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UT BME 365S > Exam 4: Immune System > Flashcards

Exam 4: Immune System Flashcards

1
Q

primary functions of the immune system

A
  1. protects the body from disease-causing invaders (pathogens and antigens)
  2. removes dead or damaged tissues and cells (inflamed cells, old blood cells)
  3. recognize and remove “abnormal self” cells (cancer cells)
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2
Q

key features of immune system

A

specificity: enable body to distinguish “self” from “non-self”

memory: immune response is stronger in the second stimulation

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3
Q

what happens if the immune system fails?

A

incorrect response: autoimmune diseases (type 1 diabetes or IBD

overactive response: allergies, allergic hypersensitivity reactions

lack of response: immunodeficiency diseases, AIDS, HIV

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4
Q

types of lymphoid tissue

A

primary: thymus gland and bone marrow

secondary: lymph nodes and spleen

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5
Q

primary lymphoid tissue

A

role: nurture immune cell development

naive immune cells have not encountered the proper antigens

cells involved in the immune response form and mature

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6
Q

secondary lymphoid tissue

A

role: get matured immune cells to interact with pathogens and initiate a response

categories: encapsulated and unencapsulated diffuse lymphoid tissues

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7
Q

bone marrow

A

spongy tissue inside some bones like hip and thigh bones

contains stem cells that can develop into red blood cells and white blood cells (immune cells) that can fight infections

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8
Q

thymus gland

A

on the chest between the lungs

makes T lymphocytes which help fight infection

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9
Q

lymph node

A

small bean shaped structure

filter substances that travel through the lymphatic fluid

contain white blood cells that help the body fight infection and disease

connected to each other by lymph vessels

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10
Q

spleen

A

largest lymphoid organ in the body

immune cells in the spleen monitor blood for foreign invaders

phagocytes in the spleen trap and remove old red blood cells

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11
Q

basophils and mast cells

A

release chemicals that mediate inflammation and allergic responses

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12
Q

granulocytes

A

white blood cells whose cytoplasm contains prominent granules

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13
Q

phagocytes

A

engulf and ingest their targets

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14
Q

cytotoxic cells

A

kill the cells they are attacking

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15
Q

antigen-presenting cells

A

display fragments of foreign proteins on their cell surface

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16
Q

neutrophils

A

50-70% of all white blood cells

1-2 days life span

ingest and kill 5-20 bacteria

make pus: thick fluid caused by infection that includes white blood cells and cellular debris

chemotactic migration to chemical signals such as IL-8, leukotriene that induces production of ROS such as H2O2 and inflammation

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17
Q

eosinophils

A

associated with allergic reactions and parasitic diseases

pink-orange color

1-3% of all leukocytes

life span of 6-12 hours

location: GI tract, lungs, epithelium of urinary and genital tracts, and connective tissue of skin

produce ROS (reactive oxygen species such as superoxide, peroxide), cytokines, and enzymes (elastase in asthma)

attach to large antibody-coated parasites and release substances that kill them

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18
Q

basophils and mast cells

A

located in the systemic circulation (0.5-1% of circulating WBCs)

mast cells are found in the local tissues

dark violet granules

contain chemicals that are involved in immune and allergic responses such as histamine, heparin, and cytokines

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19
Q

dendritic cells

A

characterized by long, thin processes that resemble the dendrites of the neuron

APCs: present antigens to lymphocytes to activate them

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20
Q

antigen-presenting cells

A

recognize and capture antigens

dendritic cells, macrophages, and B cells

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21
Q

monocytes

A

precursor cells of macrophages and dendritic cells

circulating version of macrophages and DC

spend ~8 hours in transit from the bone marrow to tissues where they differentiate into macrophages

