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Immuno/Micro/Viro > Test 1 > Flashcards

Test 1 Flashcards

1
Q

immunity means latin:

A

free from burden -

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2
Q

immunology

A

study of host defenses against infectious disease and neoplasm and the undesrable consequences of immune interactions

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3
Q

two types of immunity:

A

innate and adaptive immunity

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4
Q

innate immunity

A
  • 1st line of defense against microorganisms
  • quick but not really powerful
  • no memory
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5
Q

adaptive immunity

A
  • composed of antibody - (humoral) and cell-mediated immunity
  • specific immune response against antigens (stimulate antibody generation
  • exhibit immmunologic memory: faster and more vigorous secondary response
  • slower but more powerful resonse
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6
Q

5 features of adaptive immunity

A

-specificity: specific for a particular antigen
-cell membrane receptors on lymphocytes that pick out antigens
-lymphocyte has just one specificity
-immune response are generated toward determinant
epitopes - antibody part that recognizes antigen sequence

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7
Q

adaptive immmunity is faster bc

A

memory cells - 2, 3, 4 … time exposed you get a much stronger response

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8
Q

what binds the antigen?

A

epitope of antibody

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9
Q

self regulation of immune response

A
  • get rid of antigen and then get antibodies out

- activated lymphocytes dye within a short period of time via apoptosis

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10
Q

physical barriers an d broken what begins?

A

INNATE RESPONSE
skin- (prevents invasion, pH5.5+fatty acids)
lungs - (cilia, mucous, surfactant protein A and D enhance phagocytosis)
stomach and vagina - (acidity)
saliva - (lysozyme, phospholipase A, histatins-antimicrobial)
tears-washa way microbes, lysozymes and phospholipase A)
mucous nose and nasopharynx- (traps microorg)
small intestins - (alpha defensins–>anti fungal or bacterial)

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11
Q

innate imunity characteristics

A
  • antigen non specific (macrophage will eat it no matter what)
  • exists prior to exposure to antigen
  • not enhanced following exposure to antigen (no memory as with adaptive)
  • always available bc it does not depend on the clonal expansion of antigen specific cells
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12
Q

process of phagocytosis

A

1) attachment - non-specific, encapsulated microorganisms need to be opsonized (coating of a microbe/particle with antibody or complement to facilitate phagocytosis
2) ingestion phase- pseudopods wrap around the microbe until they meet and fuse together (zipperig), once inside it is a phagosome
3) digestion phase-lysosome fuse with phagosome to produce a phagolysosome. Enzyme degrades phagosome components
4) disposal phase-AA, sugars, ipids, and nucleotides may cross the phagolysosome membrane to be utlized by the phagocyte; if a macrophage eats too much is dies (neutrophils)

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13
Q

two basic phagocytes

A

macrophages and neutrophils

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14
Q

macrophages

A

PRIMARY FUNCTIONS (NON IMMUNE): remove dead cells ,inhaled particles, aged RBC, secrete hormones toregulate granulocyte and erythrocyte pools

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15
Q

neutrophils

A

polymorphonuclear cells with small cytoplasmic
(PMN cells)
-50% found in circulation and other half in marginal pool(bound to endothelial cells)

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16
Q

receptors for phago

A
  • mannose
  • scavenger receptors - bind bacterial components=lipopolysaccharide)
  • CD14 (receptor for lipopolysaccharide)
  • toll like receptors
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17
Q

respiratory burst:

A

uses Oxygen to make compound to destroy stuff

  • increase consumption of o2 during phagcytosis via NADPH oxidase
  • NADPH oxidase - generates superoxide anion
  • other enzymes can produce-hydrozyl radical, singlet oxygen, hypochlorite, hypobromite
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18
Q

other functions of phago

A

chemotaxis-process that guides neutrophils to where they need to be
-looking for chemotactic gradient (C5a, leukotriene -arachodonic acid metabolite, chemokines)

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19
Q

natural killer cell

A
  • not antigen specific
  • large granual lympocyte
  • first line of defense for VIRUS infected cells
  • mediate ADCC (antibody dependent cell mediated cytotoxicity) - antibody coated cells will be destroyed
  • interleukin cultured NK cells = lymphokine activated killer cells- finds and kills tumor cells
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20
Q

complement cascades

A
  • sequentially activated soluble proteins that are activated in the innate immune response
  • results: pores in the cell surface — deah by osmotic lysis AND opsonizes antigen to promote phagocytosis
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21
Q

several ways to activate complement proteins:

