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A&P 2 > Immune system > Flashcards

Immune system Flashcards

1
Q

1st line of defense

A

surface barriers: skin, mucous membranes

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2
Q

2nd line of defense

A

internal defenses: cells, inflammation, proteins (interferons, complement), fever

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3
Q

3rd line of defense

A

adaptive/specific system

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4
Q

mucous membranes defenses

A

acidity, HCl in stomach, lysosyme enzyme in saliva and most fluids, mucin

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5
Q

3 types of phagocytes

A

macrophages
dendritic (free floating)/Kupffer (fixed)
neutrophils

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6
Q

steps of phagocytosis

A

i. Adherence: phagocyte adheres to pathogens or debris. Certain pathogens are able to allude adherence due to lacking receptors or having a certain chemical structure. In these cases phagocytes can put a handle on the cell and then grab the handle to pull them in “opsonization”.
ii. Phagocyte forms pseudopods that eventually engulf the particles, forming a phagosome (phagocytic vesicle that is inside the phagosome and contains the pathogenic particles).
iii. Lysosome filled with enzymes and chemicals fuses with the phagocytic vesicle forming a phagolysosome.
iv. Enzymes digest the pathogenic particles, leaving residues.
v. Exocytosis of the vesicle removes the residual material from inside the phagocyte.

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7
Q

respiratory/oxidative burst

A

vi. Some pathogens are too large or too severe to be phagocytized, instead a respiratory/oxidative burst is used where chemicals similar to bleach/peroxide are released to kill these pathogens. This usually kills the phagocytes in the process.

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8
Q

NK cells

A

type of lymphocyte

ii. Functions: looks for “not self” on the flag and destroy it
iii. Mechanism of destruction: similar to cytotoxic T-cells but not specific. Cytotoxic which damages the cell membrane. Granzymes cause cells to undergo apoptosis

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9
Q

functions of inflammation (4)

A

prevents spread, alerts adaptive immune system, disposal of debris, preparation for repair

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10
Q

inflammation mechanism of activation

A

i. Pattern recognition receptor (toll like receptors) activate
ii. Cytokines which impact another type of cell.
iii. Histamines are released: vasodilation, increases bloodflow. Also increases capillary permeability.
iv. Kinins and prostaglandins do the same thing that histamines do. Kinins also increases sensitivity to pain.
v. 20 proteins are activated “complement”.
vi. Vasodilation causes hyperemia: “a lot of blood”/redness and heat

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11
Q

viii. Leukocytosis-inducing factor (inflammation)

A

increases WBC and make them migrate to injury

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12
Q

margination

A

WBC cling to capillary walls

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13
Q

what helps WBC know where to exit the capillary

A

cellular adhesion molecules and Chemotaxins: cellular debris leading the phagocytes to the right location

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14
Q

selectins and integrins

A

xi. Endothelial tissue near the injury will sprout selectins which are cellular adhesion molecules.
xii. Phagocytes also sprout cellular adhesion molecules called integrins

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15
Q

pus

A

cellular debris in the interstitial fluid all mixed together

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16
Q

5 cardinal signs of inflammation

A
  1. Redness
  2. Heat
  3. Swelling
  4. Pain
  5. Impairment
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17
Q

interferon functions

A

: block protein synthesis and thus virus activity, activate macrophages and NK

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18
Q

complement 3 mechanisms of activation

A

all activate C3 (the common pathway)

ii. Classical pathway: activated by antibodies.
iii. Lectin pathway: activated by lectin binding to specific sugars on organism’s surface.
iv. Alternative pathway: activated spontaneously when lack of inhibitors on microorganism’s surface allows process to proceed.

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19
Q

common pathway results (OIL)

A
  1. Opsonization: coats pathogen surfaces which allows for phagocytosis through adherance.
  2. Enhances inflammation—more vasodilation, permeability, attraction of leukocytes
  3. Lysis: Membrane Attack Complex(MACs) insert into the target cell membrane, creating pores which allow for lysis (destruction) of the cell
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20
Q

fever function

A

a. increase body temp tends to inhibit pathogen activity. Also causes the liver to hold on to zinc and magnesium which are minerals that many pathogens depend on for replication.

21
Q

fever mechanism

A

): hypothalamus sets the “thermostat” higher when an infection is detected: pyrogen secretion causes this. Body increases its temperature mainly via shivering. Shivering happens through contraction of skeletal muscles, and because muscles are inefficient, 60% of the energy that goes into it is let out as heat. Defervescence is the body temperature returning to normal by pyrogen going away, causing the hypothalamus to order the body to start sweating.

22
Q

3 characteristics of adaptive system

A
  1. Specific: good guy A only looks for bad guy A instead of self/not self
  2. Systemic: the response is systemic, through the whole body, not local
  3. Memory:
23
Q

humoral immunity

A

fluid, B cells (B lymphocytes)

24
Q

where are B cells produced and educated and hang out

A

produced and educated in red marrow, hang out in lymph

25
Q

activation of B cells

A

a. They are activated when they encounter a cell they are specifically taught to protect against. They turn into a plasma cell and start producing antibodies at a very high rate. 2000 antibodies per second for 4-5 days.