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22
Q

macrophages

A

primary scavengers for the tissues

can ingest up to 100 bacteria

remove dead blood cells and dead neutrophils

antigen presenting cells

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23
Q

lymphocytes

A

responsible for acquired immune response

5% of all lymphocytes are in circulation and the rest are located in lymphoid tissues

make up 20-35% of all circulating white blood cells

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24
Q

t lymphocytes

A

cell-mediated imkmunity

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25
Q

b lymphocytes

A

antibody-mediated immunity

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26
Q

types of immunity

A
  1. physical and chemical barrier
  2. innate immune system (all animals possess)
  3. adaptive immune system (all vertebrates possess)
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27
Q

innate immune system

A

non-specific

begins within minutes to hours

produces general inflammatory response when pathogens penetrate physical barriers

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28
Q

adaptive immune system

A

can adapt to defend against any invader

response to a first exposure to a pathogen may take days

important when the innate immune system cannot defend against an attack

provides the immune system with “memory”

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29
Q

components of the innate immune system

A
  1. professional phagocytes: macrophages and neutrophils
  2. complement system: proteins that tag stuff for destruction
  3. natural killer (NK) cells: mast cells and basophils
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30
Q

macrophages

A

patrol periphery

become activated when they find an invader

when activated:
1. send signals to recruit other immune system cells (neutrophils)
2. become vicious killers (phagocytosis)
3. present antigen to adaptive immune system

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31
Q

what activates macrophages

A

chemotaxins: bacterial toxin, cell wall components

tissue injury debris: fibrin, collagen fragments

chemotactic cytokines by leukocytes

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32
Q

mechanism of attachment during phagocytosis

A

patterning recognition receptor to binding

binding to antibody

hydrophobicity

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33
Q

patterning recognition receptor to binding

A

phagocytic cells’ patterning recognition receptor can bind bacteria directly by surveilling the pathogen-associated molecular pattern

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34
Q

binding to antibody

A

phagocytic cells can bind the Fc portion of antibody

binding of several antibodies on macrophages activates phagocytosis and microbial killing

35
Q

hydrophobicity

A

hydrophobic groups tend to attach to the hydrophobic surface of cells

may explain the recognition of damaged cells, denatured proteins, etc

36
Q

mechanism of killing and digestion during phagocytosis

A

lactoferrin

oxygen and the oxygen burst

nitric oxide (NO)

37
Q

lactoferrin

A

protein that inhibits bacteria by depriving them of iron which it binds with an extremely high affinity

38
Q

oxygen and the oxygen burst

A

intracellular killing of many bacteria requires the uptake of oxygen by the phagocytic cell

reactive oxygen species are highly toxic to microorganisms

NO produced from arginine is another reactive oxygen containing compound that is highly toxic to microorganisms

39
Q

complement proteins

A

about 30 plasma and cell membrane proteins

present in tissues and blood

attach to surfaces of bacteria and viruses
- 1. target them for destruction by phagocytes or by making pores
- 2. form membrane attack complexes

recruit other immune cells from blood

40
Q

functions of complement system

A

opsonization and phagocytosis

lysis

agglutination

neutralization of viruses

chemotaxis

activation of mast cells and basophils

inflammatory effects

41
Q

opsonization and phagocytosis

A

opsonins are used to tag foreign antigens and strongly activates phagocytosis by both neutrophils and macrophages

42
Q

lysis

A

combination of multiple complement factors can directly rupture the cell membranes of bacteria or other invading organisms

43
Q

agglutination

A

the complement products also change the surfaces of the invading organisms, causing them to adhere to one another promoting agglutination (clumping of particles together)

44
Q

neutralization of viruses

A

complement enzymes and other complement products can attack viruses and thereby render them non-virulent

45
Q

chemotaxis

A

chemical stimulus initiates the movement of neutrophils and macrophages

46
Q

activation of mast cells and basophils

A

cells become activated which causes them to release histamine, heparin, and several other substances into the local fluids

47
Q

inflammatory effects

A
  1. increase blood flow further
  2. increase the capillary leakage of proteins
  3. coagulate the interstitial fluid proteins in the tissue spaces, preventing movement of the invading organism through the tissues
48
Q

natural killer cells

A

innate response against viral infection

innate immune response because they lack antigen-specific cell surface receptors

release granzyme (protease)

