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BIOL 440 > Exam 4 > Flashcards

Exam 4 Flashcards

1
Q

What kind of defense is skin and how does it protect against infection?

A

first line of innate defense

  1. physical barrier: cannot enter unless cut, collagen helps prevent jabs
  2. chemical factors: has low pH, salt, lysozyme - breaks down cell walls
  3. competition with normal bacteria/microbial antagonism
  4. epidermal dendritic cells - nonspecific phagocytosis - fingerlike projections that intercept invaders
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2
Q

What kind of defense do mucous membranes serve as and what are some examples?

A

first line or innate defense - contains tightly packed epithelial cells in thin layer

  • mucous traps pathogens
  • dilated cells clear mucus from respiratory system
  • lysozyme in nasal mucous
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3
Q

What are some other first line defenses against infection?

A

stomach - low pH in gastric juice prevents most microbial growth

lacrimal glands - tears remove pathogens and contain lysozyme

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4
Q

Define plasma and formed elements

A

plasma - liquid portion of blood that contains complement proteins and immunoglobulins - important for host defense

formed elements - cells and cell fragments
- includes RBC, leukocytes (WBC) and platelets

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5
Q

define hematopoiesis. What do lymphoid turn into? What to myeloids turn into?

A

development of stem cells in bone marrow to formed elements - RBC, platelets and leukocytes
- differentiation due to chemical signals called cytokines

lymphoid - lymphocyte - specific defense

Myeloid - turns into 4/5 leukocytes (besides lymphocyte) and platelets

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6
Q

What are the leukocytes?

A
  1. Neurtrophil - most common
  2. Monocyte - float in blood, can turn into macrophage
  3. Eosinophil - binds to eosin
  4. Lymphocyte - NK lymphocytes function in innate defense
  5. Basophil - associated with allergies/common cold
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7
Q

What are the steps of phagocytosis?

A
  1. chemotaxis - attraction of phagocytes to microorganism due to chemotactic factors that attract leukocyte
  2. adherence - attachment of phagocyte to microorganism - binding of complementary chemicals and opsonization increasing binding sites
  3. ingestion - engulfment of microorganisms by endocytosis - creates phagosome (food vesicle)
  4. digestion - breakdown pf microorganism in phagolysosome
  5. elimination - exocytosis of undigested remnants of microorganism
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8
Q

what is the complement cascade?

A

set of serum proteins that are important for directing a rapid host defense
three pathways - classical, alternative and lectin

outcomes - opsonization and phagocytosis

  • membrane attack complex and cell lysis of invading microbes
  • inflammation

all pathways meet at C3 protein and splits it into C3a and C3b

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9
Q

What is the classical pathway for the complement cascade

A

initiated by antibodies bound to the microbe

  • bind to antigen, produces complement 1,2,4 proteins
  • activated C3b for opsonization
  • activates C3a, C4a, and C5a for inflammation
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10
Q

what is the alternative pathway for complement cascade

A

initiated by microbial cell wall polysaccharides that interact with factors B, D, P

  • works with Cb3 on cell wall and splits more C3
  • C3b accumulates and works as an opsonin
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11
Q

what is the lectin pathway of the complement cascade

A

initiated by lectin binding to mannose on fungi, bacteria and viruses
- begins series of enzyme activities as in the classical pathway

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12
Q

what are the outcomes of a complement cascade?

A
  1. opsonization - microbes are covered by antibodies and C3b complement proteins that enhance phagocytosis
  2. inflammation - stimulates chemotaxis of leukocytes
    - stimulates basophils and mast cells to release histamine
    - involved C3a, C4a, C5a
  3. membrane attack complex (MAC) - cytolysis
    - complement proteins form a hole in microbe membrane
    - involved C5b, C6, C7, C8, C9: complement fixation
  4. inactivation of complement - occurs quickly, breakdown of activated complement
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13
Q

What is the role of interferon type 1?

A

alpha and beta interferon is produced by virus infected cells

  • stimulates other cells to make antiviral proteins (AVP) that destroy protein production in cell so that the virus cannot be replicated
  • when second cell is infected with virus, AVP is activated and stops protein synthesis
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14
Q

what is an interferon?

A

a protein molecule released by a host cell to nonspecifically inhibit the spread of viral infections

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15
Q

what is the role of interferon type 2?

A

gamma interferon - “macrophage activation factor” for phagocytosis

  • produced by activated T and NK lymphocytes
  • NK - natural killer - can kill some tumor, releases cytokines
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16
Q

what are the 4 symptoms of inflammation? what is the function of inflammation?

