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Immuno Year 1 > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

Key features of the
adaptive immune system

A
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2
Q

The adaptive immune response is __________

A

specific: unique antigen receptors cap of recog antigens of specific microbe
diverse: # antigens vitually limitless - lots of different antigen receptors

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3
Q

down side to having such a diverse repertoire of antigens

A

number of cells capable of recognizing any one antigen is fairly small

solution? clonal expansion

  • Daughter cells bare antigen receptor identical to that expressed by the parent cell.
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4
Q

“Clonal Selection” hypothesis

A
  • Lymphocyte clones specific for different antigens develop before encounter with these antigens.
  • Antigen recognition triggers the expansion of lymphocytes of a specific clone.
  • Thereby specifically increasing the number of cells capable of recognizing/fighting the current infection.
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5
Q

Once the infection is cleared, the adaptive response ….

A

declines (contracts), however, long lived memory cells remain

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6
Q

Long-lived memory cells allow for …

A

more rapid and enhanced response upon reencounter with antigen

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7
Q

At 15 months of age, a child received a measles-mumps-rubella (MMR) vaccine. At age 22, she is living with a family in Mexico that has not been vaccinated and she is exposed to measles. Despite the exposure, she does not become infected. Which of the following properties of the adaptive immune system is illustrated in this scenario?

A.Self Tolerance

B.Diversity

C.Specialization

D.Memory

E.Specificity

A

Memory

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8
Q

All lymphocytes are morphologically similar

true/false

A

true!

no difference!

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9
Q

how can different kinds of lymphocytes ID?

A

unique surface proteins

CD (cluster of differentitation) numerial disgnation

detect CD molecules using antibodies

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10
Q

The most common method used to detect the presence of bound antibody is a technique called

A

flow cytometry

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11
Q

CDs of

B cells

T cells

NK cells

A

B: 19, 20, 21

T: 2,3

  • CD4: 4
  • CD8: 8

NK: 16, 56

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12
Q

B cell function

A

mediate humoral immunity: prod antibodies

  1. recognize soluble antigens
  2. present antigens on surface –> activates B cell
  3. naive T and B cells rise to effector cells (plasma for B)
  4. produce soluble antibodies with the same specificity as the membrane bound Ag receptor
  5. antibodies combat: neutralize, phago, complement sys
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13
Q
A

Activated effector B cell (Plasma cell)

large cytop: abundant mito & RER –> prod antibody

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14
Q

T cell function

A

detect antigens derived from foreign proteins or pathogens that have entered into host cells

T cells recognize small fragments of the antigen that have been broken down and presented by antigen presenting cells

  1. APC captures Ags –> breakdown
  2. fragment presented to T cell via MHC (major histocompatability complex)
  3. TCR (t-cell antigen receptor): recog fragment presented –> activates T-cell
  4. cell mediated imunity
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15
Q

CD4 antigen recognization and effector function

A

microbial antigen presented by APC

activ macrophages, inflammation, activ T and B lymphocytes

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16
Q

CD8 antigen recognition, effector functions

A

infected cell expressing microbial antigen

killing infected cell

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17
Q

CD4/CD25 lymphocytes

A

regulatory

suppressing of immune response

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18
Q

CD16/CD56 lymphocytes

A

NK

killing of infected cell

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19
Q

B and T cell development

A

both origin from hematopoietic stem cells in bone marrow

maturation:

  • b = bone marrow
  • t = thymus

upon release, they are mature –> circulate b/w blod and peripheral lymph organs for antigen response

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20
Q

T lymphocytes

naive cell

activated/effector

memory

Ig isotype

affinity of IG produced

effection functions

A
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21
Q

b cell deficiencies

A

abnormalities:

  • absent/reduced follicles & geminal centers in lymphoid organs
  • reduced serum Ig levels

consequences:

  • pyrogenic bac infections
  • enteric bacterial and viral infections
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22
Q

t cell deficiencies

A

abnormalities:

  • reduced T cell zones in lymophoid tiss
  • reduced DTH rxns to common antigens
  • defective prolif response to mitogens in vitro

consequences:

  • viral/intracell microbial infections
    • p. jiroveci
    • atyp mycobac
    • fungi
  • virus associated malignancies
    • EBV assoc lymphoma
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23
Q

innate immune deficiencies

A

abnormalities:

  • variable

consequences:

  • pyrogenic bac & viral infections
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24
Q

Memory cells are derived from…

purpose?

