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MicroBio > Test 4 Chapter 18 > Flashcards

Test 4 Chapter 18 Flashcards

1
Q

Adaptive Immunity

A

Takes time to develop, but memory allows for a more robust secondary response.

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2
Q

Innate Immunity

A

Born with it, attacks everything, memory, primary defender in first exposure.

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3
Q

Humoral Immunity

A

Antibody mediated immunity. B cells, plasma cells, antibody production.

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4
Q

B lymphocytes

A

B Cells. Differentiate into plasma cells when activated

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5
Q

Plasma cells

A

will produce antibodies

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6
Q

Antibody production

A

Effectors who will eliminate bacteria

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7
Q

Cell Mediated Immunity

A

Cellular immunity. T lymphocytes (T Cells). Multiple subtypes

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8
Q

Antigen

A

Molecules that stimulate an immune response. varies among organisms and strains. 3D structure contains epitopes. antigen may have multiple epitopes

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9
Q

Epitope

A

antigen determining region. this is was immune system responds to.

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10
Q

Multiple epitopes good or bad for immune response.

A

Multiple epitopes is a good thing. You can have an immune response directed at multiple epitopes on the same anitgen. multiple modes of attack on the same antigen,

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11
Q

Antibody Structure - Glycoproteins

A

Four protein chain held together by disulfide bonds. Heavy chains (2) Light chains (2)

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12
Q

Antibody Structure - Fab Region

A

Fragment Antigen-Binding region. Portion of an antibody molecule responsible for recognizing and binding to specific antigens

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13
Q

Antibody Structure - Fc Region

A

Fragment crystallizable region. Tail region that interacts with cell surface receptors called Fc receptors.

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14
Q

lgC antibodies

A

Most prevalent antibody in serum, crosses placenta, fixes complement. Titer to check for antibodies to see if you’re immune

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15
Q

lgM antibodies

A

Initial antibody produced and fixes complement

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16
Q

lgA antibodies

A

Present in body fluids and only antibody to leave the body.

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17
Q

lgD antibodies

A

B cell receptor

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18
Q

lgE antibodies

A

Anti-parasitic and pro-inflammatory

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19
Q

Neutralization antibodies

A

lgG, lgM, and lgA. antibodies cover all the epitopes. If all epitopes are covered antigen can’t do anything

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20
Q

Opsonization antibodies

A

lgG. Phagocytosis easier

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21
Q

Agglutination antibodies

A

lgG and lgM. Clumping of antigen antibody complexes. Makes it easier for macrophages to get rid of antigen

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22
Q

Complement Activation antibodies

A

lgG and lgM. Classic pathway activation

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23
Q

Antibody-dependent cell-mediated cytotoxicity (ADCC) antibodies

A

lgG

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24
Q

Major Histocompatibility Complexes (MHC) I

A

Identification tags. Found on all nucleated cells - mature red blood cells do not have a nucleus. Present normal self-antigens as well as abnormal or non-self antigens

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25
Q

Major Histocompatibility Complexes (MHC) II

A

Found on antigen-presenting cells. Macrophage, Dendritic cells - Phagocytic. B cells - Non-phagocytic. present abnormal or non-self antigens

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26
Q

MHC I - Antigen presentation

A

Longer alpha protein chain: spans membrane. antigen binding cleft.
Smaller Beta protein:

27
Q

MHC II - Antigen Presentation

A

Alpha and Beta chains similar length. Antigen binding cleft spans both chains

28
Q

T-Cell Production and Maturation

A

T-cells originate in red bone marrow. Released from marrow as thymocytes. Thymocytes migrate to the thymus for maturation.

29
Q

Thymic Selection

A

Development of T-cell receptor (TCR) and negative selection. Interact appropriately with MHCs and positive selection. Removal of self-reactive T cells.

30
Q

Regulatory T-Cells and Thymic Selection

A

Remove any self-reactive T-cells that escaped the thymus

31
Q

Self tolerance

A

Do not have t-cells that react to your cells

32
Q

CD4+ T Cells

A

Helper T-Cells and Regulatory T-Cells

33
Q

Helper T Cells and Immunity

A

Recognize antigens present on MHC II. Memory Cells.

34
Q

Regulatory T Cells and Immunity

A

Recognize antigens present on MHC II. Inhibit immune response.

35
Q

CD8+

A

Cytotoxic T Cells

36
Q

Cytotoxic T Cells and Immunity

A

Recognize antigens presented on MHC I. Memory Cells

37
Q

T Cell Receptor

A

Have epitope binding site for pathogen recognition. lgD

38
Q

Naïve helper T cell encounters APC

A

APC is displaying epitope on MHC II. TCR binds to epitope on MHC II forming MHC II-TCR Complex. CD4 binds to and stabilizes complex. APC and T cell secrete cytokines that activate the helper T Cell

39
Q

Th1

A

Stimulate cytotoxic T Cells. Sounds the alarm. Produces memory Tc Cells. Stimulates Macrophages, neutrophils, and NK Cells

40
Q

Th2

A

Stimulate B cell activation. Production of plasma cells and memory B cells. direct antibody class switching.