A

redness (rubber), edema (swelling), pain (dolor), localized heat (calor)

can confine and/or destroy harmful agent (microbe, physical/chemical agent)

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17
Q

What are the steps of inflammation?

A
  1. tissue injury - pressure due to inflammation
  2. vasodilation - increase blood vessel diameter
    - caused by histamine release from mast cells and basophils
    - prostaglandin and leukotrienes increase permeability of blood vessels - allows for phagocytes to move n and delivery of antimicrobial chemicals
    edema - accumulation of fluids around injury site
    - allows for host defense cells to reach infection site
    - causes pressure on nerve endings - pain
  3. phagocyte migration and phagocytosis
    - margination: attachment of leukocytes (neutrophils and monocytes) to blood vessel endothelium
    - diapedesis - leukocytes squeeze between cells of blood vessel and move toward injury site
  4. clotting factors accumulate to confine injury
  5. tissue repair
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18
Q

What are the advantages that fever gives the host?

A
  • increased body temperature is above optimum for pathogens and slows their growth
  • increased rate of chemical reactions in body to fight microbes
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19
Q

what are the chemical signals for a fever?

A
  • microbial products of exogenous pyrogens
  • phagocytes released endogenous pyrogens (IL1)
  • pyrogens cause hypothalamus to release prostaglandins
  • prostaglandin reset hypothalamus at higher temperature and results in fever
  • nerve impulse cause shivering, higher metabolic rate and inhibition os sweating and vasoconstriction
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20
Q

What is immunity and who can perform it?

A

the agility of an organism to resist specific foreign organisms or substances
- performed by vertebrates only

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21
Q

In specific immunity what are the two types?

A
  1. humoral - antibody mediated immunity
    - antibodies made by B cells circulate in the plasma and attack extracellular pathogens and toxins
  2. cell-mediated - carried out by t cells
    - involves cell-cell interactions that attack intracellular pathogens
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22
Q

What are the primary lymphoid organs?

A 
bone marrow (B cell development)
- all cells in immune system are derived rom the stem cells in the bone marrow

thymus (T cell development)

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23
Q

what are the secondary lymphoid organs?

A

tonsils, spleen, lymph nodes
- lymph nodes located at neck, groin axilla and abdomen and facilitates interaction between immune cells and body material (through medulla)

MALT - mucosal associated lymphoid tissue - contains most of the odds lymphocytes

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24
Q

what are antibodies

A

proteins found in blood serum - secreted immunoglobulin that is involved in specific immunity
- has high specificity to specific antigen

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25
Q

what is an antigen and what are some variables that affects its ability to cause a response

A

substance that causes an immune response

shape, seize and complexity

  • bigger/more complex = more epitopes = better antigen
  • can be too small to be detected for immune response
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26
Q

what is an epitopes

A

the specific part of the antigen that is recognized by the immune system - makes antibodies that respond to it
- can change over time - ex. why we need new flu vaccine

27
Q

how do eosinophils kill pathogens without phagocytosis?

A

secrete antimicrobial chemicals against pathogens that are too large to inject like parasitic worms, also binds to LPS to form barrier that kills Gram -

28
Q

how do NK lymphocytes kill pathogens without phagocytosis?

A

secretes toxins into surface of virally infected cells and neoplasms

29
Q

how do neutrophils kill pathogens without phagocytosis?

A

enzyme in CM can make O2-, H2O2, hypochlorite
enzyme makes NO and triggers inflammation
extracellular traps (NET) - fibers from cell suicide traps Gram -/+

30
Q

what is the structure of an antibody

A

variable region - antigen binding site - binds specifically to epitope

Fc - heavy chains - determines what type of antigen - held together by disulfide bonds

light chains also held to heavy chain by S-S

31
Q

what are some ways that antibodies kill pathogens?

A
  1. agglutination - clumping of pathogenic agent to hinder it from harming host and increasing chance of phagocytosis
  2. neutralization - bind to critical point of toxin so that it can no longer function against the host
  3. opsonization - antibodies bind to pathogenic agent by Fc receptor to stimulate phagocytosis
  4. antibody-dependent cellular cytotoxicity - ADCC
    - Fc region binds to NK cells causing it to lyse cell target by releasing proteins into it
    - perforin: forms tubular structure in target CM
    - granzyme - enters cells and triggers apoptosis
32
Q

describe IgG antibodies

A

most common
best at getting into extracellular spaces
can cross placenta from mother to fetus
involved in complement activation, opsonization, neutralization, ADCC and inflammatory response

33
Q

describe IgM antibiodies

A

1st antibody secreted by activated B lymphocyte in response to antigen
pentameter structure - unable to cross placenta
most efficient at complement activation and involved in agglutination and neutralization

