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BIOL 1260 > week 7 - adapative immunity > Flashcards

week 7 - adapative immunity Flashcards

1
Q

inflammation

A

When your body encounters an offending agent (like viruses, bacteria or toxic chemicals) or suffers an injury, it activates your immune system.

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2
Q

Cite four examples of stressors which may stimulate the inflammatory response.

A

The inflammatory response (inflammation) occurs when tissues are injured by bacteria, trauma, toxins, heat, or any other cause The damaged cells release chemicals including histamine, bradykinin, and prostaglandins. These chemicals cause blood vessels to leak fluid into the tissues, causing swelling

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3
Q

Explain the general purpose(s) of the inflammatory response.

A

The inflammatory response is a defense mechanism that evolved in higher organisms to protect them from infection and injury. Its purpose is to localize and eliminate the injurious agent and to remove damaged tissue components so that the body can begin to heal.

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4
Q

vasodilation

A

the widening of blood vessels as a result of the relaxation of the blood vessel’s muscular walls

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5
Q

vascular permeability during inflammation

A

Increase in vascular permeability is a conclusive response in the progress of inflammatio

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6
Q

chemotaxis

A

Chemotaxis is the process by which phagocytes follow the cytokine “scent” to the infected spot.

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7
Q

fibrin formation

A

Coagulation is initiated by the activation of thrombin, which, in turn, triggers fibrin formation by the release of fibrinopeptides. Fibrin is cleaved by plasmin, resulting in clot lysis

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8
Q

exudate formation

A

Exudates are inflammatory in nature and occur because of vascular permeability caused by the release of inflammatory mediators from the inflamed tissue. Neutrophils are typically the predominant cell type in most exudates, but macrophages and, to some extent, lymphocytes are also increased

Exudate is fluid that leaks out of blood vessels into nearby tissues

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9
Q

fibrinogen

A

a) source/origin of component in the system a glycoprotein complex, produced in the liver
b) stage of the inflammatory process in which it is primarily/ initially involved Stage 4
c) function of the component in the progress of the inflammatory process is the formation of fibrin that binds together platelets and some plasma proteins in a hemostatic plug

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10
Q

monocyte

A

a) source/origin of component in the system Myeloid stem cell
b) stage of the inflammatory process in which it is primarily/ initially involved Stage 2
c) function of the component in the progress of the inflammatory process becomes a macrophage when it leaves blood, engulf pathogens and display on surface

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11
Q

neaurophils

A

a) source/origin of component in the system Myeloid stem cells
b) stage of the inflammatory process in which it is primarily/ initially involved Stage 2
c) function of the component in the progress of the inflammatory process engulf and destroy bacteria and pathogens

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12
Q

postagladnins

A

a) source/origin of component in the system
b) stage of the inflammatory process in which it is primarily/ initially involved Stage 1,4
c) function of the component in the progress of the inflammatory process They control processes such as inflammation, blood flow, the formation of blood clots

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13
Q

kinins

A

a) source/origin of component in the system Urinary tract?
b) stage of the inflammatory process in which it is primarily/ initially involved Stage 1/2
c) function of the component in the progress of the inflammatory process Increase blood flow throughout the body. Make it easier for fluids to pass through small blood vessels.

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14
Q

histamine

A

a) source/origin of component in the system Are screteed from mast cells and basophils
b) stage of the inflammatory process in which it is primarily/ initially involved Stage 1
c) function of the component in the progress of the inflammatory process histamines boost blood flow in the area of your body the allergen affected. This causes inflammation, which lets other chemicals from your immune system step in to do repair work. Histamines then dock at special places called “receptors” in your body

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15
Q

mast cell

A

a) source/origin of component in the system Myeloid stem cell
b) stage of the inflammatory process in which it is primarily/ initially involved Stage 1
c) function of the component in the progress of the inflammatory process Release specific chemicals (histamine) that cause inflammation (increased bloodflow)

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16
Q

Explain the physiological changes which occur to produce each of the following signs/symptoms of local inflammation

A

a) redness the dilation of small blood vessels
b) swelling Some of the chemicals cause fluid to leak into your tissues, resulting in swelling
c) heat small blood vessels in the tissue to become wider (dilate), allowing more blood to reach the injured tissue
d) pain the swelling and buildup of tissue starts pressing against nerve endings
e) loss of function (not always) pain that inhibits mobility or from severe swelling that prevents movement in the area

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17
Q

5 effects of histaimnes

A

a) capillary and arteriolar diameter

increases

b) capillary permeability

increases

c) bronchial smooth muscle movement

constriction of the air passageway

d) activity of sensory nerve endings

Produces itches/pain

e) mucous secretions

increases

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18
Q

antihisatmine

A

a) the definition

Reverse the action of histamine

b) its mechanism of action

relieve symptoms of allergies, such as hay fever, hives, conjunctivitis and reactions to insect bites or stings.

