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BIOL 432 > Non-specific immunity > Flashcards

Non-specific immunity Flashcards

1
Q

What defines and constitutes the first line of defense?

A

1st line - chemical and mechanical barriers
- surface membrane barriers
- skin and mucous membranes and their secretions

mechanical
- stratified squamous ET (stratum corneum) of skin
- mucous membranes lining body cavity

Chemical
- acidity of skin secretions
- HCl and digestive enzymes of stomach/small intestine
- bactericidal enzymes of saliva and tears
- mucous traps of digestive and respiratory tracts

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2
Q

What are some components of the 2nd line of defense?

A

phagocytosis, natural killer cells, fever, inflammatory response

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3
Q

how does phagocytosis contribute to nonspecific immunity? what cells are responsible?

A

macrophages and neutrophils and eosinophils
- none require specific receptors on surface
- ingest any foreign cells

intracellular digestion
release of free radicals, defenses
opsonization - coating of complement protein and antibodies to enable phagocytosis of foreign cells/particles

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4
Q

how do natural killer cells contribute to nonspecific immunity? what do they develop from? what do they have receptors for?

A

develops from same line as T ells - non specific form of lymphocyte
- does have receptors for constant region of antibody, but does not require recognition

kills cancer cells/virus infected cell before activation of immune system
- similar to killer T cell: releases perforin and granzyme B
- perforin pokes holes in cell membrane, granzyme ruptures inside of the cell

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5
Q

how do fevers contribute to nonspecific immunity? what organ is in charge of regulation body temperature?

A

leukocytes and macrophages release pyrogens
- pyrogens - reset body temperature by causing hypothalamus to increase temperature

increased temperature inactivates bacterial enzymes
- sequesters ion and zinc needed by bacterial enzymes into liver and spleen
- increases metabolic rate of cells

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6
Q

how does the inflammatory response contribute to nonspecific immunity?

A

inflammation brings increased number of phagocytic ells and plasma proteins to the invaded area
- help isolate, destroy or inactivate the foreign cells/virues
- remove debris
- prepare for healing or repair

begins with flood of cytokines (inflammatory chemicals) released into the ECF by injured tissue
- 5HT and histamine in crease permeability

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7
Q

describe the role of the following chemicals in the inflammatory response: prostaglandins, plasma bradykinin, histamine and heparin
what affect do steroids have on inflammation?

A

prostaglandins - vasodilation, increase capillary permeability
plasma bradykinin - vasodilation, increase permeability
histamine - vasodilation and increased permeability
heparin - prevents clotting and injury site

steroids decrease inflammatory response and decrease healing

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8
Q

what if interferon? what releases it? what are its functions?

A

anti-microbial protein synthesized in cells that are infected by a virus
- also released by activated lymphocytes, macrophages

function - simulate neighboring cells to make antiviral proteins which prevent replication of the virus
- does not protect infected cells
- autocrine/paracrine: travels short distance to warn other cells
- antiviral effects: activation of macrophages and mobilization of NK

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9
Q

what is complement? what are the two pathways?

A

anti-microbial proteins - similar to clotting proteins
- produced by liver
- activated in cascade

classical pathway - involves activation by Fc fragment of antibody
- rapid - linked to immune system (specific)

alternate pathway - does not need antibody (nonspecific)
- triggered by complement activation
- triggered by polysaccharides of bacterial coat

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10
Q

what are the first steps of the classical and alternative pathway? describe the following steps

A

classical - antibody exposure activates C3
alternate - complement/sugar interaction activates C3

  1. C3b binds to target cell surface
  2. triggers insertion of membrane attack complexes (MAC)
    4, form and stabilizes opening in target cell membrane
  3. interferes with target cells ability to release Ca
  4. provides binding sites for macrophages/neutrophils
  5. stimulates basophils/mast cells to release histamine
  6. attracts neutrophils
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11
Q

Describe the 3 ways complement destroys pathogens: enhanced inflammation, opsonization, cytolysis

A

enhanced inflammation - complement C3a stimulates mast cells/basophils to release inflammatory chemicals

opsonization - complement C3b makes bacteria easier to phagocytose by coating surface
- serve as binding sites for macrophages and neutrophils

cytolysis - complement C3b leads to rupture of target cells
- triggers insertion of MAC proteins which allows cytoplasm to leak out

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12
Q

Describe what C3a/b and C5a/b do in the complement pathway

A

C3/5a - triggers mast cells/basophils to release histamine and increase inflammatory response

C3b - binds to surface of bacteria for opsonization - increases changes of phagocytosis
- OR can bind to C5 and split it

C5b - binds with C6-9 and makes donut like opening - MAC
- causes cytolysis

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13
Q

describe specificity and memory of the specific immune response

A

specificity - immunity directed against particular pathogen
- immune system has ability to recognize particular substance

memory - ability of immune system to recognize the repetition of previous event
- provides more rapid response

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14
Q

what is an antigen? define the following: hapten, antigenic determinant, antigenic receptor, and epitope

A

antigen - substance that stimulated the immune response
- typically large molecule - protein, polysaccharide, lipids

hapten - molecules of low molecular weight that are too small to be antigenic on their own, but can become antigenic by binding larger molecule

antigenic determinant - immunogenic site on the antigen that antibodies or T lymphocytes can bind

antigenic receptor - molecules on the surface of B/T lymphocytes which recognize and combine with particular antigenic determinants

epitope - specific sequence of AA/polysaccharides on antigen surface that would fit variable component of an antibody

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15
Q

do T cells make antibodies

A

no, but they have receptors on their surface that function similarly to antigens
- receptor specific to antigen epitope
- can get multiple responses to same antigen due to different epitopes on surface

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16
Q

what is a polyclonal response? how is this possible?