A

classical pathway - requires antibody-IgM (5 antibody bound together) or two IgG next to each other

alternative pathway- just needs microbial surface for components (proteins) to bind to, no antibody needed

mannose binding lectin- factors bind mannose residues expressed on whatever needs to die

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22
Q

what does MAC do? membrane attach complex

A

osmotic lysis - forms holes in membrane

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23
Q

C3b

A

sticks to microbes and phagocytes recognize it

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24
Q

anaphylatoxins

A

C3a, C4a, and C5a, bind to receptors on mast cells and basophils = histamine release

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25
Q

chemoattractant

A

C5a-stimulates chemotaxis of neutrophils

C3a - may be chemoattactant

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26
Q

immune complex removal

A

C3b-coated immune complexes - bind to erythrocytes and immune proteins–> removed by phagocytic cells in the liver and spleen

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27
Q

DAF

A

decay accelerating factor - completes for the binding of C3b to prevent the formation of convertases

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28
Q

if missin C5-C9 (membrane hole thing)

A

succeptible to Neisseria infections and meningitdis

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29
Q

if missing one of proteins (C1 inhibitor) to keep classical in check

A

herreditary angioedema= around larynx = closing of breathing pathway

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30
Q

interferons

A

interfere with viral replication

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31
Q

acute phase proteins

A

produced by the liver = c-reactive, mannose binding lectin (MBL), fibrinogen, and serum amyloid A protein
stimulated by interleukin 6 (produced by macrophages in response to infection)

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32
Q

C-reactive protein (CRP)
and
MBL

A

obsinents- coats microbes so they are more easily phagocytosed

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33
Q

components of innate immunity:

A 
phagocytes
Natural killer cells
complement
interferon
acute phase proteins
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34
Q

next line of defense after breach of phsical barreirs:

A

macrophages and neutrophils

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35
Q

chemokines

A

released by macrophage a a site of infection to attact neutrophils

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36
Q

CD59 regulation:

A

prevents binding of C9 to complete the MAC

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37
Q

DAF and CD59

A

paroxysmal nocturnal hemoglobinuria (intravascular lysis of rbc by complement)

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38
Q

deficiency of C1q, C1r, C1s, C4, & C3

A

increase of pyogenic (pus producing) infections

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39
Q

most common complement deficiency=

A

C2

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40
Q

emotional stress or trauma leads to

A

complement activation + bradykinin production –> edema in skin and larynx

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41
Q

C1 INH restricts WHATand regulates WHAT?

A

restricts sponteneous activation of C1 in plasma

regulates Hageman factor - gives ride to HAE in absence of INH

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42
Q

type 1 INF=

A

inhibit viral rep via paracrine action
enhance cytolytic capability of NK cells
increase cellular expression of class 1 MHC molcules

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43
Q

interleukin 6

A

produced by macophages to stimulate liver to proudct acute phase reactants

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44
Q

cardinal signs of inlamation

A 
Rubor (redness)
Tumor (swelling)
Calor (heat)
Dolor (pain)
LOSS OF FUNCTION
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45
Q

purpose of inflammation

A

1) remove any pathogenic insult,
2) remove injured tissue
3) institute wound healing (or scarring if the tissue cannot be repaired).

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46
Q

outcomes of acute inflamation

A
  1. Resolution is characterized by removing of any offending agents and restoration of normal tissue architecture.
  2. Abscess formation proceeds if the offending agent is walled off by inflammatory cells and destruction of the walled off tissue by released products of PMN’s occurs.
  3. Scarring can result if the tissue is irreversibly injured in spite of the elimination of the offending agent.
  4. Chronic inflammation may ensue if acute inflammation fails to remove the offending agent.
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47
Q

what is acute inflamation

A
  • accumulation of fluid + neutrophils

- measured in hours or days

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48
Q

what is chronic inflammation/hallmarks of chronic inflammation

A
  • offending agent cannot be removed during acute inflammation
  • presence of lymphocytes and macrophages (NO NEUTROPHILS)
  • weeks, moths, or years
  • tissue destruction is mediated by enzymes released by macrophages ex) elastase, collagenase, phosphateases, lipases
  • attempts at healing proceed (angiogenesis and fibrosis)
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49
Q

overview: process of acute inflammation -

A

1) immediate vasoconstriction: via sympathetics - GOES AWAY VERY QUICKLY
2) collagen or basement membrane disruption
3) mast cell degranulation result of direct trauma(including injury, cold and heat) and the presence of the anaphylatoxins C5a and C3a. And platelets release serotonin after contact with collagen.
4) Histamine also causes an increased vascular permeability of venules leading to the escape of a protein rich fluid known as an exudate. In addition, mast cells and endothelial cells can synthesize and secrete platelet activating factor (PAF). PAF potently increases vascular permeability.
5) Within 6 – 24 hours, neutrophil extravasation begins leading to the accumulation of phagocytic cells in the affected tissues.
7) Starting at 24 - 48 hours after the start of inflammation, monocytes and macrophages begin to be the predominant cell type.

