibody to many others. (in the plasma)

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60
Q

Describe the IgA dimer. (Secretions)

A

Main role:

  • bathe and protect mucosal surfaces from pathogens
  • can survive harsh environments
  • comprises of 70% of all immunoglobulins in mammals
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61
Q

Describe the IgD.

A
  • Always found attached to B cell - acts in activation

- Binds to basophils and mast cells - activating microbial factors in response to respiratory infections.

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62
Q

Order of humoral response:

A
  1. Exposure to antigen (e.g. chicken pox)
  2. B cells that do not become plasma cells become MEMORY B CELLS. These are capable of responding to the antigen later on.
  3. When they become active it is called the second humoral response.
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63
Q

What is the timeline of the primary humoral response?

A

Several days to produce antibodies and the are rarely enough

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64
Q

What is the timeline of the secondary humoral response?

A

Only takes several hours to evoke a response and it produces a massive amount of antibodies

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65
Q

Acquired humoral immunity: How is an active and passive immunity acquired naturally?

A

Active: Infection - contact with a pathogen
Passive: Antibodies passed from the mother to the foetus via placenta or via breast milk

66
Q

Acquired humoral immunity: How is an active and passive immunity acquired artificially?

A

Active: Vaccine: Dead or attenuated pathogen
Passive: Injection of immune serum (antibodies: gamma globulin)

67
Q

What is passive humoral activity?

A

Differs from active immunity in the antibody source and the degree of protection
B cells are not challenged by antigens
Immunological memory does not occur
Protection ends when antibodies naturally degrade in the body

68
Q

What is active humoral activity?

A

B cells encounter antigens and produce antibodies against them

69
Q

What is cell-mediated immunity mediated by?

A

T cells.

They play major roles in initiation, maintenance and regulation of the immune response.

70
Q

T cells are best suited for cell-to-cell interactions. They target what?

A
  • Cells infected with viruses, bacteria, or intracellular parasites.
  • Abnormal or cancerous cells
  • Cells of infused or transplanted foreign tissues.
71
Q

T cell ‘cell to cell’ interactions involve?

A

The activation of:

  • Macrophages
  • Natural killer cells
  • Cytotoxic T-lymphocytes
  • Release of cytokines in response to an antigen.
72
Q

What are the two major population of T cells that mediate cellular immunity?

A
  • CD4+ cells (T4 cells) are T helper cells (T*H)

- CD* cells (T8 cells) - these are cytotoxic T cells (TC) they destroy cells harbouring foreign antigens.

73
Q

What are self-antigens?

A

Our cells are dotted with protein molecules (self antigens) - they are not antigenic to us - however strongly antigenic to others.

74
Q

What are MHC proteins?

A

The major histocompatibility complex is a large locus on vertebrate DNA containing a set of closely linked polymorphic genes that code for cell surface proteins essential for the adaptive immune system. These cell surface proteins are called MHC molecules.

75
Q

What is the function of the MHC molecule?

A

The function of MHC molecules is to bind peptide fragments derived from pathogens and display them on the cell surface for recognition by the appropriate T cells.

76
Q

What are the two classes of MHC proteins?

A

Class I MHC proteins

Class III MHC proteins

77
Q

Where are Class I MHC proteins found?

A

Virtually in all body cells. When a foreign antigen is bound to a class I MHC protein it is a indication to the immune system to terminate the cell as it is abnormal.

78
Q

Where are Class II MHC proteins found?

A 
Only found in the membrane pf antigen-[resenting cells and lymphocytes. 
A foreign antigen bound to a class II MHC protein is another indication to the immune system. It is saying. "This antigen is dangerous. Get rid of it."
79
Q

What is different about T cells to B cells regarding antigens?

A

T cells need to be presented and antigen.

This is done through.

  • Infected cells
  • A macrophage, an activated B cell or dendritic cells that has engulfed the antigen.
80
Q

What does a macrophage do after engulfing an antigen?

A

Macrophages express parts of it externally, in combination with one of the macrophages own proteins (MHC protein)

81
Q

What are the three stages in Helper T cell activation?