A

antigen stimulated lymphocytes

surv long periods of time in absence of antigens

repond rapidly to reappearnce of pathogen in higher #s compared to naive state( primary respnose)

  • enhanced secondary response
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25
Q

Antigen Presenting Cells play a critical role in the activation of

A

T cells.

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26
Q

Dendritic cells (DCs)

A

the most important APC

reside in the tissues most commonly used as portal of entry for pathogens

  • skin, mucosal tissues

capture protein antigens of microbes –> carry to reginal lymphoid tissues for T-cell presentation

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27
Q

follicular dendritic cells (FDCs)

A

display antigens that stimulate the activation/differentiation of B cells.

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28
Q

A 2 year old boy is evaluated for a immunodeficiency disease. He appears to have a normal number of CD3+ cells, however, there are no CD19+ cells found in the blood or peripheral lymphoid organs (spleen, lymph nodes). Which of the following cell types is this boy deficient in?

A.B cells

B.CD4 T cells

C.CD8 T cells

D.NK cells

E.Neutrophils

A

A.B cells

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29
Q

Consider the 2 year old boy in the previous case found to be deficient in CD19+ cells. Which of the following capabilities would this child’s immune system lack?

A.The presentation of antigen by MHC molecules

B.The recognition of antigen derived from an intracellular pathogen

C.The mobilization of neutrophils during the first few hours of an infection

D.The production of antibody against extracellular pathogens

E.The maintenance of the epithelial barrier

A

A.The production of antibody against extracellular pathogens

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30
Q

“fourth modality of cancer treatment”

A

Immunotherapy

next to chemo, radiation, sx

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31
Q

Innate immunity

A

Cellular and biochemical defense mechanisms in place before infection - rapid response

limits infections before adaptive

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32
Q

Adaptive immunity

A

shaped by exposure to infectious agents

increases in magnitude and defensive capabilities with each successive exposure

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33
Q

Features of innate immunity

A

Also called native, natural immunity

  • epithelial barriers
  • Present from birth

In place prior to infection –> responds rapidly to infection

  • no memory, ie, it is not any faster after second exposure

Is involved in the triggering and amplifying the adaptive immune response

Can be activated by molecules released from damaged or necrotic cells

Does not respond to structures present on normal host cells

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34
Q

Features of adaptive immunity

A

adapts to infection

pathogen-specific immunity

  • tailored to the specific type of infection

Enhanced by repeated exposure= = memory!

Often use the cells and molecules of the innate immune system to eliminate microbes

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35
Q

The cellular mediators of the innate and adaptive immune systems are derived from…

A

a common hematopoietic stem cell.

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36
Q
A

Neutrophil

Bloodstream, 1,800-7,800/ml

Multilobed nucleus, small pink granule

Short-lived

Phagocytosis and activation of bactericidal mechanisms

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37
Q
A

Monocyte

Bloodstream, 0-900/ml

Bean-shaped nucleus

CD14 positive

•Phagocytosis, recruited to sites of inflammation, differentiate into tissue macrophages

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38
Q
A

Macrophage

Tissues

Ruffled membrane,cytoplasm with vacuoles and vesicles

CD14 positive

Phagocytose microbes, dead cells,

secrete cytokines

present antigen

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39
Q
A

Dendritic cell

Epithelial, tissues

Long cytoplasmic arms

Antigen capture, transport and presentation

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40
Q
A

Mast cell

Tissues, mucosa, & epithelia

Small nucleus, cytoplasm packed with large blue granules

Release of granules containing histamine, etc., during allergic responses, anti-helminth responses

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41
Q
A

Eosinophil

Bloodstream, 0-450/ml, some in the epithelial tissues

Bilobed nucleus, large pink granules

Killing of antibody-coated parasites

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42
Q
A

Basophil

Bloodstream, 0-200/ml

Bilobed nucleus, large blue granules

Nonphagocytic, release

pharmacologically active substances

during allergic responses

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43
Q
A

Natural killer (NK), lymphoid origin

Express CD16, 56

Bloodstream, less than 10% of lymphocytes

Lymphocytes with large cytoplasmic granules

Kill tumor/virus cell targets or Ab-coated target cells (ADCC)

