Exam 4: Immune System Flashcards

(84 cards)

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
b lymphocytes
antibody-mediated immunity
26
types of immunity
1. physical and chemical barrier 2. innate immune system (all animals possess) 3. adaptive immune system (all vertebrates possess)
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innate immune system
non-specific begins within minutes to hours produces general inflammatory response when pathogens penetrate physical barriers
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adaptive immune system
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"
29
components of the innate immune system
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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macrophages
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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what activates macrophages
chemotaxins: bacterial toxin, cell wall components tissue injury debris: fibrin, collagen fragments chemotactic cytokines by leukocytes
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mechanism of attachment during phagocytosis
patterning recognition receptor to binding binding to antibody hydrophobicity
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patterning recognition receptor to binding
phagocytic cells' patterning recognition receptor can bind bacteria directly by surveilling the pathogen-associated molecular pattern
34
binding to antibody
phagocytic cells can bind the Fc portion of antibody binding of several antibodies on macrophages activates phagocytosis and microbial killing
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hydrophobicity
hydrophobic groups tend to attach to the hydrophobic surface of cells may explain the recognition of damaged cells, denatured proteins, etc
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mechanism of killing and digestion during phagocytosis
lactoferrin oxygen and the oxygen burst nitric oxide (NO)
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lactoferrin
protein that inhibits bacteria by depriving them of iron which it binds with an extremely high affinity
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oxygen and the oxygen burst
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
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complement proteins
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
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functions of complement system
opsonization and phagocytosis lysis agglutination neutralization of viruses chemotaxis activation of mast cells and basophils inflammatory effects
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opsonization and phagocytosis
opsonins are used to tag foreign antigens and strongly activates phagocytosis by both neutrophils and macrophages
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lysis
combination of multiple complement factors can directly rupture the cell membranes of bacteria or other invading organisms
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agglutination
the complement products also change the surfaces of the invading organisms, causing them to adhere to one another promoting agglutination (clumping of particles together)
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neutralization of viruses
complement enzymes and other complement products can attack viruses and thereby render them non-virulent
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chemotaxis
chemical stimulus initiates the movement of neutrophils and macrophages
46
activation of mast cells and basophils
cells become activated which causes them to release histamine, heparin, and several other substances into the local fluids
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inflammatory effects
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
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natural killer cells
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
release of histamine
released by mast cells and basophils initiates inflammatory response induce WBC recruitment from the blood stream
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histamine action
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
adaptive/acquired immune system
two main components fight pathogens outside of cells: b lymphocytes/antibody-mediated immunity fight pathogens inside of cells: t lymphocytes/cell-mediated immunity
52
function of antibodies
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
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b cells
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
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when a b cell binds antigen...
b cells are activated and differentiated into plasma cells plasma cells secrete antibodies at the rate of approximately 2000 molecules per second
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how do T cells identify virus infected cells?
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
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MHC class I molecules
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
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MHC class II molecules
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
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lymphocytes clones and memory effects
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
primary immune response
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
secondary immune response
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
bacteria
cells have membrane and cell wall can survive outside the host can reproduce without a host can be killed or inhibited by antibiotics
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how do bacteria cause disease?
invade the host reproduce and overgrow deplete nutrients, ions, and oxygen secrete organic wastes produce toxins that disturb the normal functions of cells
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immune response to bacteria
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)
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virus
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
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how do viruses cause disease?
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
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immune response to viruses
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
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human immunodeficiency virus (HIV)
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
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COVID 19
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
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mRNA vaccine
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
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sensitization
initial exposure to an allergen
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allergic reaction
secondary exposure to same allergen causes more antibody binding to mast cells for release of histamine
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anti-histamine
decreases vascular permeability decreases bronchoconstriction
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corticosteroids
reduce general inflammatory response
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epinephrine (adrenaline)
constricts blood vessels intramuscular or intravenous injection
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autoimmune disease
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
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multiple sclerosis
white matter of the brain and spinal cord
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rheumatoid arthritis
joint lining
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type 1 diabetes
the pancreas
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lupus
kidneys and other organs
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guillan barre syndrome
peripheral nerves
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rheumatoid arthritis treatment
stimulation of the vagus nerve prevents cytokine production which reduces activation of cells which traffic to the joint
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immune checkpoint inhibitor
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
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chimeric antigen receptor T (CAR-T) cell therapy
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
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CRISPR-editing for allogenic CAR-T therapy
knocks out MHC 1 and TCR for prevention of immuno-response