A
  1. Antigen recognition
  2. Clonal secretion (T cell)
  3. interleukin secretion
82
Q

What is secreted in the 3rd stage of Helper T cell activation?

A
  • Neutrophils & Macrophages (non specific defence)
  • Cytotoxic T cells (cellular immunity)
  • B cells (humoral immunity)
83
Q

What are the stages of cytotoxic T cell activation?

A
  1. Antigen recognition - connects with immature cytotoxic T cell
  2. Clonal selection: Activated cytotoxic cells and memory T cells.
  3. Activated cytotoxic T cells - Lethal Hit on - infected/cancer/target cell.
  4. Target cell dies
84
Q

When does hypersensitivity of the immune system occur?

A

it occurs when the normal immune mechanisms produce an exaggerated response to an antigen, or an inappropriate response to self antigens.

85
Q

What are the four categories of hypersensitivities?

A

Types I, II, III, IV

86
Q

What are each of the hypersensitivity disorders mediated by?

A

I, II & III are mediated by antibody responses

IV is mediated by the cytotoxic cells of the immune system.

87
Q

Briefly, what hypersensitivity is type I?

A

Immediate or anaphylactic

88
Q

Briefly, what hypersensitivity is type II?

A

Cytotoxic

89
Q

Briefly, what hypersensitivity is type III?

A

Complex-mediated

90
Q

Briefly, what hypersensitivity is type IV?

A

Cell-mediated

91
Q

What is the mechanism of Type I hypersensitivity?

A

Free antigens cross link IgE on mast cells ad basophils releasing vasoactive biomolecules

  • fast response
  • basis for anaphylaxis
92
Q

What are Type I hypersensitivity examples?

A

Anaphylaxis

Asthma

93
Q

What is the antigen for Type I hypersensitivity?

A

Soluble (airborne)

94
Q

What is the mediator for Type I hypersensitivity?

A

IgE

95
Q

What is the mechanism of Type II hypersensitivity?

A

Antibody (IgG or IgM) binds to antigen on host or transplant cell that is perceived by the immune system as foreign. This leads to cellular destruction via complement (e.g. MAC) or antibody dependant cell mediated cytotoxicity (ADCC)

96
Q

What are examples of Type II hypersensitivity?

A

Autoimmune disease

Blood transfusion reactions

97
Q

What is the antigen in Type II hypersensitivity?

A

Cell or Matrix

98
Q

What is the mediator for Type II hypersensitivity?

A

IgG or IgM complement MAC

99
Q

What is the mechanism of Type III hypersensitivity?

A

Antibody IgG binds soluble antigen, forming a circulating immune complex. This can deposit in the vessel walls of joints and the kidney, initiating a local inflammatory reaction (massive neutrophil infiltration).

100
Q

What are examples of Type III hypersensitivity?

A

Rheumatoid arthritis

Lupus

101
Q

What is the antigen for Type III hypersensitivity?

A

Soluble

102
Q

What is the mediator for Type III hypersensitivity?

A

IgG
Complement
Neutrophils

103
Q

What is the mechanism for Type IV hypersensitivity?

A

Memory Th 1 cells activate macrophages and Tc cells causing an inflammatory response, ultimately leading to tissue damage.

104
Q

What are some examples of Type IV hypersensitivity?

A 
Contact dermatitis
MS
Coeliac
Graft rejection
DM type I
105
Q

What is the antigen for Type IV hypersensitivity?

A

Soluble or cell associated

106
Q

What is the mediator for Type IV hypersensitivty?

A

T cells.

107
Q

What is Type I hypersensitivity also called?

A

Immediate hypersensitivity

108
Q

Type I hypersensitivity is mediated by the production of what?

A

IgE antibodies following an initial exposure to an antigen or hapten.

109
Q

What are the stages of reaction in a Type I?

A
  1. Allergen - dust mite, cat hair - invades body
  2. Plasma cell produces large amounts of IgE
  3. IgE then attaches to mast cells. Process of sensitisation.
  4. Histamine - In the second response to the allergen mast cells release massive amounts of histamine.
110
Q

In a type I hypersensitivity reaction, after histamine is released - What occurs?

