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A+P 2 > chapter 21 module 3 and 4 > Flashcards

chapter 21 module 3 and 4 Flashcards

1
Q 
Antibodies
-also called 
\_\_\_\_ secreted by \_\_\_\_
-Make up \_\_\_\_ portion of blood
-Bind with
A
  • also called Immunoglobulins (Igs)
  • proteins secreted by plasma cells
  • Make up gamma globulin portion of blood
  • Bind with specific antigen detected by B cells
  • Five Ig classes
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2
Q

Basic antibody structure

A

Basic antibody structure
-Overall T- or Y-shaped

  • antibody monomer consists of four polypeptide chains
  • –Two identical heavy (H) chains
  • –Two identical light (L) chains

-Variable (V) regions at one end of each arm combine to form two identical antigen-binding sites

  • Stems
  • -constant (C) regions
  • -Area that determines antibody class
  • Determines:
  • -Type of cells and/or chemicals that antibody can bind
  • -How antibody class functions to eliminate antigens
  • –Example: some antibodies fix complement, some circulate in blood, some are found in body secretions
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3
Q

Antibody classes

A

Five major classes: IgM, IgA, IgD, IgG, and IgE

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4
Q

IgM

A
  • Pentamer
  • Agglutinating agent
  • Fixes and activates complement
  • first class secreted during primary response
  • activates complement
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5
Q

IgA

A

(secretory IgA)

  • Monomer or dimer
  • In mucus and other secretions (saliva, sweat, milk)
  • Helps prevent entry of pathogens
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6
Q

IgD

A
  • Monomer attached to surface of B cells

- Functions as B cell receptor

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7
Q

IgG

A
  • Monomer
  • 75–85% of antibodies in plasma
  • From secondary and late primary responses
  • Crosses placental barrier
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8
Q

IgE

release what

A
  • Monomer active in some allergies and parasitic infections

- Causes mast cells and basophils to release histamine

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9
Q

Antibodies (Changing Classes/Drop adds for B Cells?)

almost all secondary response can be

A
  • Plasma B cells can switch from making one class of antibodies to another
  • -Still for the same antigen
  • For example
  • -IgM is released during primary response, but plasma cell can switch to IgG for secondary response
  • -Almost all secondary responses are IgG
  • -Switching from IgM to IgA or IgE can also occur
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10
Q

Antibody targets and functions

How?

A

Antibodies do not destroy antigens

  • Inactivate and tag them
  • Form antigen-antibody (immune) complexes

How?

  • Neutralization
  • Agglutination
  • Precipitation
  • Complement fixation

PLAN

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11
Q

Neutralization

A
  • Simplest mechanism
  • One of most important mechanisms
  • Antibodies block specific sites on viruses or bacterial exotoxins
  • Prevent antigens from binding to receptors on tissue cells
  • Antigen-antibody complexes undergo phagocytosis
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12
Q

Agglutination

A
  • Bind to two antigens at the same time
  • –Remember: each antibody has two arms; each arm has a variable region that can bind to an antigen
  • Antigen-antibody complexes cross-link into large clumps
  • -Example: clumping of mismatched blood cells
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13
Q

Precipitation

A
  • Not on cells
  • Soluble molecules are cross-linked
  • Complexes precipitate out of solution
  • Phagocytes engulf them
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14
Q

Antibodies (Compliment Actions)

A

Complement fixation and activation

  • Main antibody defense against cellular antigens
  • –bacteria, mismatched RBCs
  • Several antibodies are bound close together on same antigen
  • Complement-binding sites on their stem regions align
  • -Alignment triggers complement fixation, which leads to cell lysis, as well as other complement functions
  • -Example: amplification of inflammatory response, opsonization
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15
Q

Parasitic infections by worms such as Ascaris and Schistosoma require different immune attack strategies

A

Worms are too big for regular PLAN attack (Precipitation, Lysis (by complement), Agglutination, or Neutralization)

  • IgE antibodies still play a critical role in worm’s destruction by binding to surface of worm, marking it for destruction by eosinophils
  • Eosinophils bind to exposed stems of IgE, which triggers eosinophils to release their toxic contents onto prey, lysing it from the outside
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16
Q

Summary of antibody actions

  • Antigen-antibody complexes do not
  • Instead they prepare
  • Antibodies are for
  • -they do not invade
  • -EXCEPTION: antibodies can act
A
  • Antigen-antibody complexes do not destroy antigens
  • Instead they prepare them for destruction by innate defenses
  • Antibodies are for extracellular pathogens
  • -they do not invade solid tissue unless lesion is present
  • -EXCEPTION: antibodies can act intracellularly if attached to virus before it enters cell
  • –Activate mechanisms that destroy virus
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17
Q