34
Q

describe IgA antibodies

A

found in mucous membranes and body secretions
- tear ducts, mammary glands, mucous membranes, breast milk, saliva
agglutinates and neutralizes
J chain and secretory components keep IgA in mucous membranes

35
Q

describe IgE antibodies

A

mostly a signaling molecule
present in small amounts of blood serum
involved in allergic response
defense against parasitic worms

36
Q

describe a B cell receptor

A

antigen receptor that contains two antigen binding sites identical to binding sites of secreted antibody

  • specific to each epitope, only one epitope per B cell
  • ability to respond to 10^9 antigens
37
Q

what happens when an epitope binds to a BCR

A
  1. B cell divides and secretes antibodies into blood and lymph
  2. plasma cells and antibodies act against same original epitope
  3. plasma cells no longer present BCR and secrete antibodies - affinity to antigen gets progressively better
  4. also produces memory cells that can remain in suspended animation for months/years n lymph tissue
38
Q

describe the differences between a primary and secondary specific immune response

A

primary - small amount of antibodies formed over days to weeks

secondary - large amounts of antibodies due to clones, response much quicker than primary response

  • immune system ready
  • memory cells makes IgG and IgM faster and stronger
39
Q

what is apoptosis?

A

programmed cell death

  • B and T cells unstimulated by antigen will go through
  • B ant T cell that are stimulated by self antigen will go through
40
Q

what is tolerance?

A

surviving lymphocytes survive and respond only to foreign antibodies and is tolerant to self antigens
- if they react to auto antigen it goes through apoptosis and clonal deletion - all daughter cells killed

41
Q

describe the role of helper T cells

A

have CD4 protein
assists B cell in antibody production and assists cytotoxic T cells
- provides necessary signals (cytokines) growth factors needed for immune response

42
Q

describe the role of cytotoxic T cells

A

have CD8 protein
destroy target cells on contact
- cells with infected virus or pathogen
- abnormal cells

43
Q

how do T cell recognize antigens?

A

can only recognize epitopes that are bound to MHC proteins
- do not bind to native antigens
antigen processing - modification of antigen for recognition by T cells
APC = antigen presenting cells

44
Q

what is the MHC

A

major histocompatibility complex (HLA in humans)

  • binds to antigen and carries it to cell surface
  • broad in binding: can bind to 1000s of epitopes

MHC I: cytotoxic T cells
MHC II: helper T cells

45
Q

what are cytokines? describe the following: TNF, chemokines, interleukins, interferons, growth factors.

A

regulatory proteins that function as intracellular signals

TNF: tumor necrosing factor - secreted by macrophages and T cells to kill tumors, regulate immune response and inflammation

chemokines - chemotactic cytokines - signal to leukocytes to move to inflammation/infection

interleukins - signal among leukocytes and other cells

interferons - inhibit spread of vital infection
- INF- gamma - potent phagocytic activation secreted by TH1

growth factors - stimulate leukocytes to divide

46
Q

describe B cell activation by T helper cells

A
  1. antigen presenting: APC present MHC II with epitopes
    - enduced Th with CD4 with complementary TCR to bind
    - releases IL1 to differentiate Th - Th2
  2. Clonal selection - Th2 binds to B specific cell, releases IL4 that activated B cell and causes it to proliferate
    - creates clones of plasma cells - releases antibodies
    - also creates memory cells
47
Q

describe the cytotoxic t cell response

A
  1. antigen presentation: MHC I presents epitope for Tc (CD8)
  2. helper t differentiation: MHC II of the Th (CD4) also binds to epitope of dendritic cell
    - dendritic cell release IL12 - stimulates TH- TH1
    - TH1 secretes IL2
  3. Clonal expansion: signal from dendrite and IL2 from TH1 signal Tc cells to release IL2
    - triggers Tc division into memory T cells and Tc
  4. self stimulation: Tc daughter cells produce IL2 receptors and their own IL2 - no longer need APC or Th
    - leaves lymph and attacks infected cells
48
Q

What is acquired immunity

A

the protection developed against specific microbes or foreign substances

49
Q

describe natural active vs passive immunity

A

active - body mounts an immune response against ex. flu

passive - newborns get IgG antibodies that cross placenta, IgA from breast milk
- baby is not actively producing these antibodies

50
Q

describe artificial active vs passive immunity

A

active - vaccines that introduce antigens mounts immune response

passive - inject antibodies - typical for toxins or pathogens that act to quickly for immune response

51
Q

what is a vaccine

A

organisms or fractions of organisms that is used to induce active immunity
- acquire immunity without disease symptoms or severity

52
Q

describe attenuated vs inactivated vaccines

A

attenuated - live vaccine with weakened microbes - can be more risky

inactivated: safer, requires booster
- whole agent - contains killed microbes
- subunit - contains components of organism

53
Q

describe toxoid vs recombinant vaccines

A

toxoid - contains inactivated toxins, require multiple childhood doses and reinoculation every 10 years

recombinant - express antigen in genes - isolate antigen protein in vaccine
- virulence is deletes from pathogen

54
Q

describe passive immunization. what does it \entail?