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19
Q

platlete adhension

A

First, platelets contact and stick to damaged parts of blood vessels, such as collagen (which will now be exposed, they were on the opposite side of the endothelium Adhesion activates the platelets, and they change appearance and activity dramatically

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20
Q

plalete release reaction

A

They start forming projections that allow them to attach to each other, and they also begin to release their vesicles.

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21
Q

platlete plug, BLOOD COAGULATION

A

So all of the platelets in the area are activated thanks to the signals being released. And they all stick together and aggregate, forming a plug.The plug of course, limits blood loss

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22
Q

coagykation

A

the action or process of a liquid, especially blood, changing to a solid or semi-solid stat

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23
Q

5. Use the following outline to begin a description of the three stages of the clotting mechanism:

A

Extrinsic pathway Plasma Tissue damage————— > prothombinase (prothrombin activator)

Coagulation Factors Intrinsic pathway Platelet Factors Platelet damage ————— > prothrombinase (prothrombin activator) Plasma Coagulation Factors

STAGE II Prothrombinase Prothrombin ———————- > Thrombin

STAGE III Thrombin Fibrinogen ———————— > Fibrin

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24
Q

contents in platlet cytoplasm

A

Platelets contain dense granules, lambda granules and alpha granules

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25
Q

platlets in blood clotting

A

a) site of formation/origin/source of substance

Platelets, also called thrombocytes, are derived from megakaryocytes, which are derived from stem cells in the bone marrow

b) stage(s) of clotting mechanism in which it plays a role

1

c) function in the clotting mechanism

Your platelets will clot (clump together) to plug the hole in the blood vessel and stop the bleeding.

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26
Q

issue thromboplastin

A

a) site of formation/origin/source of substance

usually derived from placental sources

b) stage(s) of clotting mechanism in which it plays a role

2

c) function in the clotting mechanism

catalyzing the conversion of prothrombin to thrombin.

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27
Q

prothrombinase (prothrombin activator)

A

a) site of formation/origin/source of substance

Thrombin activation occurs on the surface of activated platelets

b) stage(s) of clotting mechanism in which it plays a role

2

c) function in the clotting mechanism

catalyzes the conversion of prothrombin to thrombin

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28
Q

prothrombin

A

a) site of formation/origin/source of substance

Produced in liver

b) stage(s) of clotting mechanism in which it plays a role

3

c) function in the clotting mechanism

acts to transform fibrinogen, also present in plasma, into fibrin

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29
Q

thrombin

A

a) site of formation/origin/source of substance

Prothrobinase,tissue throboplasmis

b) stage(s) of clotting mechanism in which it plays a role

3

c) function in the clotting mechanism

converts fibrinogen to fibrin

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30
Q

fibrinogen

A

a) site of formation/origin/source of substance

mainly synthesized by hepatocytes

b) stage(s) of clotting mechanism in which it plays a role

3

c) function in the clotting mechanism

helps to form a stable blood clot at the site of vascular disruption

31
Q

fibrin

A

a) site of formation/origin/source of substance

Formed from fibrinogen

b) stage(s) of clotting mechanism in which it plays a role

3

c) function in the clotting mechanism

forms a hemostatic plug or clot over a wound site.

32
Q

calicum

A

a) site of formation/origin/source of substance

bone

b) stage(s) of clotting mechanism in which it plays a role

1

c) function in the clotting mechanism

responsible for complete activation of several coagulation factors, including coagulation Factor XIII (FXIII)3

33
Q

viatmin k

A

a) site of formation/origin/source of substance

Leafy foods

b) stage(s) of clotting mechanism in which it plays a role

1-3

c) function in the clotting mechanism

Vitamin K helps to make four of the 13 proteins needed for blood clotting

34
Q

thrombus

A

a blood clot that forms in a vessel and remains there

35
Q

embolus

A

anything that moves through the blood vessels until it reaches a vessel that is too small to let it pass. When this happens, the blood flow is stopped by the embolus. An embolus is often a small piece of a blood clot that breaks off

36
Q

anticoagulant therapy

A

Anticoagulant therapy is used prophylactically and/or to treat intravascular clotting problems by decreasing the coagulation of the blood.