T cells provide defense against

  • Some T cells
  • Some T cells release
A

intracellular antigens
-cells infected with viruses or bacteria, cancerous or abnormal cells, foreign (transplanted) cells

  • Some T cells directly kill cells
  • Some T cells release chemicals that regulate immune response
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18
Q

Two populations of T cells

A

CD4, CD8

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19
Q

CD4 cells

A
  • are based on which receptors are displayed on their surface
  • CD4 cells
  • -usually become helper T cells (TH)
  • –can activate B cells, other T cells, and macrophages
  • -direct adaptive immune response
  • -Some become regulatory T cells, which moderate immune response
  • Can also become memory T cells
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20
Q

CD8

–CD4 or CD8 cells are

A
  • become cytotoxic T cells (TC)
  • destroy cells “harboring” foreign antigens
  • Also become memory T cells
  • -Helper, cytotoxic, and regulatory T cells are activated T cells
  • -CD4 or CD8 cells are naïve T cells
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21
Q

T cells require ____ to be displayed by

Two classes of MHC proteins:

Both types are synthesized in

A

T cells require antigens to be displayed by MHC to respond to them

Two classes of MHC proteins:

  • Class I MHC proteins
  • –displayed by all cells except RBCs
  • Class II MHC proteins
  • –displayed by APCs (dendritic cells, macrophages, and B cells)

-Both types are synthesized in ER and bind to peptide fragments

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22
Q

Class I MHC proteins
antigen can be:
Class I MHC activates

A
  • Bind with short fragment (8–9 amino acids) of endogenous antigen,
  • -Protein synthesized inside cell
  • -Endogenous antigen can be:
  • –Self-antigen-normal proteins of cell
  • -Nonself antigen-abnormal proteins found in infected or abnormal cell
  • Class I MHC activates CD8 cells
  • -Act as antigen holders
  • -form “self” part that T cells recognize
  • -Inform cytotoxic T cells of microorganisms hiding in cells (cytotoxic T cells ignore displayed self-antigens)
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23
Q

Class II MHC proteins
–Have been
recognized by what kind of T cell
signal what kinds of cells

A
  • Bind with longer fragments (14–17 amino acids) of exogenous (extracellular) antigens
  • -Have been engulfed and broken down in a phagolysosome by antigen-presenting cell
  • Class II MHC proteins recognized by helper T cells
  • -Signal CD4 cells that help is required
24
Q

clone formation

A
  1. antigen presentation
    - dentritic cell engulfs an exogenous antigen, processes it, and displays its fragments on class II MHC protein.
  2. Double recognition
    - CD4 T cell recognizes antigen-MHC complex. Both TCR and CD4 proteins bind to antigen-MHC complex. Co-stimulatory molecules ind their receptors
  3. Clone formation
    - activated CD4 T cells proliferate (clone), and become memory and effector cells.
25
Q

Cytokines

  • Mediate
  • Includes
  • IL-2 is a key
  • Encourages activated T cells to
A
  • Chemical messengers of immune system
  • Mediate cell development, differentiation, and responses in immune system
  • Include interferons and interleukins
  • –Interleukin 1 (IL-1) is released by macrophages and stimulates T cells to
  • –Release interleukin 2 (IL-2)
  • –Synthesize more IL-2 receptors
  • IL-2 is a key growth factor, acting on same cells that release it and other T cells
  • –Encourages activated T cells to divide rapidly
  • Other cytokines amplify and regulate innate and adaptive responses
  • –Example: gamma interferon—enhances killing power of macrophages
26
Q 
Helper T (TH) cells
Play central role in 
-Activate both
-Once primed by APC presentation of antigen, helper T cells:
--Help activate 
--Induce 
--Secrete
-Without TH,
A
  • Play central role in adaptive immune response
  • Activate both humoral and cellular arms
  • Once primed by APC presentation of antigen, helper T cells:
  • -Help activate B cells and other T cells
  • -Induce T and B cell proliferation
  • -Secrete cytokines that recruit other immune cells
  • Without TH, there is no immune response
27
Q

Helper T cells help in humoral immunity

A
  1. Th cell binds with self-nonself complexes of a B cell that has encountered its antigen and is displaying it on MHC II on its surface
  2. Th cell releases interleukins as co-stimulatory signals to complete B cell activation.
28
Q

Amplification of innate defenses

A
  • Amplify responses of innate immune system
  • -Activate macrophages, leading to more potent killers
  • -Mobilize lymphocytes and macrophages and attract other types of WBCs
29
Q