A
  • Fluid outpours from capillaries
  • Release of mucus
  • Constriction of bronchioles
111
Q

Specifically what occurs in a Type I hypersensitivity reaction?

A
  1. Sensitisation - Allergen(dust mite, cat hair) invades body > Peptide forms on macrophage > Th cell attaches to APC > communicates with B cell which presents antigen on surface.
  2. Plasma cell in retaliation produces large amounts of IgE > releases them
  3. IgE attaches to mast cells and basophils
  4. Second exposure: Mast cells release massive amounts of histamine
  5. Fluid out pours from capillaries
    mucous is released
    bronchioles constrict.
112
Q

Mild forms of type I hypersensitivities include:

A
  • Rhinitis (hay fever)
  • Mild allergies
  • Urticaria (Hives)
  • Atopic dermatitis
  • Mild asthma
113
Q

Severe forms of type I hypersensitivities include:

A

Severe allergies leading to anaphylaxis

Severe asthma

114
Q

What are mild signs of a type I hypersensitivity reaction?

A

Localized redness and swelling of the skin as seen in urticaria, increased mucus production and swelling of the epithelial tissue of the sinus cavity seen in rhinitis (hay fever).

115
Q

What are severe signs of a type I hypersensitivity reaction?

A

Severe signs include decreased airway capacity (via bronchial constriction or mucus production) seen in asthma, or reduced blood pressure via systemic vasodilation in anaphylaxis.

116
Q

What is anaphylaxis?

A

Anaphylaxis is a severe systemic response to the inflammatory vasodilation.

117
Q

Q. What will happen when arterioles vasodilate throughout the body?

A

A

118
Q

What will happen when the bronchioles constrict?

A

A

119
Q

What can also cause bronchoconstriction?

A

Acetylcholine, leukotrienes and prostaglandins can all cause bronchoconstriction.

120
Q

What does systemic vasodilation cause?

A

It causes relative hypovolemia and a decrease in blood pressure. Bronchoconstriction leads to reduced ventilation and reduced oxygen availability.

121
Q

What are the most significant clinical signs of anaphylaxis?

A

Hypoxaemia and Hypotension

122
Q

What is hypoxaemia due to?

A

Due to a bronchospasm, hypersecretion of mucus and swelling of the upper airways

123
Q

What causes hypotension?

A

Systemic vasodilation

124
Q

What are some responses due to hypotension and hypoxaemia?

A
  • Tachycardia
  • Confusion
  • Loss of consciousness

Other signs also which are considered as type I hypersensitive = rashes, localised oedema.

125
Q

How is anaphylaxis treated?

A

It is treated as a medical emergency - with the use of adrenaline and saline to restore blood pressure.

126
Q

Adrenaline stimulates alpha-adrenergic receptors - Why is this a reason we use adrenaline?

A

This action decreases the increased vascular permeability and the vasodilation that occurs during anaphylaxis.

127
Q

We use adrenaline because it activates beta-2 adrenergic receptors in the lungs, why?

A

Because it relaxes bronchial smooth muscle, thereby relieving bronchospasm, increasing vital capacity, decreasing residual volume, and reducing airway resistance.

128
Q

The action of adrenaline is believed to result in?

A

The increased production of cyclic adenosine 3’,5’-monophosphate (c-AMP). Increased c-AMP concentrations also inhibit release of mediators of immediate hypersensitivity from cells, especially from mast cells.

129
Q

What is Type II hypersensitivity also known as?

A

Antibody dependant cytotoxic hypersensitivity

130
Q

What is Type II hypersensitivity mediated by?

A

It is mediated by the production of IgG or IgM antibodies - These bind to self-antigens or antigenic determinants formed by molecules like drugs being bound to normal cells (e.g. RBCs)

131
Q

When antibodies are bound to cells this activates what?

A

Immune cell mediated cytotoxic responses to destroy those cells. In some cases where the antibodies bind to receptor proteins on cells this can also disrupt the normal functions of the receptor, either by causing uncontrollable activation or by blocking receptor function.

