FINAL immunity Flashcards

1
Q

Briefly describe the innate immune system

A

Non specific, quick response, no memory. Consists of external defenses, inflammation, NK cells, complement system

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2
Q

Briefly describe adaptive immunty

A

Ramps up over time via cell signaling, specific, creates memory so it can identify recurring antigens and respond quickly on subsequent exposure. Antibody and cell- mediated.

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3
Q

Describe the first line of defense- physical and biochemical barriers

A

Physical barriers that cover the body and protect from damage/ infection (i.e., skin normal microbiome)

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4
Q

Describe the second line of defense- inflammation

A

Systematic process that responds to cellular or tissue damage (regardless of type of insult). Rapid initiation of interactive systems limits tissue damage, destroy contaminating infectious microorganisms, initiate the adaptive immune response, and begin healing.

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5
Q

Four characteristcs of inflammation

A

1) occurs in vascularized tissues
2) activated rapidly after damage (within seconds)
3) depends on activity of cellular and chemical components
4) non specific

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6
Q

Briefly describe the process of inflammation

A

Vasodilation, increased vascular permeability, white blood cells adehere to endothelium and migrate into vessel

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7
Q

What cells are involved in innate immunity?

A

Phagocytes, macrophages, mast cells, neutrophils, eosinophils, basophils, NK cells, dendritic cells

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8
Q

What cell bridges the innate and adaptive immune system?

A

Dendritic (presents antigens)

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9
Q

This cell type destroys infected host cells to stop the spread of infection

A

NK cells

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10
Q

These cells circulate through the body looking for potential threats to engulf and destroy

A

Phagocytes

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11
Q

These cells are a phagocytic cell that has left the circulatory system to hunt for pathogens; it also releases cytokines to signal and recruit other cells to an area where there are pathogens

A

Macrophages

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12
Q

What is the role of Mast cells in innate immunity?

A

Found in mucous membranes and connective tissue. Important for wound healing. When activated, release cytokines and granules containing chemical molecules to create and inflammatory cascade. Key player in mounting allergic response.

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13
Q

What cell is the first to arrive at the site of an infection?

A

Neutrophils

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14
Q

What do eosinophils do in the innate immune response?

A

Target parasites, involved in allergic response
Secrete highly toxic proteins and free radicals to kill bacteria and parasites

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15
Q

What do basophils do in innate immune response?

A

Granulocyte that attacks multicellular parasites
Release histamine

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16
Q

What is the complement system?

A

Typically acts are part of innate immune system
Activation produces factors that destroy pathogens directly or can activate or increase the activity of many other components of the inflammation/ adaptive immune response. Very potent against bacteria.

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17
Q

3 pathways of complement system

A

Classical- activated by antibodies
Alternative- activated by substances found on surface of infectious organisms like bacteria and yeast
Lectin- activated by plasma proteins that recognize the carbohydrate patterns on many pathogenic microorganisms

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18
Q

Describe the complement cascade

A

1) opsonization (foreign particles marked for phagocytosis- i.e. coated by opsonins)
2) chemotaxis (attraction of macrophages to a chemical signal (diffuse from a site of inflammation)
3) cell lysis (break down/ destruction of the membrane of foreign cells
4) Agglutination- antibodies cluster and bind pathogens together

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19
Q

Name characteristics for the adaptive immune response

A

Inducible- effectors of the immune response (lymphocytes and antibodies) do not pre- exist; infection induces production in response to foreign antigen
Develops more slowly (7-14 days to respond)
Very specific- lymphocytes and antibodies induced in response to infection are very specific to infecting microbe
Effectors are long lived and systemic (long term immunological protection/ memory response against specific infections)

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20
Q

What is meant by the term “humoral immunity”

A

antibodies circulating in blood defending against extracellular microbes/ toxins). Generated by plasma cells (produce antibodies) and memory B cells (long lived memory cells that become activated once a subsequent infection occurs with the same microbe)

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21
Q

What is meant by the term “cellular immunity”

A

Effector T cells circulate in blood and tissues and defend against intracellular pathogens (i.e., viruses) and cancer cells. Consists of t reg cells, t cytotoxic cells, th cells, and memory t cells

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22
Q

What T cell identifies and kills target cells?

A

T cytotoxic

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23
Q

What T cell assists in the clonal selection process?

A

T helper

24
Q

What T cells supress inappropriate immune response

A

T regulatory

25
Q

What T cells have a long memory that becomes activated once a subsequent infection occurs with the same microbe?

A

Memory T cells

26
Q

What T cells have a long memory that becomes activated once a subsequent infection occurs with the same microbe?

A

Memory T cells

27
Q

What is passive immunity?

A

Preformed antibodies are administered to individual (i.e., exposed to infectious agent without having pre-existing vaccine induced immunity) (i.e., new born receiving maternal antibodies via breast milk, Rh immunoglobulin to manage Rh incompatibility, IgG given for GBS)

28
Q

What immunoglobulin is more abundant?

A

IgG

29
Q

What immunoglobulin is first produced in the initial response to antigens?

A

IgM

30
Q

What immunoglobulin is found in blood and bodily secretions?

A

IgA

31
Q

What immunoglobulin is the primary cause of allergies?

A

IgE

32
Q

What immunoglobulin has the primary function of being an antigen receptor on the surface of early b cells?

A

IgD

33
Q

What is clonal diversity vs. clonal selection?