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50
Q

collagen/basement membrane exposed: process of acute inflamation

A
  • The collagen and/or basement membrane activates Hageman factor (another name for factor XIIa of the coagulation system).
  • Hageman factor converts prekallikrein into kallikrein, plasminogen into plasmin and activates the coagulation system (ultimately to convert fibrinogen into fibrin).
  • –Kallikrein cleaves C5 into C5a and C5b fragments.
  • –Kallikrein also cleaves high molecular weight kininogen into bradykinin (which induces pain and edema).
  • –Plasmin cleaves C3 into C3a and C3b fragments.
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51
Q

mast cell degranulation: process of acute inflamation

A
  • Degranulation due to: direct trauma, injury, cold, heat, anaphylatoxins (C3a-from plasmin, C4a, C5a-from kallikrein)
  • Mast cells synthesize prostaglandin E2, from arachidonic acid derived from plasma membrane phosphatidylcholine, to induce pain.
  • Mast cells release preformed histamine from their intracellular granules. This histamine along with platelet-derived serotonin causes vasodilation of arterioles and new capillary beds in the affected tissue. The increased blood flow causes the heat and redness characteristic of inflammation.
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52
Q

What causes PAIN and EDEMA in acute inflammation?

A

bradykinin

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53
Q

histamine: process of acute inflamation

A
  • The increase in vascular permeability is caused by endothelial cells lining the blood vessels becoming separated, thus allowing fluid (a protein-rich exudate) from the blood to accumulate in the tissues.
  • The protein-rich exudate increases the osmotic pressure of the interstitial fluid and, along with the increased hydrostatic pressure due to vasodilation, causes fluid accumulation in the tissues known as edema.
  • Whereas histamine is relatively short-lived, mast cells also synthesize leukotriene (LT) C4, LTD4 and LTE4 from arachidonic acid which provide a sustained increased in vascular permeability. (takes longer to get there but effect is longer)
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54
Q

What cuases HEAT and REDNESS in acute inflamation?

A

vasodialation

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55
Q

What causes PAIN in acute inflammation?

A

PGE2

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56
Q

histamine results in:

A
  • inc vascular permeability caused by gaps between endothelial cells
  • exudate increases osmotic pressure of interstitial flud –> inc hydrostatic pressure due to vasodialation, causes accumulation of flud (EDEMA)
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57
Q

neutrophil extravasation is basically and steps

A
  • -neutrophils moving from the blood stream to where they are needed
    1) rolling - endothlial cells have p-selectin in Weiber palade bodies - brought to surface and neutrophils have PSGL-1 (p-selectin glycolipi-1) that binds P-selectin on endothelial cells (slows neutrophil-low affinity binding); E-selectin appears later on endothelial cell
    2) binding - HIGH AFFINITY interaction bw LFA-1 (upregulated by neutrophils) and ICAM-1= STOP ROLLING
    3) extravasation - both endothelial and neutro have CD31 (PECAM-1); concentrated at inracellular junctions;neutro squeeze bw endothelial cells and penetrate basement membrane via metalloproteinases
    4) chemotaxis (C5a) - chemokines bind proteoglycans to form solid matrix gradient; PMNs eat extracellular bacteria to prevent spread; PMNs release toxic substances that damage host tissue and increase inflamation
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58
Q

6-24 hrs: process of acute inflammation

A
  • neutrophil extravastion leads to phagocytotic cells inthe tissues
  • stasis of circulation (vasodialation which slows down movement of stuff in blood) –> margination of PMNs along vascular endothelium
  • neutrophils passing through affected tissue detect changes on endothelium
  • neutrophils are the first line of defense against extracellular bacteria and some yeast pathogens
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59
Q