NK cells induce virus-infected cells to commit suicide (apoptosis)

secrete antiviral cytokines (interferons)

interferons interfere with viral reproduction in the body

49
Q

release of histamine

A

released by mast cells and basophils

initiates inflammatory response

induce WBC recruitment from the blood stream

50
Q

histamine action

A
  1. opens pores in capillaries: release of plasma protein causes local edema/swelling
  2. dilates blood vessels increasing blood flow: bring about hot, red, swollen area around the wound or infection site
51
Q

adaptive/acquired immune system

A

two main components

fight pathogens outside of cells: b lymphocytes/antibody-mediated immunity

fight pathogens inside of cells: t lymphocytes/cell-mediated immunity

52
Q

function of antibodies

A
  1. activates b lymphocytes
  2. acts as opsonins
  3. causes antigen clumping and inactivation of bacterial toxins
  4. activates antibody-dependent cellular activity
  5. triggers mast cell degranulation
  6. activates complement
53
Q

b cells

A

lymphocytes that make antibodies

b cell receptors on the surface

100 million different types of b cells that each have different surface receptors

b cell receptors are so diverse they can recognize every organic molecule

54
Q

when a b cell binds antigen…

A

b cells are activated and differentiated into plasma cells

plasma cells secrete antibodies at the rate of approximately 2000 molecules per second

55
Q

how do T cells identify virus infected cells?

A

antigen presentation

all nucleated cells have major histocompatibility complexes on the surface

when virus invades the cell, fragments of viral protein are loaded onto MHC proteins

T cells inspect MHC proteins and use this as a signal to identify infected cells

56
Q

MHC class I molecules

A

all nucleated cells

infected cells display viral antigens on MHC I

cytotoxic T cells recognize a cell with foreign antigen fragment and kills the cell

57
Q

MHC class II molecules

A

macrophages, b lymphocytes, and dendritic cells

helper T cells recognize a cell with foreign antigen fragment on its MHC II

helper T cells secrete cytokines that enhance the immune response

58
Q

lymphocytes clones and memory effects

A

at birth, each clone of lymphocytes is represented by only a few cells called naive lymphocytes

exposure to an antigen triggers clonal expansion and the immune response

59
Q

primary immune response

A

clone of B and T cells are built up over the course of 1 week

when the infection is over, these cells die off and the ones that remain are memory cells

B lymphocytes become plasma cells which can secrete antibodies to treat the disease in the future

peak antibody concentration occurs about 2 weeks after exposure

60
Q

secondary immune response

A

memory cells can activate more easily and reproduce effector and memory cells that will turn into plasma and secrete antibodies

peak antibody concentration occurs around 3 weeks post exposure, BUT antibody concentration rises immediately after exposure to yield a faster response that is also stronger

in just a few days, secondary immune response will yield the peak amount of antibodies that were secreted in the primary immune response

aka: can become stronger faster

61
Q

bacteria

A

cells have membrane and cell wall

can survive outside the host

can reproduce without a host

can be killed or inhibited by antibiotics

62
Q

how do bacteria cause disease?

A

invade the host

reproduce and overgrow

deplete nutrients, ions, and oxygen

secrete organic wastes

produce toxins that disturb the normal functions of cells

63
Q

immune response to bacteria

A

complement proteins make membrane attack complex that lyses bacteria

complement proteins activate mast cells that secrete chemotaxins and histamine (chemotaxins attract circulating leukocytes that will ingest and disable bacteria or secrete antibodies)

64
Q

virus

A

contains nucleic acid core (DNA or RNA) with protein envelope

uses the intracellular machinery to reproduce
- virus causes host cell to lyse OR viral particles will bud from the host cell surface)

cannot be killed with antibiotics

65
Q

how do viruses cause disease?

