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MicroBio > Test 4 Chapter 18 > Flashcards

Test 4 Chapter 18 Flashcards

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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
Major Histocompatibility Complexes (MHC) II
Found on antigen-presenting cells. Macrophage, Dendritic cells - Phagocytic. B cells - Non-phagocytic. present abnormal or non-self antigens
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MHC I - Antigen presentation
Longer alpha protein chain: spans membrane. antigen binding cleft. Smaller Beta protein:
27
MHC II - Antigen Presentation
Alpha and Beta chains similar length. Antigen binding cleft spans both chains
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T-Cell Production and Maturation
T-cells originate in red bone marrow. Released from marrow as thymocytes. Thymocytes migrate to the thymus for maturation.
29
Thymic Selection
Development of T-cell receptor (TCR) and negative selection. Interact appropriately with MHCs and positive selection. Removal of self-reactive T cells.
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Regulatory T-Cells and Thymic Selection
Remove any self-reactive T-cells that escaped the thymus
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Self tolerance
Do not have t-cells that react to your cells
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CD4+ T Cells
Helper T-Cells and Regulatory T-Cells
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Helper T Cells and Immunity
Recognize antigens present on MHC II. Memory Cells.
34
Regulatory T Cells and Immunity
Recognize antigens present on MHC II. Inhibit immune response.
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CD8+
Cytotoxic T Cells
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Cytotoxic T Cells and Immunity
Recognize antigens presented on MHC I. Memory Cells
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T Cell Receptor
Have epitope binding site for pathogen recognition. lgD
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Naïve helper T cell encounters APC
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
Th1
Stimulate cytotoxic T Cells. Sounds the alarm. Produces memory Tc Cells. Stimulates Macrophages, neutrophils, and NK Cells
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Th2
Stimulate B cell activation. Production of plasma cells and memory B cells. direct antibody class switching.
41
Naïve cytotoxic T cells encounter cell displaying epitope presented on MHC I
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
How cytotoxic T cells kill the target cell
Perforins make holes in plasma membrane. Granzymes go through holes and cause apoptosis.
43
cytokine storms
An unregulated immune response triggered by a superantigen. Toxic shock syndrome toxin. Staphylococcal enterotoxins.
44
Superantigen and MHCII-TCR
Super antigen can cause MHCII-TCR binding even if epitope does not match the antigen binding site
45
Cytokine storm Signs/Symptoms
Decrease in blood pressure, shock, multi-organ failure, death
46
B cell receptors (BCRs)
are monomers of lgD and lgM. Two identical heavy chains and two identical light chains held together by disulfide bonds.
47
B cell Production and Maturation
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
T-independent activation of B cells
T-Independent antigens present. Clonal expansion and differentiation into plasma cells. Produce lgM. Short-lived, less robust, no memory
49
T-Independent antigens
Repetitive epitope unity allowing for cross-bridge of multiple BCRs Polysaccharide capsules, LPS, etc
50
T-dependent activation of B cells
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.
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Primary Response
First exposure to antigen Lag period of ~10 days lgM peak around 14 days lgG peak around 21 days You get and feel sick
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Secondary response
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
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Natural Active Immunity
Got sick, exposed to pathogen. Immune response activated. Memory developed.
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Natural Passive Immunity
Fetus or infant. IgA cross placenta, or breast milk. Antibodies received from someone else.
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Artificial Active Immunity
vaccine. Exposure, didn’t get sick. Memory developed
56
Artificial Passive Immunity
You’re given antibodies. No memory.
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Herd Immunity
artificial activity immunity. When a vulnerable population rely on the majority to be vaccinated.
58
Edward Jenner
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
live attenuated vaccines
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
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Inactivated vaccines
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
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subunit vaccines
Contain antigens only – key antigens Low risk vaccines – no pathogen present Anthrax, Whooping Cough
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toxoid vaccines
not going to get sick Inactivated bacterial toxin Diptheria, Tetanus TDap – Tetanus, Diphtheria, A cellular protasis
63
conjugated vaccines
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
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MicroBio (17 decks)

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