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Clin Microbio > Specific Autoimmune Diseases > Flashcards

Specific Autoimmune Diseases Flashcards

1
Q

What are the two types of out body’s defenses?

A

Non-Specific (Innate)

Specific (Adaptive)

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2
Q

Give an overview of Specific Defenses (5 things)

A
  1. ) takes time to develop after birth (optimum reached later in life)
  2. ) 3rd line of defense after non-specific
  3. ) Enhancement (improves after each encounter)
  4. ) has memory (best immunity)
  5. ) Specific- given cells and proteins protected only against one or a few different pathogens
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3
Q

What are the 2 types of Specific/Adaptive response?

A 
Antibody mediated (Humoral)
Cell-Mediated
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4
Q

What is the end goal of Antibody/Humoral mediated response?

A

to activate specific B lymphocytes–> activated B lymphocytes –> secrete antibodies

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5
Q

What is an Antibody?

A

an antimicrobial protein complex

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6
Q

What is the end goal Cell-Mediated response?

A
  • activate specific cytotoxic T Cells (Tc)

- protect against viruses , cancer cells, and other cellular intracellular pathogens

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7
Q

what do Tc cells do?

A

find cancer cells and infected host cells and kills them

*Intracellular pathogens–> all viruses, some cellular pathogens

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8
Q

What is an antigen?

Where are they found?

A

any molecule that can stimulate a specific immune response; generally big molecules
includes: proteins, glycoproteins, nucleic acids, polysaccharides
Found= on viruses, prokaryotes, eukaryotes, humans

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9
Q

what is the normal function of an antigen?

A

attachment, transport, invasions, adhesives, enzymes (others)

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10
Q

What are the antigen classes ?

A
  • Self Antigens
  • Non-self antigens (foreign antigens)
  • Tumor antigens (altered-self antigens)
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11
Q

what is an epitope?(5)

A
  • antigenic determinant
  • smaller part of an antigen that is actually “recognized” as self, non self, or altered self
  • recognized by B or T lymphocytes via their unique surface receptors
  • what a secreted antibody will specifically bind to
  • a specific epitope may be found on more than 1 antigen-thus, a single antigen will posses many different epitopes and many of the same type
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12
Q

what is an epitope composed of?

A

Composed of 6-10 amino acids, 6-10 monosaccharides

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13
Q

A body’s specific defenses must learn to distinguish self from non-self, and self from altered-self.
What else must it learn?

A

It must learn to not respond to normal self (immunological tolerance) but respond to non self and altered self

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14
Q

The Immune Recognition/ Discrimination recognition is at the molecular level and involves receptors on unique _________ and ________ and coreceptors.

A

B and T lymphocytes

T helper and cytotoxic T cells

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15
Q

Primary Lymphoid Tissues = ________ and ________;

describe what happens in these tissues

A

Where B and T lymphocytes mature

  • learn to recognize non-self and respond (alloreactive)
  • learn to recognize self and not respond (not autoreactive); *cells that fail to do this are eliminated
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16
Q

Secondary Lymphoid Tissue= _________, ___________, _________;
describe what happens here

A
  • lymph nodes, lymph nodules, MALT
  • location where where B and T lymphocytes first meet epitope/antigen brought by antigen presenting cells
  • Lymphocytes circulate between the blood and secondary lymphoid tissues
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17
Q

What is similar about T and B Lymphocytes

A
  • each is covered by 1000s of identical surface receptors that can “recognize” 1 or a few closely related epitopes
  • non covalent bounds
  • 10-100s of millions of different types of B and T cell
  • receptors are membrane
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18
Q

B lymphocytes prior to exposure are referred to as_____

A

naive B-cells

they have a low state of readiness

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19
Q

What is the difference between B and T lymphocytes?

A

B: cell receptors remembrance bound forms of antibody
T: membrane bound protein receptors, but not antibody

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20
Q

Can B,T, and NK lymphocyte be distinguished from each other?

A

not morphologically, but they have different surface antigens which can identify them–> referred to as cluster differentiation

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21
Q

what are 3 main aspects of adaptive immune response?