A

virus invades the host cell
- binds to membrane receptors
- endocytosis brings virus into the cell

virus takes over the cell
- use viral nucleic acid and host cell resources to make new viral nucleic acid and proteins

more virus is released from host cell
- virus causes the host cell to lyse OR viral particles bud from the host cell surface

66
Q

immune response to viruses

A

MHC I presenting
- attacked by cytotoxic T and NK cells
- granzymes
- infected cell is destroyed

MHC II presenting
- macrophage ingests the virus
- secretes cytokines for inflammatory response
- macrophage presents antigen fragments
- activates helper T cell
- activates B lymphocytes
- become plasma cells that secrete antibodies

67
Q

human immunodeficiency virus (HIV)

A

fast mutation of the viral genome
- antibodies fail to coat the viral particles for phagocytosis by macrophages
- macrophages fail to phagocytose (failed to transferred to lysosome) and virus invade macrophages

after viruses infect cells, T lymphocytes are the main defense - failed
- helper T cells are infected by the virus
- cytotoxic T cells use viral antigen-MHC I to recognize the infected cells and kill them BUT also kill T cells
- virus down regulate MHC expression to escape cytotoxic T cells

68
Q

COVID 19

A

targets angiotensin converting enzyme (ACE2) to get into host cells

ACE2 found on apical surface of the epithelium in the lung, arteries, heart, kidney, and gut

once coronavirus binds to ACE2, complex internalizes into the cytoplasm via endocytosis

in the lung, attacks type II alveolar epithelium since it has a lot of ACE2 on the surface

disrupted type II alveolar epithelium results in reduced surfactant production –> lung malfunction

damaged type II alveolar epithelium produces multiple cytokines that recruit macrophages in the lung

69
Q

mRNA vaccine

A

mRNA with instructions for making spike protein put into vaccine

mRNA enters the cell

virus spike protein is created

spike protein is recognized by the immune system and specific antibodies are produced

if infected, antibodies bind to the virus and stop it from replicating

70
Q

sensitization

A

initial exposure to an allergen

71
Q

allergic reaction

A

secondary exposure to same allergen causes more antibody binding to mast cells for release of histamine

72
Q

anti-histamine

A

decreases vascular permeability

decreases bronchoconstriction

73
Q

corticosteroids

A

reduce general inflammatory response

74
Q

epinephrine (adrenaline)

A

constricts blood vessels

intramuscular or intravenous injection

75
Q

autoimmune disease

A

immune system mistakenly attacks your body

foreign antigens that are similar to human antigens can be a trigger
- body makes antibodies BUT antibodies have enough cross-reactivity with human tissues to do some damage

76
Q

multiple sclerosis

A

white matter of the brain and spinal cord

77
Q

rheumatoid arthritis

A

joint lining

78
Q

type 1 diabetes

A

the pancreas

79
Q

lupus

A

kidneys and other organs

80
Q

guillan barre syndrome

A

peripheral nerves

81
Q

rheumatoid arthritis treatment

A

stimulation of the vagus nerve prevents cytokine production which reduces activation of cells which traffic to the joint

82
Q

immune checkpoint inhibitor

A

PD-L1 on tumor cells

PD-1 on T cells

binding of PD-L1 to PD-1 keeps T cells from killing tumor cells

blocking this binding allows the T cells to kill tumor cells
- can be accomplished by inhibiting either PD-1 OR PD-L1

in the case where it is inhibited, the T cell receptor and antigen bind, but PD-L1 and PD-1 do not

83
Q

chimeric antigen receptor T (CAR-T) cell therapy

A

white blood cells including T cells are separated out and the rest of the blood is returned to patient

T cells are engineered to find and kill cancer cells
- inactive virus inserts genes into T cells
- genes cause T cells to make CARs (special receptors) on their surfaces
- modified T cells are multiplied until there are millions of these attacker cells

CART cells put back into patient’s blood to make space and continue to multiply

CART cells identify the cancer cells with target antigens and kill them; remain in the body to prevent reemergence of cancer

84
Q

CRISPR-editing for allogenic CAR-T therapy

A

knocks out MHC 1 and TCR for prevention of immuno-response

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