41
Q

Naïve cytotoxic T cells encounter cell displaying epitope presented on MHC I

A

TCR binds to MHC I -> MHC I-TCR Complex. CD8 binds to and stabalizes complex. Cytokines direct proliferation and differentiation. Can occur without Th1, but less efficent. Secrete perforins and granzymes to kill target cell.

42
Q

How cytotoxic T cells kill the target cell

A

Perforins make holes in plasma membrane. Granzymes go through holes and cause apoptosis.

43
Q

cytokine storms

A

An unregulated immune response triggered by a superantigen. Toxic shock syndrome toxin. Staphylococcal enterotoxins.

44
Q

Superantigen and MHCII-TCR

A

Super antigen can cause MHCII-TCR binding even if epitope does not match the antigen binding site

45
Q

Cytokine storm Signs/Symptoms

A

Decrease in blood pressure, shock, multi-organ failure, death

46
Q

B cell receptors (BCRs)

A

are monomers of lgD and lgM. Two identical heavy chains and two identical light chains held together by disulfide bonds.

47
Q

B cell Production and Maturation

A

Born in and mature in red bone marrow. Test antigen-binding receptors and negative selection. Travel to spleen for final stages of maturation to naïve mature B cells. Naïve mature B cells travel to other secondary lymphoid organs.

48
Q

T-independent activation of B cells

A

T-Independent antigens present. Clonal expansion and differentiation into plasma cells. Produce lgM. Short-lived, less robust, no memory

49
Q

T-Independent antigens

A

Repetitive epitope unity allowing for cross-bridge of multiple BCRs

Polysaccharide capsules, LPS, etc

50
Q

T-dependent activation of B cells

A

Binding of antigen to BCR. Endocytosis of antigen and display on MHC II. Th2 TCR binds to MHC II. CD4 stabilizes binding. Th2 secretes cytokines to activate B cell. B cell undergoes clonal expansion and differentiate into plasma cells and memory B cells. Initial secretion of lgM then class switch to lgC.

51
Q

Primary Response

A

First exposure to antigen
Lag period of ~10 days
lgM peak around 14 days
lgG peak around 21 days
You get and feel sick

52
Q

Secondary response

A

Lag period of a few days – memory cells ready to go don’t need all activation steps
More rapid and robust production of lgG
Faster and more robust response
Often fast enough to not get sick

53
Q

Natural Active Immunity

A

Got sick, exposed to pathogen. Immune response activated. Memory developed.

54
Q

Natural Passive Immunity

A

Fetus or infant. IgA cross placenta, or breast milk. Antibodies received from someone else.

55
Q

Artificial Active Immunity

A

vaccine. Exposure, didn’t get sick. Memory developed

56
Q

Artificial Passive Immunity

A

You’re given antibodies. No memory.

57
Q

Herd Immunity

A

artificial activity immunity. When a vulnerable population rely on the majority to be vaccinated.

58
Q

Edward Jenner

A

Noted that milkmaids who developed cowpox tended to not get small pox. Hypothesized that exposure to the less virulent pathogen provided immune protection with less risk than variolation (fluid from smallpox lesion). Tested hypothesis by injecting material from cowpox lesion and later infectious small pox – boy did not develop smallpox

59
Q

live attenuated vaccines

A

weakened strain of a pathogen
Goal is subclinical infection -> get a little sick
Problems include storage, transport, development of disease, and reversion to full virulence
Chickenpox, Measles, tuberculosis

60
Q

Inactivated vaccines

A

Contain whole pathogens that have been killed or inactivated
Inactivation process must not affect key antigen structure
No active infection – immune response may be weaker than with attenuated vaccines
More stable, No risk of active infection
Influenza, Rabies, Hepatitis A

61
Q

subunit vaccines

A

Contain antigens only – key antigens
Low risk vaccines – no pathogen present
Anthrax, Whooping Cough

62
Q

toxoid vaccines

A

not going to get sick
Inactivated bacterial toxin
Diptheria, Tetanus
TDap – Tetanus, Diphtheria, A cellular protasis

63
Q

conjugated vaccines

A

a type of subunit vaccine
Capsule polysaccharide conjugated to a protein
A capsule is all that is needed in order to stimulate and train the immune system
Allows T-Dependent response to capsules
HiB, Streptococcus pneumiae

MicroBio (17 decks)

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