Cytotoxic T (TC) cells

-Activated TC cells target:

A
  • Directly attack and kill other cells
  • Circulate in blood and lymph and lymphoid organs in search of body cells displaying antigen they recognize
  • Activated TC cells target:
  • -Virus-infected cells
  • -Cells with intracellular bacteria or parasites
  • -Cancer cells
  • -Foreign cells (transfusions or transplants)
30
Q

Helper T cells help in cellular immunity
1. TH cell binds to
can now activate

A
  1. TH cell binds dendritic cell
  2. tH cell stimulates dendritic cell to express co-simulatory molecules.
  3. Dendritic cell can now activate CD8 cell with the help of interleukin 2 secreted by TH cell.
31
Q

Cytotoxic T cells deliver lethal hit using two mechanisms

A
  1. TC cell releases perforins and granzymes by exocytosis
    –Perforins create pores through which –granzymes enter target cell
    Granzymes stimulate apoptosis
  2. TC cell binds specific membrane receptor on target cell and stimulates apoptosis
32
Q

Natural Killer Cells

NK cells use same key mechanisms as

A
  • Natural killer cells recognize other signs of abnormality that cytotoxic T cells do not look for, such as:
  • –Cells that lack class I MHC proteins
  • –Antibodies coating target cell
  • –Different surface markers seen on stressed cells
  • NK cells use same key mechanisms as TC cells for killing their target cells
  • Immune surveillance
  • -NK and TC cells prowl body looking for markers they each recognize
33
Q

Regulatory T (TReg) cells

  • Important in preventing
  • -Suppress
A
  • Dampen immune response
  • Important in preventing autoimmune reactions
  • -Suppress self-reactive lymphocytes
  • -Research into using them to induce tolerance to transplanted tissue
34
Q

Autograft

A

Transplant within the same person (artery transplants)

35
Q

Isografts

A

Grafts between genetically identical twins

36
Q

Xenografts

A

Grafts taken from another animal (pig kidney transplants, etc)

37
Q

Allograft
-Success depends on
After surgery
–Patient treated with

A
  • Most common type of transplant
  • transplant from same species
  • Success depends on similarity of tissues
  • -ABO, other blood antigens, and MHC antigens are matched as closely as possible
  • After surgery
  • -Patient treated with immunosuppressive therapy
  • -Many of these therapies have severe side effects
38
Q

Organ Transplants and Prevention of Rejection (Side Effects of Immunosuppression)

A
  • Cannot protect body from foreign agents
  • -Bacterial and viral infections
  • -Leading cause of death among transplant recipients
  • Best circumstances: rejection after 10 years in 50% of patients
39
Q

Immunodeficiency:

A

congenital or acquired conditions that impair function or production of immune cells or molecules

40
Q

Severe combined immunodeficiency (SCID) syndrome

A
  • Genetic defect with marked deficit in B and T cells

- Treatment: bone marrow transplants

41
Q

Hodgkin’s disease

A
  • is an acquired immunodeficiency
  • causes cancer of B cells
  • depresses lymph node cells and leads to immunodeficiency
42
Q

Acquired immune deficiency syndrome (AIDS)

A
  • Human immunodeficiency virus (HIV)
  • interfers with activity of helper T cells
  • -Remember these guys are needed to active the immune system!
  • Symptoms
  • -Characterized by severe weight loss
  • -night sweats
  • -swollen lymph nodes
  • Opportunistic infections
  • -i.e Pneumocystis pneumonia
43
Q

Immunodeficiencies (HIV Transmission)
-HIV is transmitted via

-HIV can enter the body via:

  • HIV destroys ____thereby depressing____
  • HIV multiplies in
A
  • HIV is transmitted via body fluids
  • -blood, semen, and vaginal secretions
  • HIV can enter the body via:
  • -Blood transfusions; blood-contaminated needles; sexual intercourse and oral sex; mother to fetus

-HIV destroys TH cells, thereby depressing cellular immunity

-HIV multiplies in lymph nodes throughout asymptomatic period
∼10 years if untreated

  • No cure for AIDS
  • -four major classes of antivirals in combination help but can fail as virus becomes resistant
44
Q

Autoimmune disease

A

when immune system loses ability to distinguish self from foreign

45
Q

Autoimmunity

A

production of autoantibodies and sensitized TC cells that destroys body tissues

46
Q

Autoimmune Diseases (Examples)

A

Examples

  • Rheumatoid arthritis: destroys joints
  • Myasthenia gravis: impairs nerve-muscle connections
  • Multiple sclerosis: destroys white matter myelin
  • Graves’ disease: causes hyperthyroidism
  • Type 1 diabetes mellitus: destroys pancreatic cells
  • Systemic lupus erythematosus (SLE): affects multiple organs
  • Glomerulonephritis: damages kidney
47
Q