26
Q

naive B cells

A

a B cell that has never encountered their designated bad guy. When they bind to their antigen they are activated and two cells are formed: plasma cells and memory cells

27
Q

effector B cells

A

plasma cells

28
Q

primary response and secondary response difference in antibody levels

A

v. Primary response: antibody levels rise for 3-6 days, peak after 10. Secondary response: levels rise for 2-3 days, last for weeks to months.

29
Q

active humoral immunity

A

naturally acquired (infection), artificially acquired (vaccine—dead or attenuated pathogens)

30
Q

passive humoral immunity

A

naturally (antibodies passed from mother to fetus), artificially (injection of exogenous antibodies (gamma globulin). Passive means no cellular immunity as the antibodies are not being produced by the innate cells

31
Q

antibodies aka

A

immunoglobulins

32
Q

structure of antibodies

A

shaped like a Y. The “hands” of the Y are what binds to the antigen. The variable regions are the hands, and they can take on tons of different sequences, which is why we can have antibodies for so many different pathogens. The stem, non variable region dictates what class the antibody belongs to.

33
Q

5 classes of antibodies

A
  1. IgM: released when the first exposure happens
  2. IgG: most abundant and passed from mom to fetus. After the second exposure and towards the last stage of the first exposure.
  3. IgA: found in secretions and mucus—this is what’s passed on through breast feeding.
  4. IgD: bound to B cells
  5. IgE: allergic response
34
Q

role of antibodies PLAN

A
  1. Precipitation (soluble antigens): cling to antigens and link them together into large, heavy molecules that fall out of the solution and sink to the bottom, often the wall of a blood vessel where they can’t escape macrophages and other innate immune cells.
  2. Lysis (complement)
  3. Agglutination: reaction between an antigen and antibody (clumping).
  4. Neutralization: Masks dangerous parts of bacterial exotoxins and viruses.
35
Q

cellular immunity

A

T cells

36
Q

where T cells formed and educated

A

a. Formed in the red marrow but educated in the thymus

37
Q

steps of education for T cells

A

i. Positive selection: recognizing self-MHC. If they fail this test it results in apoptosis. If they pass the test they survive and proceed to negative selection.
ii. Negative selection: must NOT recognize self-antigen, this eliminates self-reactive T cells that could cause autoimmune diseases. Failure to recognize (bind tightly to) the self antigen results in survival and continued maturation. Out of 100 cells only 2 make it to “graduation” (immunocompetency). Upon achieving immunocompetency it sprouts 10,000 to 100,000 receptors that are specific to an antigen.

38
Q

types of T cell

A

i. CD4: naïve cell before it’s activated, becomes a receptor on a helper T cell when activated. “run the show”, don’t actually kill
ii. CD8: receptor on cytotoxic T-cells, kill pathogens similar to NK cells
regulatory/suppressive: temporarily slow down immune response to monitor the activity and see if we can stop fighting.

39
Q

class 1 MHCs

A

found on all nucleated cells. Flags say “I’ve been invaded or cancerous, kill me and all the ones that look like me!”. recognized by innate system and naive CD8 and cytotoxic T cells

40
Q

class 2 MHCs

A

found on APCs. Flags say “I’ve captured a foreign invader, this is what it looks like, help me mount a defense”. recognized by naive CD4 and helper T cells

41
Q

activation of T cells

A

c. APC that’s engulfed a pathogen will bind with a CD4 T cell that recognizes the antigen. Both CD4 protein and TCR bind to antigen-MHC.
d. Co-stimulation: “putting the car into gear” must occur for reaction to happen. Two co-stimulatory proteins bind together. Cytokines are released after co-stimulation occurs.

42
Q

anergy

A

a partially activated helper T cell where binding has happened but not co-stimulation.

43
Q

interleukins

A

e. An example of a cytokine is an interleukin, which facilitates communication between immune cells. Interleukins released after co-stimulation will induce helper T cell proliferation. Interleukins also activate B cells and tell them to start producing antibodies. They also activate cytotoxic T cells (CD8) and tell them to start killing the pathogens.

44
Q

antigenic determinants

A

different “shapes” on an antigen that different antibodies can bind with. The more different antigenic determinants an antigen has, the more reactive it is, the bigger the immune response.

45
Q

MHC

A

major histocompatibility complex, “flagpole”

46
Q

complete vs incomplete antigen

A
  1. A complete antigen has two characteristics: it causes antibodies to be formed (immunogenicity), and it’s reactive. An incomplete antigen lacks one of these. An incomplete antigen may become immunogenic when it binds to a specific protein
47
Q

hapten

A

an incomplete antigen. Ex: poison ivy. It isn’t reactive on the first exposure when antibodies start forming, but on the second exposure there is already antibodies so there is a reactive response

48
Q

APC

A

antigen presenting cells

  1. They have a specialized MHC and are able to phagocytize pathogenic cells and then display a piece of the pathogen on their flagpole. The APC go to the T lymphocytes and communicate what pathogen has infected us, so the T cells can mount an attack.
  2. Types: dendritic, Langerhans, macrophages, B cells
49
Q

4 types of hypersensitivity

A

i. Type 1 anaphylactic: IgE on mast and basophils
ii. 2 cytotoxic: cell attacks antibodies (blood reaction)
iii. 3 antigen-antibody complex (eludes phagocytosis)
iv. 4 delayed, cell mediated

A&P 2 (8 decks)

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