132
Q

What are some examples of Type II hypersensitivity?

A
  • Autoimmune diseases where antibodies are produced that bind to normal cell receptors
  • Hemolytic disease of the new born.
  • Hyperacute graft rejection, during blood transfusion or organ graft rejection.
  • Certain drug allergies.
133
Q

When is it that haemolytic diseases occur in newborns?

A

Haemolytic disorders occur in newborns when maternal IgG antibodies cross the placenta. Most commonly this condition develops in rhesus factor negative (RhD) negative mother with RhD+ foetus.

134
Q

Type III hypersensitivity is also called?

A

Immune complex-mediated hypersensitivity

135
Q

Type III hypersensitivity occurs when?

A

When unattached antigens enter the blood circulation and activate and exaggerated immune response (IgG and IgM mediated) that results in the formation of a large amount of antigen-antibody complex.

These complexes build up in capillaries and accumulate in joints or the glomeruli of the kidneys.

136
Q

Type III hypersensitivity antigen/antibody complexes then activate the classical complement pathway leading to:

A
  1. Systemic inflammation - Due to C5a triggering mast cells to release inflammatory mediators
  2. Local influx of neutrophils - Due to C5a signalling, resulting release of neutrophil lysosomes leading to tissue destruction and further inflammation
  3. Membrane attack complex lysis - Of surrounding tissue cells - due to the membrane attack complex
  4. Aggregation of platelets - resulting in the formation of microthrombi that block capillaries.
  5. Activation of macrophages.
137
Q

What else is type IV hypersensitivity called?

A

‘Cell mediated hypersensitivity’

138
Q

Why is Type IV hypersensitivity different to the other types of sensitivities?

A

It is different because it is mediated by immune cells (i.e. T Cells) rather than requiring antibodies. Because of the involvement of cellular mechanisms these responses are also slower that antibody mediated mechanisms, taking 48-72hours, rather than minutes. Hence type IV hypersensitivity is also known as delayed hypersensitivity.

139
Q

What is alloimmunity?

A

A delayed type of hypersensitivity (type IV) reaction caused by a reaction of immune system to antigens on transplanted cells from the same species eg transplanted organs and blood transfusions.

140
Q

Alloimmunity can occur when?

A
  • In the recipient after transfusions of fluids such as blood or plasma
  • In the recipient after allografts (grafts)
  • In the foetus after maternal antibodies have passed through the placenta into the foetus, as in haemolytic disease of the new-born and fetomaternal all immune thrombocytopenia.
141
Q

What is the ABCDs of hypersensitivity?

A

I - Allergic, Anaphylaxis and Atopy
II - Antibody
III - Immune complex
IV - Delayed

142
Q

What are some examples of autoimmune diseases?

A

Autoimmune diseases occur with the loss of the immune system’s ability to distinguish self from non self.

143
Q

Autoimmune diseases occur with the loss of the immune system’s ability to distinguish self from non self. What does this mean?

A
  • Normally, self reactive immune cells are killed in the lymphoid organs or supressed by regulatory T Cells.
  • in at autoimmunity, self-tolerance thus breaks down.
144
Q

What is immunodeficiency?

A

A state where the immune system is unable to respond appropriately because part of the system is defective, missing or has itself been compromised by disease.

145
Q

How are immunodeficiencies classified?

A
  • Primary immunodeficiencies (mostly genetic aetiology)

- Secondary immunodeficiencies - which are acquired or result from extrinsic factors.

146
Q

Briefly differentiate between primary and secondary immunodeficiency.

A

Primary immunodeficiencies are distinct from secondary immunodeficiencies that result from other causes, such as viral or bacterial infections, malnutrition, immunoglobulin (Ig) loss, malignancy or treatment with drugs that induce immunosuppression.

147
Q

Primary Immunodeficiencies (PIDS) are classified broadly by?

A
  • Disorders of Innate Immunity

- Disorders of Adaptive Immunity

148
Q

What are two examples of Disorders of Innate Immunity?