A
  1. ) Specficity- immune cells recognize and react w/ individual molecules (antigens) via direct molecular interactions
  2. ) Memory- immune response to specific antigen is faster and stronger upon subsequent (initial antigen exposure induces growth and division of antigen-reactive cells–> results in multiple copies of antigen reactive cells
  3. )Tolerance- immune cells not able to react w/ self antigen and self reactive cells are destroyed during development of the immune response
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22
Q

Describe Antibody Mediated Response (6 steps)

A
  1. ) APC pathocytizes pathogen and processes epitopes. It puts pathogen’s epitopes in its MHC class II molecules
  2. ) APC presents epitope via its T cell receptors to Th cells–> specific Th cells that recognize the epitope are activated
  3. ) B cells bind the antigen specifically using membrane bound antibody receptors.–> next, B cells endocytose the antigen and process it down into epitope–> these epitopes are placed in their MHC class II molecules–> B cell activated into plasma cell via cytokines from Th cells–> plasma cells secrete antibody
  4. ) Activated Th cells present the epitope in their MHC class II molecule to the membrane bound antibody receptors on B cells that recognize that same epitope
  5. ) B cells are activated–> undergo clonal expansion into plasma cells and memory cells
  6. ) plasma cells synthesize and secrete antibody against specific epitopes on specific antigen on specific pathogens
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23
Q

What is a plasma cell (2)

A
  • an activated B cell (also known as an effector B cell)

- secrete antibody against specific epitopes

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24
Q

describe the structure of an antibody

A
  • Y shaped
  • composed of 4 polypeptide chains held together by disulfide bonds (2 identical heavy chains and 2 identical light chains)
  • each chain is composed of several globular functional domains (constant, variable, hyper variable)
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25
Q

Where is the Constant region? Describe it

A
  • region located between the carboxyl terminus of polypeptides and the variable region that has the same amino acid sequence from antibody to antibody
  • includes Fc region (fragment crystallizable)
26
Q

What are variable regions? what are hyper variable regions?

A
  • Variable: amino acid sequence varies from antibody to antibody made by different B cells
  • Hyper variable: unique amino acid sequence near amino end of polypeptides
  • varies from antibody to antibody made by different B cells
  • includes the antigen binding sites region
27
Q

The _____ form of antibody has 2 identical (but unique to the B cell) antigen binding site

A

monomeric form

28
Q

The _____ form of antibody has 4 identical (but unique to B cell) antigen binding sites,___ monomers held together by ____ and ______

A
  1. Dimeric Form
  2. 2
  3. secretory piece
  4. J chain
29
Q

The _____ form of antibody has 10 identical (but unique to the B cell) antigen binding sites. It is composed of ___ monomeric units joined to each other by ____ _______ ____

A
  1. Pentameric form
  2. 5
  3. J chain polypeptide (valence=10)
30
Q

True or False: All antibodies made by the same B cell have identical antigen binding sites.
Explain your answer.

A

True
-because they are all identical, can bind to the same epitope/s
-

31
Q
  1. ) A given B cell can potentially make up to ___ different classes of antibody.
  2. ) Does each class have their own antigen bindings sites or are they all the same?
  3. ) What does this mean?
A
  1. ) 5
  2. ) they are all the same (each class has the same antigen binding sites)
  3. ) means they can bind to the same epitope

-(other differences between the 5 classes)

32
Q

Concerning IgG:

  1. ) how many antigen binding sites
  2. ) properties
  3. ) distribution
A
  1. ) 2
  2. ) major circulating antibody (~80% of antibodies in blood serum); four subtypes; some activate complement; monomer
  3. ) extracellular fluid, blood, and lymph; can cross blood vessel wall and placenta
  4. ) opsonin; activate complement, bind to viruses and toxins and block their effects (neutralization)
33
Q

Concerning IgM:

  1. ) how many antigen binding sites
  2. ) properties
  3. ) distribution
  4. ) function
A
  1. ) 10 (pentamer) or 2 (monomer)
  2. ) 5-10% antibodies in serum; usually on service of naive (unactivated) B cell; pentamer
  3. ) Blood and lymph (usually in bv b/c too big to enter tissues); monomer is B cell surface receptor
  4. ) strong complement activator; opsonin; first antibody to appear after immunization
34
Q

Concerning IgA:

  1. ) how many antigen binding sites
  2. ) properties
  3. ) distribution
  4. ) function