A

administration of antibodies to pt immediately without waiting for an immune response
- vaccine contains antisera: serum and gamma antibioses
- can be administered intravenously
rabes, tetanus

not long lasting, no memory B cell production

55
Q

what are hybridomas and what is its role with monoclonal antibodies

A

hybridoma - cell lines created by fusing and antibody producing plasma cell and myeloma cell so that it reproduces continuously
- produces many of the desired antibody - monoclonal antibody

56
Q

what is the ELISA test

A

ELISA : enzyme linked immunoabsorbent assay

  • anti-antibodies that are chemically linked to color changing enzymes help to identify particular molecules
  • color change only occurs if the anti-antibody is bound to antigen
57
Q

what are some immunological disorders?

A

hypersensitivity - immune response occurs in an exaggerated of inappropriate fashion that causes harm to the host

autoimmune disorders - host immune system attacks itself

immunodeficiency - absence of normal immune response

58
Q

describe hypersensitivity type I

A

immediately response after exposure to allergen

localized anaphylaxis
upper respiratory system- allergic rhinitis - hay fever
lower respiratory system - asthma
GI tract - food allergy

acute anaphylaxis - rapid suffocation by contraction of bronchial smooth muscle exceeds body’s ability to adjust - tx with epi

prevention of anaphylaxis by desensitization: injection of dilute amounts of allergen

59
Q

describe the mechanism of how hypersensitivity type I develops

A

1st exposure
- cytokine stimulate B cells - become plasma cells and produce IgE
= IgE sensitize basophils, eosinophils and mast cells that will make the resent to future exposures to allergen

2nd exposure
- allergen binds to IgE molecule on sensitized cells and causes degranulation
degranulation - mast cells release histamine:
- dilates blood vessels - local redness and swelling
- simulation of muscle secretion - leads to congestion of airways
- constriction of bronchial airways - leads to wheezing
- stimulation of nerve endings - leads to itching and pain

60
Q

describe cytotoxic ii hypersensitivity

A

cytotoxic Rxn - antibodies bind to cell surface of antigens in host cells
- results in phagocytosis and complement activation

ex. transfusion reaction
- agglutination of foreign RBC
- activation of complement system
- hemolysis - lysis of RBC releases hemoglobin into the bloodstream and can cause kidney damage

ex. Rh antigens in newborns
1st pregnancy - Rh - mom and Rh + baby: mom makes anti-Rh antibodies bc of baby - IgM molecules only
2nd pregnancy - Rh - mom has another Rh + baby - produces IgG anti Rh - can cross placenta and destroy baby’s RBC’s - enlarged liver and spleen
Rhocam injection given to mother after first birth to prevent - destroys fetal RBC before mom can produce anitbodies

61
Q

describe immune complex type III hypersensitivity

A 
antibody antigen complexes form in circulation and get deposited in organs and cause inflammatory damage 
- complement and neutrophils activated
- damage from inflammation 
examples 
- hypersensitivity pneumonitis 
glomerulonephritis - affected kidneys
62
Q

describe cell mediated or delated type IV hypersensitivity

A

T lymphocytes activated by antigen
memory cells produced
subsequent exposure to antigen, memory T cells release cytokines
macrophages accumulate at site of hypersensitive reaction
inflammation and tissue damage occurs

contact dermatitis
tuberculin hypersensitivity - TB test
Graft rejection due to MHC incompatibility - rejected by immune system
- prevented by tissue typing and immunosuppressive drugs

63
Q

what is an autoimmune disease

A

immune system is hypersensitive to self antigens
how it happens
- loss of self tolerance
- cross reaction: antibodies against foreign antigen recognize a self antigen that looks similar

64
Q

what are some examples of autoimmune disorders

A

RA - immune completes of IgM, IgG and complement is deposited in joints
- inflammation and restriction of cartilage in joints

SLE - lupus - autoanitbodies made against many self components including DNA
- antibody-antigen completes cause inflammation ex. glomerulonephritis

BIOL 440 (8 decks)

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