37
Q

asprin as an anitplalete

A

a) how it is administered

spirin can be administered via the oral, rectal, and intravenous (IV) route

b) site and type of action

reduce the signs and symptoms of inflammation

Works by irreversibly inhibiting the enzyme cyclo-oxygenase (COX-1) which is required to make the precursors of thromboxane within platelets. This reduces thromboxane synthesis. Thromboxane is required to facilitate platelet aggregation and to stimulate further platelet activation.

c) most common undesirable effects of its use

May cause extra bleeding

38
Q

tissue-plasminogen activator

A

a) when and how it is administered

IV, within hours of when stroke symptoms start

b) site and type of action

it works by dissolving blood clots that block blood flow to the brain

c) most common undesirable effects of its use

Extra bleeding

39
Q

phaogens

A
  1. Phagocytes must be able to adhere to a pathogen before it can engulf it; to counteract this, pathogens are coated with complement proteins called opsonins.
  2. Neutrophils and macrophages destroy pathogens by engulfing them, acidifying the phagolysosome (pathogen-containing vesicles associated with a lysosome within the phagocyte), and digesting the contents with lysosomal enzymes.
  3. When phagocytes cannot ingest their targets, they may release chemicals lethal to pathogens.
40
Q

natural killer cell

A

Natural killer cells are able to lyse and kill cancer cells and virally infected cells before the adaptive immune system has been activated, and they secrete chemicals that enhance the inflammatory response.

41
Q

inflammation

A
  1. Inflammation is beneficial because it prevents the spread of damage, disposes of debris and pathogens, alerts the adaptive immune system, and sets up repair.
  2. The four cardinal signs of acute inflammation are redness, heat, swelling, and pain.
  3. Inflammation results from the release of inflammatory chemicals from damaged cells that cause vasodilation, and increased capillary permeability, which allows fluid containing clotting factors and antibodies to enter the tissues.
42
Q

after inflammation

A

a. Injured cells produce leukocytosis-inducing factors that induce neutrophils to enter the blood from the bone marrow, increasing their number.
b. Inflamed endothelial cells produce CAM proteins that mark the cell—a process called margination.
c. Continued signaling causes diapedesis, in which neutrophils squeeze into the tissues between endothelial cells of the capillary walls. d. Inflammatory chemicals create chemical trails that encourage chemotaxis of neutrophils and other WBCs into the site of damage.

43
Q

anitmricobial protein

A

Antimicrobial proteins enhance the innate defenses by attacking microorganisms directly or by hindering their ability to reproduce.

  1. Interferons are small proteins produced by virally infected cells that help protect surrounding healthy cells by causing synthesis of proteins that interfere with viral replication.
  2. Complement refers to a group of about 20 plasma proteins that provide a major mechanism for destroying foreign pathogens in the body.
    a. Three pathways by which complement can be activated are: the classical pathway, involving antibodies to bind pathogens and complement; the lectin pathway, in which lectin proteins bind to sugars on the surface of the microorganism, and then bind to and activate complement; and the alternative pathway, triggered when complement factors interact on the surface of microorganisms.
44
Q

fever

A

Fever, an abnormally high body temperature, is a systemic response to microorganisms.

  1. Pyrogens produced by leukocytes and macrophages act on the hypothalamus, causing a rise in body temperature.
45
Q

3 aspect of adpative immune response

A

There are three important aspects of the adaptive immune response:

  1. The adaptive defenses recognize and destroy the specific antigen that initiated the response.
  2. The immune response is a systemic response; it is not limited to the initial infection site.
  3. The immune system has memory; after an initial exposure, the immune response is able to recognize the same antigen and mount a faster and stronger defensive attack.
46
Q

humoral immunity

A

Humoral immunity is provided by antibodies produced by lymphocytes present in the body’s “humors” or fluids.

47
Q

cellular immunity

A

Cellular immunity is based on direct attack of microorganisms by lymphocytes and has living cells, rather than free proteins, as its protective factor.

48
Q

antigen

A

Antigens are substances that can mobilize the adaptive responses, and are the targets of all adaptive immune responses.

  1. Complete antigens have immunogenicity, the ability to stimulate the proliferation of specific lymphocytes and antibodies, and reactivity, the ability to react with the activated lymphocytes and antibodies.
  2. Haptens are incomplete antigens that are not capable of stimulating the immune response, but if they interact with proteins of the body, they may be recognized as potentially harmful.
49
Q

antigenic determinants

A

Antigenic determinants are a specific part of an antigen that are immunogenic and bind to free antibodies or activated lymphocytes

50
Q

self anitgens

A

Self-antigens are the body’s antigens that are not antigenic to itself, only to others, and are identified as “self” by MHC (major histocompatibility complex) proteins on the surface of cells.

51
Q

lymphocytes

A

Lymphocytes originate in the bone marrow and, when released, become immunocompetent and self-tolerant in either the thymus (T cells) or the bone marrow (B cells).