**SEE SLIDE 42

A
  1. ) 2 or 4
  2. ) 5-10% antibodies in serum- most common form= in mucus membranes and body secretions (mucus, saliva, tears, and breast milk); most abundant antibody in body; important circulating antibody; major secretory antibody; monomer
  3. ) Secretions (saliva, colostrum, cellular, and blood fluids); monomer in blood; dimer in secretions
35
Q

Concerning IgD:

  1. ) how many antigen binding sites
  2. ) properties
  3. ) distribution
  4. ) function
A
  1. ) 2
  2. ) 0.2% serum antibodies; monomers; minor circulating antibody; mostly membrane bound on naive B cells surfaces
  3. ) Blood and lymph; B lymphocyte surfaces
  4. ) as a receptor
36
Q

Concerning IgE:

  1. ) how many antigen binding sites
  2. ) properties
  3. ) distribution
  4. ) function
A
  1. ) 2
  2. ) 0.002% serum antibodies; monomer; involved in allergic reactions and parasite immunity; Fc region binds to receptors on mast cells and basophils
  3. ) Blood and lymph; some bind to mast cells and eosinophils (Ch4)
  4. ) Type 1 hypersensitivity- release histamine and other inflammatory mediators; Attract IgG, phagocytes, and NK cells in parasitic worm larvae infection
37
Q

what are the functions 8 functions of an antibody?

A
  1. ) neutralization
  2. ) inhibit transport proteins on cellular pathogen, growth, and replication
  3. ) Opsonization
  4. ) Initiate/activate complement pathway (classical pathway)
  5. ) Antibody dependent cellular cytotoxicity (ADCC)
  6. ) Initiate Acute inflammation
  7. ) Bind to epitopes on pathogen and prevent it from adhering to surface (IgA at body surfaces)
  8. ) Agglutination
38
Q

Elaborate on what “Neutralization” is (2)

A
  • antibody binds to virus or toxins and prevents virus or toxin from binding to receptors
  • viral or toxin neutralization
39
Q

Elaborate on what “Opsonization” is (2)

A
  • antibody binds specifically to a pathogen and enhances phagocytosis and some complement factors
  • Fc receptors on phagocyte bind to Fc constant region of the antibody bound to the pathogen
40
Q

Elaborate on what “Antibody-dependent cellular cytotoxicity” is (2)

A

-any antibody bound specifically to an epitope on a large pathogen can have a NK cell, macrophage, or eosinophil bind to the Fc region and release cytotoxic chemicals into the pathogen

41
Q

Elaborate on “Initial Acute inflammation” as it concerns function of antibody

A

IgE binds to IgE receptors on mast cell–> causes degranulation and release of inflammatory mediators

42
Q

What is Agglutination?

A

antibody binds to several pathogens–> causes them to clump together*promotes phagocytosis

43
Q

What is a Primary Immunological Response?

A
  • first exposure to specific pathogen
  • typically takes 5-10 days to see any antibody–> increases over several weeks until peak reached
  • first antibody seen= IgM
  • second antibody= IgG
  • If memory cells form as result–> immunity will develop
44
Q

What is a Secondary Immunological Response?

A
  • If memory cells form/survived–> each subsequent exposure to that pathogen will not reach disease threshold b/c stronger, quicker secondary response
  • Mostly IgG
45
Q

What is hypersensitivity? (2)

A
  • over reaction of some part of the body defenses to a foreign, but usually non pathogenic, antigen (i.e.: allergen)
  • occurs on second and subsequent exposures
46
Q

what is an autoimmune disease?

A
  • when immune system loses (or never obtained) self-tolerance and responds to hosts own healthy cells/tissues/organs (body’s defenses against awn healthy self)
  • can involve auto antibodies or auto reactive T cells
  • some types seem to involve antigen mimicry b/w non-self and self antigens on tissues
  • genetic component=-> receptor proteins and genes; maybe mutation
  • *example on slide 68
47
Q

what is an immune deficiency?