24-48 hrs after start: process of acute inflammation

A
  • monocytes and macrophages predominant cell type as PMNs are short lived cells with short halflife
  • macrophages ingest cellular debris (dead or damaged tissue and dead PMNs= heal restore normal tissue architecture
  • macrophages secrete trasforming growth factorBeta.= initiation of wound healing process (induces fibroblast migration and their prolif); stimulates secretion of collagen
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60
Q

transforming growth factor beta

A

secreted by macrophages
migration and prolif of fibroblasts
stims ecretion of collagen

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61
Q

chronic inflammation is

A

simultaneous inflammation, tissue destruction and healing

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62
Q

conditions that predispose to chronic inflamation

A

persistent infections
chronic exposure to toxic agents
autoimmune diseases

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63
Q

systemic effects of inflammation:

A

EX) fever, neutrophilia, acute phase response and shock

-due to pathogen enters bloodstream (sepsis) or during severe local injury where inflammatory mediators may be released into the blood stream

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64
Q

fever development

A

1) infection or toxin
2) macrophages make cytokines (Interleukin 1 IL-1 and tumor necrosis factor TNF)
3) IL1 and TNF make it into blood
4) move to brain – hypothalamus
5) hypothalamus produces PGE2 (nothing to do with pain)
6) PGE2 –> vasomotor center
7) vasomotorcenter instructs sympathetic nerves to vasoconstrict BV in skin
8) decrease heat dissipation
9)===>FEVER
Not producing more heat just losing less heat

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65
Q

advantages of fever:

A
  • immune system functions betetr at hgiher temp
  • host ells are more protected from the deleterious effects of TNF-alpha at higher Temps
  • pathogens grow more poorly at higher temps
66
Q

what inhibits cyclooxygenage?

A

aspirin- blocks prostaglandin E2 (PGE2) production = reduce fever

67
Q

neutrophilia

A
  • increased peripheral blood neutrophils
  • suspect bacterial infection
  • commonly accompanies acute inflamation
  • production IL1 and TNF by macrophages== accelerated release and production of PMNs from bone marrow
  • sustained release by macrophage and T-lymph derived released of granulocyte colony stimulating factor
68
Q

acute phase response:

A

macrophages make IL6 = liver to make acute phase proteins—> accelerated RBC sedimentation rate (erythrocyte sedimentation rate ESR) === CRP and MBL - obstinents to coat microbes

69
Q

too much TNF=

A
  • shock especially due to sepsis or severe injury
  • effects: systemic vasodialation and permeability = intravascular volume loss –> hypotension and shock; systemic activation of coagulation system (DIC) –> multisystem organ failure +serious bleeding

potential death

70
Q

define immunogenicity

A

The property of a molecule that allows it to induce an immune response.

  • Immunogenicity is increased when the molecule is injected along with an “adjuvant”, which prolongs the molecule’s retention in the body so that a more vigorous immune response can occur.
  • Common adjuvants include alum, mineral oil, and lipids.
71
Q

define antigenicity

A

The property of a molecule that allows it to react with an antibody. This term is used loosely to describe an immunogen.

72
Q

define hapten

A

Small molecules that cannot induce antibody formation but can react with antibody that is specific for it, i.e. it must be coupled to a carrier molecule in order to induce antibody formation. -a hapten is an antigen, but not an immunogen

73
Q

five features needed to generate immune response against immunogen

A
  1. Size: Molecules of >10,000 molecular weight are the best immunogens, although there are molecules that are smaller than this which can function as immunogens.
  2. Internal complexity: The more complex the molecule, the more capable it is to be an immunogen. For example, long linear polymers of lysine are not immunogenic, whereas smaller protein molecules can be immunogens because they are structurally more complex due to amino acid sequence and three dimensional orientation.
  3. Degradability: Immunogen processing occurs in phagocytes so that the immunogen can be presented to T-helper lymphocytes in conjunction with major histocompatibility proteins.
  4. Foreignness: Because of tolerance to self antigens, foreignness must be perceived by the immune system in order to respond.
  5. Accessibility: Areas of the immunogen that are easy to reach (i.e. not buried within the molecule) are more likely to induce an immune response. These areas of an immunogen are called immunodominant areas.
74
Q

linear determinanats/epitopes are formed by:

A

adjacent amino acids - retained with detanturation

75
Q

Conformational determinants (or epitopes) are composed

A

of amino acid residues from different parts of the protein that are brought together in space. - not retained when denatureated

76
Q

t-lymphocytes ONLY recognize…

A

LINEAR determinanats - little pieces of protein

77
Q

Neoantigens are:

A

“new antigens” formed by proteolysis, phosphorylation, or exposure of new determinants through the interaction with foreign antigens (e.g. such as virus antigens being expressed on the cell surface in conjunction with cellular proteins).