A

different components react to different epitopes on the same antigen

most naturally occurring antigens have many sites that:
- activate several different lymphocyte populations
- bind different kinds of antibodies

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17
Q

describe the role of the t lymphocyte in the immune system

A

originates in red bone marrow, mature and multiply in the thymus
- each cell recognizes only one antigenic determinant
- selection occurs in thymus

competent lymphocytes reside in diffuse lymphatic tissue, spleen, lymphatic nodules, and in the paricortical and medullary areas of lymph nodes

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18
Q

describe the role of B lymphocytes in the immune system. what happens when they are activated?

A

originate and mature in red bone marrow
- one lymphocyte produces antibodies which recognize only one antigen

reside in diffuse lymphatic tissue, spleen, germinal centers of lymphatic nodules

when activated - increase ribosomal ER and golgi apparatus
- increases amount of cytoplasm

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19
Q

describe the role of macrophages in the immune system. what do they arise from?

A

arise from monocytes in the blood

secrete chemicals which activate T/B cells
T cells secrete chemicals that activate
act as antigen presenting cella
reside in loose CT, lymph node sinuses, lung, liver sinusoids

20
Q

what is an APC? what dose a helper T cell do?

A

antigen presenting cell - must be phagocytic
- lysosome breaks down antigen into protein components and present them on the surface

T helper cells - undergoes cellular changes that recognize specific epitope of specific antigen
- cellular changes allow T helper cells to release molecules that activate T/B cells - causes them to multiply

21
Q

what is an MHC class I molecule? what is its function? what is the purpose of TAP channels on ER

A

found on any nucleated cell in the body

function - present antigens produced internally on the external surface of plasma membrane - endogenous proteins
- MHC I /antigen complex can bind to a T cell receptor to activate the T cell
- T cell can destroy the cell demonstrating MHC I/antigen complex

TAP channel - allows molecules into lumen of ER
- binding site of MHC I on inside of lumen, need to let molecule in
- TAP: transporter associated antigen processing

22
Q

once the MHCI receptor/antigen is presented, what happens next?

A

T killer (cytotoxic) cells interacts with MHC I
- CD8: specific binding site on T cytotoxic that recognized MHCI
- intermolecular binding - activates T cells, stabilizes activity

23
Q

what is the MHC class II molecule? What is its function>

A

found only on antigen-presenting cells - exogenous antigen
- macrophages, B lymphocytes, monocytes, dendritic cells

engulf foreign antigen - binds with protease enzymes to degrade antigen into antigenic components
- vesicle binds with golgi or ER

MHCII on the golgi or ER leaves and presents antigen

24
Q

What happens after MHCII receptor/antigen is presented?

A

T helper interacts with MHCII
- CD4: specific binding site on T helper that interacts with MHCII
- intermolecular binding - activates T cells, stabilizes activity

25
Q

what are cytokines? what are they involved in? describe interferon gamma, interleukin-1 and 2

A

cytokines - proteins/peptides secreted by one cell that regulates another
- involved in costimulation

interferon gamma - increases expression of MHC I/II molecules
- secreted by helper T, cytotoxic T and NK cells

interleukin-1: costimulation of B and T cells
- secreted by macrophages, B cells and fibroblasts
- need CD4 of T helper to help activate

Inerleukin-2: costimulation of B and T cells
- secreted by helper T

26
Q

describe the following T cells: delayed hypersensitivity, memory, suppressor

A

delayed hypersensitivity - respond to antigens by releasing cytokines
- promote phagocytosis and inflammation in allergic reaction

memory - responsible for memory in cellular immunity

suppressor - limit the attack and the immune system functions
possess CD8 receptors

27
Q

describe helper T cell activation

A
  1. macrophage processes antigen and displays via MCHII on its surface
  2. T helper cells interacts with molecule via TCR
  3. costimulation occurs as the macrophage releases interleukin 1 - which activated the T helper cells
  4. intermolecular-binding occurs via the CD4 molecule

can fascinate the activation of B cells or killer T cells

proliferated into more T helper and T memory cells

28
Q

describe cytotoxic T cell activation

A
  1. MHCI displays antigen on surface of target cell
  2. activation of cytotoxic T cell begins when T cell receptor binds to MHCI/antigen complex
  3. costimulation occurs when CD8 molecule binds to MHCI
  4. more costimulation occurs due to cytokines (interleukin-2) released by helper T - goes to T killer cells that recognize same antigen
  5. activated cytotoxic T cell divides exponentially

can lyse cells via perforin

29
Q

describe the proliferation of B lymphocytes

A
  1. before B cell can be activated by helper T, must process the same antigen that activated the T helper cell
    - antigen binds to B cell receptor and both taken in via endocytosis
  2. B cells uses MHCII to present antigen to T helper
  3. T helper releases interleukin-2 that stimulate B cell to divide
  4. B cell proliferates and gets converted to plasma cells - produce antibodies

also can create memory cell for subsequent exposures to the virus

30
Q

describe antibodies. what is the constant and variable regions? what are they heavy and light chains?