  1. Lymphocytes undergo selection in order to gain immunocompetence, the recognition of specific antigens, and self-tolerance, ensuring attack on the body’s own cells is prevented, by being subjected to:
    a. Positive selection, which allows only T lymphocytes that recognize MHC proteins to survive.
    b. Negative selection, which selects for T cells that do not recognize self-MHC proteins
52
Q

immunocompetnent B and T cells

A

Immunocompetent B and T cells are exported from the primary lymphoid organs, the thymus and bone marrow, to colonize the secondary lymphoid organs, such as the spleen and lymph nodes

The first encounter between a lymphocyte and antigens usually occurs in secondary lymphoid organs.

Antigen binding with a particular lymphocyte selects that lymphocyte for further development, a process called clonal selection.

53
Q

clonal selection cont.

A

Once activated by clonal selection, a lymphocyte divides, producing an entire group of lymphocytes with an identical ability to bind to a given antigen.

a. Most members of the clone become effector cells that actively fight the infection.
b. A few members of the clone become memory cells that will respond quickly to future encounters with this antigen.

Genes within lymphoid stem cells determine which foreign substances our immune system can attack and destroy by coding for a specific set of pieces that can be combined in different ways to form a variety of antigen receptor sites.

54
Q

Antigen-presenting cells (APCs)

A

Antigen-presenting cells (APCs) are responsible for activating T cells, by engulfing antigens and presenting fragments of these antigens on their surfaces, where they can be recognized by T cells.

  1. Dendritic cells are APCs located on body surfaces that have contact with the external environment: They phagocytose antigens and migrate to lymphoid organs to present antigens to T cells.
  2. Macrophages are found throughout lymphoid organs and connective tissues and present antigens to T cells in order to be activated by T cells into aggressive phagocytes.
  3. B lymphocytes present antigens to helper T cells, in order to become more fully activated B cells.
55
Q

when are B lymhocytes activated?

A

The immunocompetent but naive B lymphocyte is activated when antigens bind to its surface receptors.

  1. The activated B lymphocyte begins clonal selection, the process of the B cell growing and multiplying to form an army of cells that are capable of recognizing the same antigen.
  2. Most cells of the clone develop into plasma cells, the antibody-secreting cells of the humoral response.
  3. The cells of the clone that do not become plasma cells develop into memory cells.
56
Q

primary immune response

A
  1. The primary immune response occurs on first exposure to a particular antigen, with a lag time of about 3–6 days.
    a. After mobilization, the antibody titer in the blood rises, peaking in about 10 days, and then declines to a low level.
57
Q

secondary immune response

A

The secondary immune response occurs when someone is exposed to the same antigen for a second time, and is a faster, more prolonged, more effective response.

a. Mobilization of B cells takes only a few hours and rises to a much higher peak concentration after only 2–3 days, producing antibodies with a much higher binding affinity for the antigen that may persist for weeks or months

58
Q

active immunity

A

Active immunity occurs when the body mounts an immune response to an antigen.

a. Naturally acquired active immunity occurs when a person suffers through the symptoms of an infection.
b. Artificially acquired active immunity occurs when a person is given a vaccine.

59
Q

passive immunity

A

Passive immunity occurs when a person is given preformed antibodies.

a. Naturally acquired passive immunity occurs when a mother’s antibodies enter fetal circulation.
b. Artificially acquired passive immunity occurs when a person is given preformed antibodies that have been harvested from another person.

60
Q

anitbody structure

A

The basic antibody structure consists of four looping polypeptide chains: two identical heavy (H) chains, and two identical, shorter, light (L) chains.

a. Each chain has a variable region at one end, which varies depending on the antigen it binds, and a constant region at the other end, which is nearly identical among all members of a given class of antibodies.

61
Q

5 classses of antibodies

A

Antibodies are divided into five classes based on their structure: IgM, IgG, IgA, IgD, and IgE.

62
Q

Antibody Targets and Functions

A

a. Neutralization occurs when antibodies block specific sites on viruses or bacterial exotoxins, causing them to lose their toxic effects.
b. Agglutination occurs when antibodies cross-link to antigens on cells, causing clumping.
c. Precipitation occurs when soluble molecules are cross-linked into large complexes that settle out of solution.
d. Complement activation occurs when complement binds to antibodies attached to antigens and leads to lysis of the cell.

63
Q

two types of T cells

A

There are two major populations of T cells, based on which of the cell differentiation glycoproteins the mature cell displays: CD4 cells and CD8 cells.