78
Q

most common antigen to which the body is exposed and most immunogenic=

A

PROTEIN

79
Q

antibody characteristics:

A
  • structurally related family of glycoproteins that mediate their biological effects by binding to antigen in a very specific manner.
  • The interaction of antibody and antigen is similar in many ways to the specificity of enzymes reacting with their substrates.
  • There is exquisite specificity of antibody for antigen.
80
Q

antibodies can be found:

A
  • surface of b-lymphocytes (antigen receptors): each has it’s own specificity —- antigen native b-lymphs have both IgM and IgD
  • blood plasma and tissue fluids
  • surgace of mast cells/basophils have receptors for IgE
  • secretory fluids (mucous and milk)
81
Q

polyclonal antiserum definition-ish-

A

contains a population of antibodies which (collectively) can bind to more than one particular antigen. Each individual antibody will recognize only one antigen, but the population of antibodies will cover multiple antigen specificities.

82
Q

monoclonal antiserum definition-ish-

A

contains antibodies which bind to only one specific antigen.

83
Q

titer definition:

A

the reciprocal of the last dilution of antiserum that still yields a demonstrable antibody binding reaction. For example, if an assay which measures antibody binding to an antigen gives a demonstrable reaction at an antibody dilution less than or equal to 1/32, but not a dilution of 1/64, then the titer would be 32.

  • THE RECIPROCAL IS THE TITER
  • TITER NEEDS TO CHANGE TO SHOW ITS BEING STIMULATED BY ANTIGEN
84
Q

elecrophoresis on serum

A

bunch of peaks – most antibodies will be in gamma fraction –. antibodies also called gamma globulins - but not all found here to immunoglobulin is more acurate terms

85
Q

antibody structure

A

-2 identical heavy and light chains (arms bind antigen covalently bound) made of immunoglobulin domains (amino acids)
-heavy and light chains have constant and variable regions (vary in AA sequence) - combo of heavy and light variable regions=antigen binding site:
-hypervariable regins of variable region=contact antigen(tip of finger
-framework regions of variable region=line up hypervariable regions for binding–> framework (length of finger)
-hinge region allows for flexibility of the arms = better binding to antigen (in IgG, IgA, IgD)
-

86
Q

two forms of antibody isotypes and describe

A
  • secretory form=from memory cells - have a J chain allows formation of pentamers (IGM) and dimers or trimers (IGA)
  • membrane form=plasma membrane bound form
87
Q

antibody treated with papain and pepsin

A

papain: 2 Fab (each have antigen binding site) and Fc (no binding site)
pepsin: F(ab’)_2 ( has 2 antigen binding sites) and pFc’ (n osite) - CAN STILL CROSS LINK ANTIGENS

88
Q

IgG characteristics

A
  • most abundant of longer half life
  • secreted as monomer
  • activates complement by classical path
  • IgG1 and IgG3 can opsonize to enhance phagocytosis - important for polysaccharide coated bacteria
  • can coat tumor or virus infected cells to facilitate ADCC
  • cross placenta to protect fetus
  • in mother’s milk - taken up by gut in infant and into blood
  • primary antibody produced in secondary immune response
89
Q

IgM characteristics

A
  • 10% total antibody
  • secreted as pentamer
  • predominant form in primary immune response
90
Q

IgA caracteristics

A
  • 15% of total
  • mediator of mucosal immunity
  • in tears, saliva, clostrum, milk
  • monomeric in serum
  • (LUNGS GUT UROGENITAL)**
  • dimer in secretions
  • IgA dimers held togetehr wtih J-chain
  • eosinophil mediated ADCC of certain parasitic infections
  • secretory component - protects antibody from being broken down- PiGIT receptor brings it through endthelial cells into lumen without destruction
91
Q

IgE characteristics

A
  • <2% total
  • secreted as monomer
  • eosinophil-mediated ADCC of certain parasites
  • binds to cell surface receptors for IgE on basophils and mast cells to mediate allergies and anaphylaxis.
  • IgE receptor is high affinity
  • secreted by plasma cells
  • sticks to basophils
92
Q

IgD characteristics

A
  • embed itself in a b-cell
  • very low concentration in serum
  • transduction of signals across the plasma membrane to result in antigen driven B-cell activation
93
Q

waht part of IgA molecule at mucosal site is not produced by b-lymphocyte?