A

Clonal diversity is the production of a large population of B and T cells (before birth) that have the ability to recognize almost any foreign antigen. Mostly occurs in primary lymphoid organs (thymus and C cell). Result is differentiation of lymphoid stem cells into B and T cells with the ability to react against almost any antigen. Immunocompetent cells.

Clonal selection- processing of antigen for specific immune response. Antigen initiated- interaction between cells in the secondary lymphoid organs. Antigen is presented by dendritic cell or macrophage to immune cell. Interaction between APC, Th cell, and immunocompetent C or T cell results in differentiation of B cells into plasma cells (to produce antibodies) and T cells into effector cells (Tc cells) (both also differentiate into memory cells).

34
Q

Where does generation of clonal diversity occur?

A

Primary lymphoid organs (thymus and bone marrow) (primarily in fetus)

35
Q

Where does clonal selection occur

A

Secondary lymphoid organs

36
Q

What cells are needed for the process of clonal selection?

A

Antigen presenting cells (dendritic, macrophages)
T helper cells
Immunocompetent B or T cells

37
Q

Describe the primary vs secondary adaptive immune response

A

Primary immune response
* Single initial exposure to an antigen > latent period during which clonal selection occurs
* After 5-7 days, detection of antibodies (IgM followed by IgG against the same antigen; produced in similar quantities)

Secondary immune response
* Second challenge by same antigen results in secondary immune response
* Rapid production of larger amount of antibody than primary response (especially IgG)

38
Q

Where are T cells derived? B cells?

A

thymus and bone marrow, respectively

39
Q

What do B cells differentiate into

A

plasma cells or memory cells

40
Q

What do T cells differentiate into

A

Tc (cytotoxic), Th (T helper), T reg (regulatory) memory cells

41
Q

What cell does HIV target

A

T helper cells

42
Q

Autoimmunity can be classified as what 3 types of hypersensitivity reactions?

A

Type II, III, or IV (mostly type III)

43
Q

What immunoglobulin is involved in Type I HR? What is happening here?

A

Ig E = allergic reaction

  • During the first exposure, macrophages and dendritic cells present the antigen to T helper cells
  • IgE antibodies are made, which attach themselves to the surface of mast cells ready to respond if there is a subsequent exposure

For subsequent exposures:
1) External antigen (allergen) binds to IgE antibodies on mast cells or basophils.
2) This results in a large release of histamine (degranulation), which is a pro-inflammatory mediator
3)This causes a rapid onset of allergic symptoms within minutes (early phase reaction) –> vessel dilation & inc permeability (edema, hives), bronchoconstriction, etc
4) Late phase reaction (8-12 hours) can also occur

44
Q

Common examples of a type I hypersensitivity rxn

A

Food allergies

Hay fever

Allergic rhinitis

Atopic dermatitis or eczema

Asthma

45
Q

What types of hypersensitivity reactions are usually seen in an alloimmune reaction?

A

Mostly Type II or IV.

(Rarely Type I or III)

Type II: ie Hemolytic disease of the newborn

Type IV: ie Graft Rejection

46
Q

Which of the 4 hypersensitivity types is cell mediated?
(The other 3 are antibody mediated.)

A

Type IV is cell mediated as it is a response initiated by T-helper cells. Leads to cytotoxicity.

47
Q

Type II Hypersensitivity Reaction - what immunoglobulin?

A

IgG, IgM

48
Q

Type III Hypersensitivity Reaction - what immunoglobulin?

A

Same as type II - IgG, IgM

49
Q

Which type of hypersensitivity reaction is a fast/immediate response?

A

TYpe I

50
Q

Which type of hypersensitivity reaction has the slowest response, taking 48-72 hours?

A

Type IV

51
Q

In which type of hypersensitivity reaction are the body’s cells attacked by antibodies? (antibody-mediated destruction of healthy cells)

A

Type II

  • Tends to be tissue specific
  • antibodies bind cell-surface antigens
    -Due to self-reactive B-cells that produce antibodies (IgM, IgG) that bind antigens on host cells, forming antigen-antibody complex at tissue site
  • involves complement system activation, which targets cells for destruction
  • leads to death of cell by phagocytosis or cell lysis
52
Q

What happens in type III hypersensitiity?

A

= Immune Complex-Mediated Hypersensitivity Reaction

  • Antibodies bind soluble antigens that were released into the blood/body fluids. This antibody-antigen complex is then deposited into tissues.
  • Not organ specific
  • Immune complex deposition into tissues/vessels causes compliment activation and recruitment for neutrophils
  • Neutrophils typically cannot phagocytose the immune complexes due to their large size
  • Most of tissue damage comes from the release of lysosomal enzymes from neutrophils
53
Q

Examples of Type II hypersensitivity reaction?

A

ITP (antibodies target platelets), autoimmune hemolytic anemia (target RBCs), rheumatic heart disease, erythroblastosis fatalis (rH incompatibility between mom and babe),

54
Q

Examples of Type III hypersensitivity rxn?

A

serum sickness, rheumatoid arthritis, poststretptococcal glomerulonephritis, lupus

55
Q

What type of cells mediate a type IV hypersensitivity rxn?

A

T cells

56
Q

What happens in Type IV hypersensitivity rxn?

A

Antigens stimulate T cells to differentiate into Tc cells and Th1 cells

Tc cells (T-cytotoxic cells) = attack and destroy cellular targets directly

Th1 (T helper cells) = involved in delayed hypersensitivity

Delayed response by sensitized T cells to antigens, resulting in release of lymphokines or other chemical mediators that cause an inflammatory response and destruction of the antigen