  1. Activated CD4 cells usually become helper T cells that activate B cells, T cells, and macrophages; some become regulatory T cells that moderate the immune response.
  2. Activated CD8 cells become cytotoxic T cells that destroy cells or other foreign substances.
64
Q

MHC (major histocompatibility complex) proteins

A

Antigen presentation through the use of MHC (major histocompatibility complex) proteins is necessary for both activation and normal functioning of T cells.

  1. Class I MHCs are found on all body cells except RBCs and display antigens synthesized from within the cell or, if infected, the MHCs may also include fragments of foreign antigens.
  2. Class II MHCs are antigens arising from outside the cell that are engulfed by the displaying cell.
  3. CD4 cells bind antigens only on class II MHC proteins; CD8 cells are activated by antigen fragments on class I MHCs, and may bind this antigen on any cell in the body.
65
Q

Activation and Differentiation of T Cells

A
  1. When T cell antigen receptors bind an antigen, the cell must accomplish a double recognition process: It must recognize both the MHC protein and the antigen it displays.
  2. Following antigen binding, a T cell must bind one or more co-stimulatory signals present on the antigen-presenting cell.
  3. Once activated, a T cell enlarges and proliferates to form a clone of cells that differentiate and perform functions according to their T cell class.
  4. Cytokines are chemical signals, such as interferons, secreted to amplify the immune response.
66
Q

roles of specific t cells

A
  1. Helper T cells stimulate proliferation of other T cells and B cells that have already become bound to antigen.
  2. Cytotoxic T cells are the only T cells that can directly attack and kill other cells displaying antigen to which they have been sensitized, through the use of perforins and granzymes, or by triggering apoptosis of the target cell.
  3. Regulatory T cells either by direct inhibition, or by causing the release of cytokines, suppress the activity of both B cells and other types of T cells.
67
Q

organ transplant and chance of rejection

A
  1. The goal of organ transplantation is to provide patients with a functional organ from a living or deceased donor.
  2. Transplant success depends on the similarity of the tissues because cytotoxic T cells, NK cells, and antibodies work to destroy foreign tissues.
  3. Allografts, the most common type of transplant, are grafts transplanted from individuals of the same species.
  4. Immunosuppressive therapy following the transplant uses drugs to suppress rejection, but results in a weakened immune system.
68
Q

immmunodeficiencies

A

Immunodeficiencies are any congenital or acquired conditions that cause immune cells, phagocytes, or complement to behave abnormally.

  1. Severe combined immunodeficiency (SCID) is a congenital condition that produces a deficit of B and T cells.
  2. Acquired immune deficiency syndrome (AIDS) cripples the immune system by destroying helper T cells, and ultimately impairing T and B lymphocyte functioning.
69
Q

autoimmune diseases

A

Autoimmune diseases occur when the immune system loses its ability to differentiate between self and nonself and ultimately destroys itself.

  1. Autoimmune disorders are treated by suppressing the entire immune system, either by blocking cytokines, or co-stimulatory factors.
  2. Failure of self-tolerance occurs when weakly self-reactive lymphocytes are activated when foreign antigens resemble self-antigens, or new self-antigens appear.
70
Q

hypersensititvies

A

Hypersensitivities result when the immune system causes tissue damage as it fights off a perceived threat that would otherwise be harmless.

  1. Immediate hypersensitivities (acute, or type I hypersensitivities), or allergies, begin within seconds after contact and last about half an hour.
    a. The initial contact produces no symptoms, but sensitizes the individual to the allergen.
    b. Subsequent contact with the same allergen results in immediate binding of the allergen to IgE antibodies on mast cells and basophils, causing a release of histamine, and promotion of inflammation.
71
Q

subacute hypersensitivities

A

Subacute hypersensitivities are caused by antibodies, take 1–3 hours to occur, and last 10–15 hours.

a. Cytotoxic (type II) reactions occur when antigens bind to antigens on specific body cells and cause phagocytosis and complement-mediated lysis of cellular antigens.
b. Immune complex (type III) hypersensitivities result when antigens are widely distributed in the body, and form large numbers of insoluble antigen-antibody complexes that cannot be cleared from an area.

72
Q

delayed hypersensitivity

A

Delayed hypersensitivity reactions are caused by T lymphocytes, activated when chemicals diffuse through the skin and bind to haptens, and can take 1–3 days to occu

73
Q

where do stem cells orginate

A

Stem cells of the immune system originate in the liver and spleen during weeks 1–9 of embryonic development; later, the bone marrow takes over this role.

74
Q

when do lymphocytes develop

A

In late fetal life and shortly after birth, lymphocytes develop immunocompetence in the thymus and bone marrow, and then populate other lymphoid tissues.

BIOL 1260 (14 decks)

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