A

secretory component/polyIG receptor - protects antibody from breakdown

94
Q

Idiotype definition

A

The collection of hypervariable regions (formed by the rearrangement of immunoglobulin gene segments) contributed by heavy and light chains to form the antigen-binding site, i.e. idiotype is the unique features of an antigen-binding site

differences in varying region

95
Q

Allotype definition

A

Differences in the constant regions of antibodies (of the same isotype) between different individuals due to the presence of multiple alleles of the constant region genes in the human population.

differences in constant region

96
Q

Avidity definition

A

overall strength of attachment which takes into account how many antigen combining sites the antibody has bound

97
Q

affinity maturation definition

A

average affinity for a population of antibodies will increase with repeated immunization with an antigen

98
Q

affinity definition

A

strength of binding for antigen of one antigen combining site ex one arm of an antibody

99
Q

define haplotype

A
  • total set of MHC genes on each chromosome
  • one haplotype from each parents
  • MHC is polygenic => multiple diferent genes within each individual
100
Q

define polymorphic

A

MHC gene expression is polymorphic- multiple variants of each gene exist in the population

101
Q

define codominant

A

MHC gene expression is codominant=alleles on both chromosomes will be expressed simulaneously

102
Q

major histocompatibility complex (MHC)

A
  • MHC proteins are expressed on the surface of nucleated cells
  • called immune response genes (Ir) because they control the protein antigens to which an individual can response
  • MHC proteins in humans=HLA (human leukoyte antigens)
103
Q

class II MHC proteins encoded by region…

A

region D genes

104
Q

class I MHC proteins encoded by region…

A

A,B, & C region genes

105
Q

D-region genes sequence

A

DP—DQ—DR

106
Q

A,B,C region sequence

A

B—C—A

107
Q

role of MHC proteins:

A
  • help t-lymphocytes become active
  • t-lymphs need their SPECIFIC antigen presented to them on a SPECIFIC mHC protein which is bound to antigen presenting cell
108
Q

ankylosing spondylitis

A

inflammation of vertebrae and spinal deformities - related to HLA-B27 (class I MHC)

109
Q

clinical uses for MHC typing

A

organ transplantation-

paternity testing

110
Q

class I MHC protein cells:

A
  • on nearly all nucleated body cells

- not on corneal epithelial cells and RBC (no nucleus)

111
Q

class I MHC proteins structure

A

-alpha 1,2,3 and Beta2 microglobulin components
-need Beta2 for cellular expression of alpha chain and hence class I
- binds 9-11 AA long sequences - T-lymph see ONLY frangments
-ends are pinched in
-

112
Q

why so much MHC polymorphism

A

protective advantage for population if everyone is different

113
Q

class II MHC protein cells

A
  • expression restricted to antigen presenting cells= denritic cells, macrophages, and B-lymphocytes
  • some in thymic epithelial cells=aids in selection of mature t-lymphocytes
114
Q

class II MHC protein structure

A
  • alpha 1 and 2 sections and beta 1 and 2 sections
  • both beta1 and alpha1 bind
  • noncovalent link bw chains
  • each chain has separate MHC genes
  • cleft can hold protein fragments 10-30 AA longs (cleft is open at both ends)
115
Q

Do antigen presenting cells present class I, II, or both?

A

Both Class I and II

116
Q

MHC restriction of immune responses:

A
  • CD4-t-lypmphs recognize peptides in self-class II MHC proteins
  • CD8-t-lymphs recognize peptides in self class I MHC proteins
117
Q

clinical importance of CD4 t lymphocytes

A

attacked by HIV

118
Q

clinical importance of CD8 t lymphocytes

A

importnat to mount response against virus

119
Q

what do t-lymphocytes recognize

A

ONLY denatured protein antigens

NOT nucleic acids, lipids, or anything else.