A

y shaped protein produced by B lymphocytes in response to antigen
constant - non-specific component
- activated NK killer, complement, mast cells and basophils

variable region - specific component

heavy chain - large interior
light chain - small exterior

both heavy and light chain have constant and variable regions

31
Q

Describe IgG antibodies

A

activated complement and functions as an opsonin to increase phagocytosis
- an cross the placenta to provide limited immune protection to the fetus/newborn

main antibody in primary and secondary responses - vaccines
active in Rh transfusion rxns

32
Q

describe IgD antibodies

A

antigen binding receptor on the surface of B lymphocytes

33
Q

describe IgM antibodies

A

pentamer - activates complement
- antigen binding receptor on the surface of B lymphocytes
active in ABO-induced transfusion reactions - agglutination

34
Q

describe IgA antibodies

A

dimer
secreted into saliva, tears, and onto surface of mucous membranes
found in breast milk to provide limited immune protection to the newborn

35
Q

describe IgE antibodies

A

binds to mast cells and basophils via constant region
- stimulates inflammatory response - causes hypersensitivities
- mast cells and basophils respond by releasing heparin/histamine

36
Q

describe the following actions of antibodies: neutralization, opsonization, agglutination, complement fixation

A

neutralization - inactivates small antigens
- toxins released by bacteria binds to antibody
- ingested by macrophage - cell dies or releases chemicals

opsonization - triggers classical pathway of complement
- coating can be complement protein or antibody
- increases likelihood of endocytosis by macrophage

agglutination - precipitation occurs when multiple cells are bound to antibody
- binds antigens together
- easier for macrophages to break down

complement fixation - activates complement cascade (classical)

37
Q

describe the primary and secondary immune response

A

primary - 1st exposure
- latent period (5-7 days): T helper must become activated before activating other lymphocytes
- activated lymphocytes begin to make antibodies - few, do not last long
- antibody levels peak at day 20

secondary - 2nd exposure to antigen
- no latent period
- antibody levels ride in minutes/hours
- plateau rather than peak may last for 6 weeks: stays high for longer period of time to protect body

38
Q

describe passive natural immunity

A

passive - another body produces the antibodies
- fetus/infant not exposed to antigen, but gets antibodies from mother
IgG - crosses placenta
IgA - breastfeeding

39
Q

describe passive acquired immunity

A

passive - another body produces the antibodies
- not natural, raised in commercial product and injected

Rhogam - Rh negative mom
- contains antibodies against D antigen - prevents mother’s primary immune response to D antigen

anti-snake venom - contains antibodies against venom toxin
- neutralizes or precipitates toxin
- prevents damage to tissue

40
Q

describe active natural immunity

A

getting sick - develop memory cells via primary response
- when secondary response comes around, high amounts of antibody are produced to protect the body from getting sick again

41
Q

describe active acquired immunity

A

acquired - commercial way of getting exposure
- do not actually get sick

T helper and B lymphocytes are activated and produce antibodies when exposed to antigen again

hepatitis, polio vaccines

42
Q

what are hypersensitivities?

A

excessive immune reaction against antigens that most people tolerate
ex. mold, dust, pollen, vaccines, bee toxins etc

43
Q

describe type I hypersensitivity. what antibody is involved?

A

allergies - IgE antibody - immediate hypersensitivity
1. initial presentation of allergen results in no symptoms but results in sensitivity
- APC present antigen fragments to T helper cells
- high # T helper cells differentiate into T helper 2 cells - released IL-4
- IL-4 stimulates B cells to secrete IgE
- IgE binds to mast/basophils

  1. later exposure to allergen results in alleged binding/crosslinking the antibodies bound to mast/basophils
  2. mast cells and basophils degranulate and release large amounts of histamine
  3. systemic reaction (anaphylactic shock) usually require that allergen enters bloodstream/distributed systemwide
44
Q

describe type II hypersensitivity. what antibodies are involved?

A

immediate hypersensitivity - IgG and IgM
- blood transfusion reactions
- glomerulonephritis
- systemic lupus erythematosus
- Rheumatoid arthritis

45
Q

describe delayed hypersensitivities. What cells are involved?

A

t lymphocyte cytokine release
- allergic contact dermatitis
- tuberculin skin test reaction

BIOL 432 (25 decks)

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