Treatment of autoimmune diseases

A
  • Suppress entire immune system
  • -Anti-inflammatory drugs, such as corticosteroids
  • -Blocking cytokine action
  • -Blocking co-stimulatory molecules
  • Research
  • -Activating regulatory T cells; inducing self-tolerance using vaccines; directing antibodies against self-reactive immune cells
48
Q

Failure of self-tolerance

  • Autoimmunity may be caused by
  • Appearance of new self-antigens-How?
A
  • Autoimmunity may be caused by weakly self-reactive lymphocytes that are activated by:
  • Foreign antigens that resemble self-antigens
  • -Antibodies against foreign antigen may cross-react with self-antigen
  • Appearance of new self-antigens-How?
  • -Gene mutations
  • -Changes in self-antigens by hapten attachment or infectious damage
  • -Release of novel self-antigens by trauma to barrier
49
Q

Hypersensitivities

  • immune responses to perceived
  • Classification based on
  • Antibodies cause
A

-immune responses to perceived (otherwise harmless) threat that cause tissue damage (uggghhhh pollen and dogs!)

  • Classification based on
    1. Their time course
    2. Whether antibodies or T cells are involved
  • Antibodies cause immediate and subacute hypersensitivities
  • T cells cause delayed hypersensitivity
50
Q

Immediate hypersensitivity

A
  • Also called acute (type I) hypersensitivities (allergies)
  • -Seconds after contact with allergen
  • –antigen that causes allergic reaction
  • Initial contact with allergen is asymptomatic but sensitizes person
  • Activated IgE against antigen binds to mast cells and basophils
  • Later encounter with same allergen causes flood of histamine release from IgEs, resulting in induced inflammatory response
51
Q 
Hypersensitivities (Still Alergic!)
-Histamines causes
--Asthma can occur if allergen is 
\_\_\_\_are needed to control
-Allergic reactions can be
A
  • Histamines causes vasodilation and leakiness of the vessels, leading to symptoms of runny nose, itchy hives, or watery eyes
  • -Asthma can occur if allergen is inhaled
  • -Antihistamines are needed to control
  • Allergic reactions can be local or systemic
  • -Local reaction involves mast cells of skin or respiratory or gastrointestinal mucosa
52
Q

Systemic response is anaphylactic shock

  • Vasodilation results in
  • –Could cause
  • Treatment:
A
  • Usually seen with injected allergens
  • –example: bee sting
  • Bronchioles constrict, making breathing difficult
  • Vasodilation results in low blood volume
  • –Could cause circulatory collapse
  • Treatment: epinephrine
53
Q

mechanism of an acute allergic response

A

sensitization stage

  1. antigen (allergen) invades body
  2. plasma cells produce large amounts of class IgE antibodies against allergen
  3. IgE antibodies attach to mast cells in body tissues (and to circulation basophils)

subsequent (secondary) responses

  1. More of same antigen invades body.
  2. antigen combines with IgE attached to mast cells (and basophils), which triggers degranulation and release of histamine
  3. Histamine causes blood vessels to dilate and become Leakey, which promotes edema; stimulates secretion of large amounts of mucus; and causes smooth muscles to contract.
54
Q

Subacute hypersensitivities

Cytotoxic (type II) reactions

A
  • Caused by IgM and IgG transferred via blood plasma or serum
  • Slow onset (1–3 hours)
  • long duration 
(10–15 hours)
  • Cytotoxic (type II) reactions
  • -Antibodies bind to antigens on specific body cells, stimulate phagocytosis and complement-mediated lysis of cellular antigens
  • -Example: mismatched blood transfusion reaction
55
Q

Immune complex (type III) hypersensitivity

A
  • Antigens widely distributed in body or blood
  • Insoluble antigen-antibody complexes form
  • Complexes cannot be cleared from particular area of body
  • Intense inflammation, local cell lysis, and cell killing by neutrophils
  • Example: systemic lupus erythematosus (SLE)
56
Q 
Delayed hypersensitivities (type IV)
-Mechanism depends on 
--Example: 
-Agents act as
\_\_\_\_ skin test depends on this reaction
A
  • Slow onset (1–3 days)
  • Mechanism depends on helper T cells
  • Cytokine-activated macrophages and cytotoxic T cells cause damage
  • -Example: allergic contact dermatitis (e.g., poison ivy)
  • Agents act as haptens
  • TB skin test depends on this reaction

A+P 2 (13 decks)

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