120
Q

antigen presentation class I MHC

A

on nearly all nucleated cells except RBC and corneal epithelial cells

121
Q

antigen presentation class II MHC

A
  • dendritic cells, macrophages, and B-lymphocytes
  • express class II and present antigentic peptide fragments to t-helper lymphocytes
  • professional antigen presenting cells (APC)
  • dendritic cells are the mos tpotent antigen presenting cells
122
Q

dendritic cell characteristics

A
  • These cells are produced by the bone marrow and released into the bloodstream. Ultimately, they migrate into the tissues as long-lived immature dendritic cells.
  • Dendritic cells continuously sample their environment through phagocytosis and macropinocytosis.
  • This cell type is present in nearly every organ of the body.
123
Q

general priciple of antigen procession

A

APC activate T-lypmph–>interferon-gamma is released by t-cell–>induces more class II MHC protein on surface of APC ==== More cells to present antigen to t-lymphocytes

124
Q

typical antigen presentation scenario

A
  • dendritic cells constantly sample environment
  • during infection, immature dendritic cells take up antigen, become activated and migrate to nearest lymphoid tissue
  • in lymphoid tissue dendritic cells mature and present antigen to t-helper lymphocytes
125
Q

first cells that you want to activate in immune response?

A

t-helper cells - fed by class II

126
Q

exogenous antigen processing

A

1) exogenous antigen internalized by phagocytosis, receptor mediated endocytosis or fluid phase pinocytosis
2) processing takes 1-3 hrs
3) Class II MHC proteins are bound by the MHC class II associated invariant chain—> prevents binding of cellular proteins
4) vessicles with Class II MHC fuse with the peptide containing vesicles
5) Fusion with plasma membrane
6) absence of exogenous antigen —>class II MHC binds self peptides

127
Q

endogenous antigen processiong

A 
how it gets on class I MHC
things that already inside the cell ex) tumors, viral infected cells
1) cytosolic antigen proteins proteolytically degraded into peptide fragments by proteosome
2) peptide transported to the endoplasmic reticulum by TAP proteins
3) peptide class I MHC complexes formed in the SR and shuttled out to plasma membrane to alert t-lymphocytes of infection
4) uninfected cells, class I MHC bind self peptides
128
Q

exogenous pathway results;

A

—> produce Class II MHC—> activate T-helper cells—> antibody production effective against extracellular pathogens

129
Q

endogenous pathway results

A

—> produce class I MHC —> activate CTL’s effective against virus infected or tumor cells

130
Q

NK cells are part of which immunity/

A

Innate - theyre the patrol boat

131
Q

B and T lymphocytes are part of which immunity/

A

adaptive - big guns

132
Q

ontogeny of t-lymphocytes

A
  • prothymocytes from bone marrow migrate to the thymus (thymocytes)
  • thymocytes matuer into mature t-cells
  • memory T-cells from thymus travel to peripheral lymphoid organs
  • memory t-cells reside in the blood stream until directed to enter non-lymphoid tissues to elicit cell-mediated immune responses
133
Q

t-helper population of lymphocytes

A
  • Th1 cells –> cell mediated immunity (IgG can be produced)
  • Th2 cells –> humoral immunity (esp IgE)
  • Th17 cells –> enhance inflammation
134
Q

cytotoxic t-lymphocytes do what/

A

lyse virus infected cells

135
Q

regulatory t-lymphocytes are

A

Th3 cells, T_reg cells - suppress immunity - slowing down immune response

136
Q

T-cell antigen receptor (TCR)

A
  • tells a T-cell what it is responsible for
  • specificity for T-cell to see ITS antigen
  • TCR is not responsible for MHC restriction (function CD4 -ONLY CLASS2 and CD8-ONLY CLASS1)
  • genes encoding the TCR rearranged similar to immunoglobulin genes
  • heterodimer of disulfide-linked alpha and beta chains
  • each chain has constant and variable regions similar to antibodies
  • different antigen specificities generated by altering variable regions
  • ONLY STICK TO T-CELL .. NEVER are let loose unlike antibodies and TCR has single antigen binding site unlike B-cell antigen receptor (antibody bound to surface)
  • BOTH chains incolved in binding antigen AND MHC
  • cytoplasmic tails are not long enough to act as signal transducers =>requires CD3
137
Q

CD3 of TCR

A
  • tells the inside of the cell that TCR bound something to react to
  • EVERY T-cell has CD3
138
Q

Co-stimulatory molecules needed for a T-cell response to occur:

A
  • Aid the t-cell to become activated by triggering signal transduction
  • CD28(on T-cell) binds B7 (on APC)
  • CD40 ligand (CD40L- on T-cell) binds CD40 (on APC)
  • B7 and CD40 are expressed on ALL professional antigen presenting cells
  • suppresion without these co-stim molecules
139
Q

CD4 and CD8 molecules do waht?