A
  • Phagocytic disorders (such as chronic granulomatous disease)
  • Complement disorders (such as C2 deficiency and C3 deficiency)
149
Q

What are examples of Disorders of Adaptive Immunity?

A
  • B-Cell disorders such as X-linked agammaglobulinaemia
  • T-cell dysfuntion such as DiGeorge syndrome (DGs)
  • Combined T and B-lymphocyte disorders (such as severe combined immunodeficiency, i.e. SCID, the wiskott-aldrich syndrome.
150
Q

PIDS “Primary immunodeficiencies” are almost all?

A

Genetically acquired however an exception is “Neutralizing anti-interferon-y autoantibody- associated immunodeficiency which has been seen in over 95% of patients with disseminated infections by non tuberous mycobacteria.”

151
Q

What is a secondary immunodeficiency a result of?

A

A variety of factors - can affect a host with an intrinsically normal immune system e.g.

  • Infectious disease ‘HIV’
  • Immunosuppressive agents
  • Age Extremes ‘Young or Old’
  • Malnutrition
  • Surgery & Trauma

These all effect adaptive and innate immunity.

152
Q

The factors that lead to secondary Immunodeficiency leads to ?

A

Infection or Tumor.

153
Q

Regarding extremes of age; New-born’s. Why do they have an increased susceptibility to common and opportunistic infections and sepsis compared to older children?

A
  • New-borns have fewer B cells
  • A decreased expression of CD12 of B cells preventing them from developing specific responses.
  • Lack of maturity of secondary lymphoid organs
  • Decreased levels of neutrophils - therefore limited phagocytosis ability
  • Transfer of maternal IgG occurs at 32 weeks of gestational age. Premature babies are at an even higher risk.
154
Q

Regarding extremes of age: Advanced Age. What is happening regarding immunodeficiencies?

A
  • Decreased lymphocyte response
  • Limited capacity for thymus for generate naïve T cells therefore reduced response to new antigens
  • Restricted B cell diversity
  • Limited responses to vaccines
155
Q

How does malnutrition cause secondary immunodeficiency?

A

Worldwide cause for secondary immunodeficiency.

  • Lowered intake of proteins results in less t-Cells production.
  • Deficiency of micronutrients such as zinc and ascorbic acid contribute to weakening of mucosal barriers
  • Vitamin D is needed for macrophage activity
156
Q

How do immunosuppressive agents cause secondary immunodeficiencies?

A

This is employed in autoimmune disorders, allergic disorders, transplant rejection and graft-versus host disease (GvHD)

  • Corticosteroids inhibit T cells and inhibit cytokine production
  • Calcineurin inhibitors inhibit calcineurin which is needed for transcription and T-cell function.
  • Low concentration ctyotoxic agents for neoplasms inhibit both T and B cells proliferation
157
Q

How does surgery and trauma implicate a secondary immunodeficiency?

A
  • Patients that have undergone surgery to remove lymphoid tissue such as the spleen, tonsils and appendix have reduced B and T cell populations
  • Patients that have undergone a splenectomy are most susceptible to encapsulated bacteria such as streptococcus pneumoniae
158
Q

Name an infectious disease that is a secondary immunodeficiency

A

HIV

  • 30million infected world wide
  • 2/3 are from sub-Saharan Africa and are women or children
159
Q

What is the virology of HIV?

A
  • HIV is double stranded
  • It is a RNA retrovirus that can bind to CD4+ T helper cells and macrophages
  • HIV viral genomic RNA is converted into DNA by reverse transcriptase
  • The HIV DNA is then integrated into the host genome and uses the host cells replication mechanisms to produce more virions.
160
Q

What is the progression of HIV to aids?

A

Initially: the viremia occurs with very high HIV-1 RNA levels followed by a prolonged period during which viral replication continues with lower but measurable HIV-1 RNA levels

CD4 lymphocytes then decline and then the collapse of the immune system, high level viremia, symptoms and opportunistic infections develop and death ultimately occurs.

BMS292 (13 decks)

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