A

when one or more of the body’s defenses is absent or lost

48
Q

describe Type 1 Hypersensitivity (5)

A
  • known as allergic or anaphylactic
  • involves IgE-Mast cell interactions
  • occurs after individual first sensitized to antigen (pathogen, venom, allergen) due to specific epitopes–IgE is made in response to allergen–> binds to IgE receptors on mast cells via Fc receptors
  • occurs within 30 min (second and subsequent exposures)
  • can be localized or systemic depending on which mast cells are sensitized and how the individual was exposed
49
Q

In Type 1 Hypersensitivity, what happens when the body is exposed to the foreign antigen a second time? (and all subsequent exposure to the pathogen)

A

antigen crosslinks with 2+ IgE molecules bound to mast cells–> mast cell undergoes degranulation–> releases inflammatory mediators

50
Q

how does the antigen enter the body during localized hypersensitivity type 1?

A

inhalation or ingestion

-only mast cells along exposure route are sensitized

51
Q

how does the antigen enter the body during systemic hypersensitivity type 1?

A

injection/bite into circulation

-many mast cells around body sensitized

52
Q

describe Type 2 Hypersensitivity (6)

A
  • known as cytotoxic
  • involves IgG (or IgM) binding yo surfaces on host cells and marking them for attack
  • attack by complement(MAC), phagocytosis by macrophages, or other cytotoxic cells
  • Occurs 5-12 hrs after exposure
  • Can involved foreign antigens attaching to cell surface of host cell (i.e.: malaria and erythrocytes, virus infected cells)
  • Transfusion rejection (ABO and Rh)
53
Q

Describe Hemolytic Disease of Newborn (a Type 2 Hypersensitivity)

A
  • Rh + father and Rh- mother
  • first Rh+ child: If Rh antigens enter mother’s circulation (i.e., during birthing), mother will likely produce anti Rh+ antibody (IgG) and memory cells
  • All subsequent Rh+ babies: anti Rh+ antibody can cross placenta and attack baby’s erythrocytes–> complement and lysis of cells–> baby compensates by making large # immature cells called erythroblasts (also toxic products of erythrocyte destruction)–> after birth baby=jaundice w/ severe anemia –> severe cases often fatal
54
Q

how do you prevent Hemolytic Disease of Newborn?

A

prevent with passive immunization

-anti Rh antibody–> combines with baby’s Rh+ that enter maternal circulation

55
Q

Describe Type 3 Hypersensitivity (5)

A
  • known as immune complex mediated
  • involves IgG antibodies against soluble antigens in blood or tissue fluid
  • immune complexes form with certain ratio of antibody to antigen–> these can deposit and get trapped in small blood vessels (i.e.: glomerulus of nephron)–> this can induce inflammation and cause damage
  • occurs 3-8 hrs after exposure
  • examples= glomerulonephritis, serum sickness
56
Q

Describe Type 4 Hypersensitivity (5)

A
  • known as cell mediated–no antibody involvement
  • involves Tc , Th cells (cytokines), and macrophages
  • delayed hypersensitivity –> occurs 24-48 hrs after exposure
  • sensitization occurs when foreign epitopes (particularly those that bind to tissue cells) are phagocytize by macrophages and presented to T cell receptors–> this causes T cell proliferation/maturation and memory cells –> subsequent exposure to the antigen can result in cell-mediated hypersensitivity
57
Q

the TB skin test is an example of a Type 4 Hypersensitivity. Explain the process

A
  1. ) TB protein antigen injected into skin

2. ) If previous exposure to M. tuberculosis or BCG vaccine, inflammatory reactions appears ~1-2 days later

58
Q

what causes Allergic Contact Dermatitis?

A

Haptens from plants (i.e.: catechol in poison ivy), cosmetics, or jewelry get on skin–> in some individuals, this induces a reaction by Tc cells, macrophages

59
Q

What are the 2 forms of Immune Deficiency? Describe them

A
  1. ) Hereditary Form:
    - usually due to recessive mutations (1 copy inherited from each parent) in the genes for key proteins in stem cells for leukocytes
    i. e.: Severe Combined Immunodeficiency
  2. ) Acquired
    - due to disease, cancers, chemicals
    i. e.: AIDS
60
Q

Describe Severe Combined Immunodeficiency (4)

A
  • can be due to several different mutated alleles
  • most autosomal on X-linked
  • affects lymphoid precursor cells
  • severest form lacks any functional B or T lymphocytes

Clin Microbio (3 decks)

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