A

-MHC restriction with Class 2 (CD4) and Class 1 (CD8)

140
Q

CD4 characteristics:

A
  • transmembrane glycoprotein w/ single polypeptide
  • on 65% of mature t-lymphs
  • most CD4-expressing lymphocytes are T-helper cells**
  • present in small quantities on the surface of macrophages
141
Q

CD4 functions:

A

cell adhesion molecules
signal transduction
restricts T-cell responses to recognizing only class II MHC proteins (binds invariant regions of Class II MHC proteins)

142
Q

CD8 characteristics

A

composed of a homodimer or heterodimer

most CD8 expressing lymphocytes are cytotoxic t-lymphocytes

143
Q

CD8 protein functions

A

cell adhesion
signal transduction
restricts t-cell responses to recognizing only class I MHC proteins (CD8 binds to invariant regions of Class I MHC proteins)

144
Q

activation of T-cell details:

A

-need multiple TCR to bind to multiple MHC pepdtide complexes

145
Q

what do interleukin 2 and IL2 receptor do?

A

For autocrine growth - dont have very many t-cells for somthing until theyre activated — when they are activated you want ++++++ tons and then some to hang around for memory later on

146
Q

t-lymphocytes only respond to…

A

processed antigen

147
Q

activated of T-cell follows

A

the binding of TCR to the antigen MHC complex

148
Q

additional signals for activation are provided by …

A

costimulatory molecules

149
Q

Th1 and Th2 activation

A

1) native CD4 t-cell (uncommitted)
2) proliferating t-cell
3) immature effector t-cell (T_H0)
4a) Th1 cell - activates macrophages: induces B-cells to produce opsonizing antibody (IL12)
4b) Th2 cells to make neutralizing antibody: has various effects on macrophages(IL-4)

Direction to4a/4b is done by presence of interleukin-12 or interleukin-4

Unless inflamation is present to induce macrophages to produce IL12, the Default path produces Th2 cells

150
Q

interleukin -12

A
  • produced by macrophages and dendritic cells

- produces Th1 cells = cell mediated immunity

151
Q

interleukin 4

A
  • produced by mast cells or antigen activated t-cells

- produces Th2 cells = antibody .. humoral?

152
Q

other factors in Th1 and Th2 activation

A
  • peptides in large quantities = induce Th1
  • peptides in small quantities = induce Th2 (allergens)
  • peptides that bind strongly to T-cell antigen receptor cause Th1 responses
  • peptides that bind weekly = Th2 responses
153
Q

cytokine secretion pattern:

A
  • Th1 cells –> interferon-gamma and IL2
  • Th2 cells —> IL4, IL5, IL10, IL13
  • Th3 cells and T_reg lymphoc –> transforming growth factor-beta
154
Q

Th1 cytokine response:

A
  • cell-mediated immune response against intracellular pathogens (virusrs and bacteria)
  • interferon-gamma - activates the microbial activities of macrophages and stimulates B-cells to produce IgG antibody
  • IL2 (with interfon-gamma) generates cytotoxic t-lymphs which kil lvirus infected host cells
  • INH Th2
155
Q

Th2 cytokine response:

A
  • IgE antibody and mast cell mediated immune reactions against helminth (worm) infestations
  • INH Th1
156
Q

t-helpers

A

CD4+

they coordinate everything - make sure that b-cells make antibodies and cytotoxic t-cells go kill some things

157
Q

Cytotoxic t-cell activation (CTL)

A

destroy inracellular microbes (virus/bacteria), tumor cells, transplanted tissues and organs
-prior to differentiation, pre-CTLs do not have cytolytic capabilities - they are inside circulating as pre-CTLs

158
Q

Pre-CTL–>CTL requirements

A
  • endogenous peptide presented on class i MHC
  • costim molecule interactions: CD28 on CTL and B7 on target
  • Th1-derived interferon-gamma and IL2
159
Q

steps how CTL kills

A

1) target cell binding and recognition of class I MHC and antigen - tumor cell, bacteria, etc
2) CTL activation
3) delivery of lethal hit
4) disengagement from the target cell to attach another target cell
5) DEATH of target

160
Q

CTL principle killing mechanism

A
  • delivery of perforins (form hole in membrane) to target cell surface –> osmolytic lysis
  • granzyme B –> enters through perforin pores and acti ates caspases –> appoptosis of the target cell
161
Q

CTL secondary killing mechanism

A

-binding of CTL-expressed Fas ligand to target cell Fas protein –> activates caspases –> apoptosis

Immuno/Micro/Viro (14 decks)

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