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44
Q
A

Lymphocyte - adaptive immunity

Bloodstream, 1,000-4,000/ml, lymph nodes, spleen, submucosa and epithelia

Large, dark nucleus, small rim of cytoplasm

B cells (CD19, 20, 21) produce Ab

TH cells (CD3, 4) regulate immune responses

CTLs (CD3, 8) kill infected, altered cells

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45
Q
A

Plasma cell - adaptive immunity

Lymph nodes, spleen, MALT, & bone marrow

Small dark nucleus, intensely staining golgi apparatus

End cell of B-lymphocyte differentiation, produce Ab

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46
Q

Humoral immunity

A

mediated by antibodies - proteins made by B cells

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47
Q

Cell-mediated immunity

A

responsible for the defense against intra-cellular microbes, and is mediated by T cells.

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48
Q

A previously health 8 year old boy is infected with an upper respiratory tract virus for the first time. During the first few hours of infection, which one of the following events occurs?

A.A lymphocyte response rapidly controls the infection.

B.An immune response dominated by neutrophils and monocytes keeps the infection under control

C.Killer CD8 T cells destroy infected epithelial cells

D.Antibody neutralizes the virus and prevents the spread of infection

E.Memory B cells quickly become activated to secrete antibody

●

●

A

A.An immune response dominated by neutrophils and monocytes keeps the infection under control

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49
Q

Foreign substances recognized by B and T lymphocytes are called

A

antigens

specific portion of antigen that is recognized by lymphocyte is called an epitope.

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50
Q

, B and T cells recognize antigen in what ways

A

T: only protein antigens

B & antibodies: many - prteins, carbos, nuc-acids, lipids

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51
Q

T and B lymphocytes that have not yet encountered antigen are said to be

A

naïve

“immunologically” inexperienced, and are in an “inactivated” state

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52
Q

Protective immunity against a microbe is induced by

A

host’s T and B cell recognition of, and response to the foreign antigen.

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53
Q

active immunity

A

whose lymphocytes have responded to microbial antigens and are protected from subsequent exposures to that microbe

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54
Q

Passive immunity

A

immune to antigen without previous exposure

  • txf serum/lymphocytes of immunized person
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55
Q

Many of the functions of the cells of the innate and adaptive immune systems are mediated by the release of

A

cytokines

conceptually sim to hormones - local and systemic

Have highly pleiotropic effects: multiple effects from single source

Chemokines attract other cells

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56
Q

In a normal individual, a primary infection is cleared from the body by

A

combined effects of innate and adaptive immunity.

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57
Q

Communication between elements of the innate and adaptive immune response

A
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58
Q

A standard treatment of animal bite victimes, when there is a possibility that the animal was infected with the rabies virus, is administration of human immunoglobulin preparations containing anti-rabies virus antibodies. Which type of immunity would be established by this treatment

A.Active humoral immunity

B.Passive humoral immunity

C.Active cell-mediated immunity

D.Passive cell-mediated immunity

E.Innate immunity

A

A.Passive humoral immunity

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59
Q

immune system tree

A
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60
Q

Most pathogens gain entry to the tissues through

A

skin, respiratory tract, or gastrointestinal tract

surfaces are protected by continuous epithelia that provides a physical and chemical barrier

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61
Q

The epithelium is colonized by normal flora

A
  • Compete for nutrients and colonization
  • Stimulate secretion of antimicrobial substances at epithelial surfaces
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62
Q

Epithelial Mechanical Barriers

A

Tight junctions

Mucus - prevent adherence pathogen to epithelial cells

Mucociliary elevator - microorg trapped in mucus pushed out by beating of cilia

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63
Q

Epithelial Chemical Barriers

A

skin:

  • sweat: anti-microbe FA

mucous memb:

  • HCl (parietal cells) - lowers pH
  • tears/saliva - enz dig
  • defensins/cathelicidins: direct toxicity
  • sufactants - opsonin - “coats” mic-org –> targ it for destruction by phago
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64
Q

Pathogen Associated Molecular Patterns (PAMPs)

A

innate immune sys recog limited # microbial products shared among broad groups

NOT present on host cells - often structures essential for surv % infectivity

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65
Q

Recognition of PAMPs is mediated by

A

•Pattern Recognition Receptors (PRR)

major fam = toll-like receptors (TLRs)

nod-like receptors (NLR) - microbial products, dmg tissue

ROG-like receptors (RIG-I, MDA-5) - recog viral rna

c-type lectin receptors - recog mannose residues

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66
Q

Innate immune receptors mediate these functions:

A
  1. Stimulate production of effector molecules and cytokines that induce innate responses and also influence down-stream adaptive immune responses
  2. Stimulate pathogen phagocytosis
  3. Chemotactic function, guide phagocytes to site of infection
67
Q

TLR pathway

A
68
Q

NOD-like cytosolic receptors (NLRs)

A

senses bac products & substances indicated cell dmg/death

NLRP-3 engagement –> combines with caspase 1 (complex = inflammasome)–> activ –> convert IL-1b into active form –> secreted

IL-1 induces infla and fever

69
Q

Sterile (non-infectious) Inflammatory NLRP3 activators & associated diseases

A

monosodium urate cyrstals - gout

beta-amyloid plaques - alzheimer’s

free FA, islet amyloid polypeptide - DM

ox-LDL, cholesterol crystals - atherosclerosis

70
Q

Defective TLR Signaling

A
71
Q

•MyD88 Deficiency

A

•Recurrent and severe pus-forming or pyogenic bacterial infection

72
Q

•IRAK4 Deficiency

A

•Recurrent severe bacterial infections (cellulitis, arthritis, meningitis, osteomyelitis, organ abscesses, and sepsis)

73
Q

•UNC93B Deficiency and TLR3 Mutations

A

•Increased susceptibility to encephalitis caused by herpes simplex virus

74
Q

•IKK/NEMO

A
  • Ectodermal dysplasia with immunodeficiency
  • Immunodeficiency ranges in severity from recurrent sinopulmonary infections extreme susceptibility to mycobacteria and opportunistic organisms
75
Q

Carl is a 1 month old healthy child who has not, as yet, received any childhood vaccines. He presents with his first episode of otitis media that is successfully treated with antibiotics. Which of the following immune components contributed the most to the clearing of the infectious agent during the first few days of the infection?

●

A.Antigen receptors on B lymphocytes

B.Toll like receptors on macrophages

C.Cytokines that promote antibody production

D.T cell responses to bacterial antigens

E.Memory B cells

A

A.Toll like receptors on macrophages

76
Q

macrophage populations

A
77
Q

Tissue Resident Innate Immune Cells

A

Macrophages

Dendritic Cells

Mast Cells

78
Q

Dendritic cells

A
79
Q

The inflammatory cytokines _______ (as well as the microbe itself) stimulate endothelial cells to express the adhesion molecules ___________

A

IL-1 and TNF-α

E and P selectin

80
Q

what makes “rolling”

A

shear forces made by blood flwo

weak binding of selectins

81
Q

neutrophil mig relies mainly on…

A

LFA1: ICAM-1 & MAC-1/ICAM-1 interactions, CSCR1 CXCR2 binding to chemokine IL-8

82
Q

monocytes mainly utilize

A

VLA-4:VCAM-1 interactions

CCL2 binding with CCR2

83
Q

Leukocyte Adhesion Deficiency

A

rare, auto-recessive

dec mvmt leukocytes to inflam sites & dec tight adhesions

  • absent/deficient expr the β2 integrins, LFA-1 and Mac-1
    • heterodimers of CD18/CD11 due to var mut in CD18 gene

symp:

  • delayed sep of umb cord
  • recurr infections of skin, lungs, GIT, perirectal

tx: BMT, stem cell txplant

84
Q

It is generally thought that a limited amount of inflammation at the site of vaccination helps to stimulate a strong adaptive immune response to the vaccine antigens. Which of the following substances, if introduced with the vaccine, would best serve the purpose of attracting a neutrophil infiltrate into the area?

A.G-CSF

B.IL-8

C.Prostaglandin

D.E selectin

E.TNFalpha

A

A.IL-8

85
Q
A

Neutrophils: PMN

dom in acute inflam, most abundant

first responders to most infections (part bac/fungi)

fx: enter cell –> phago

86
Q

neutrophil granules

A

specific

  • lysozyme
  • collagenase
  • elastase

azurophilic

  • defensins
  • cathelicidins
87
Q

G-CSF

A

granulocyte colon stim fac

  • prod neutrophils (reserve in BM and released during infection)
    • lifespan = 6 hrs

elev during infection

88
Q
A

Monocytes

monocytes –>extravasc tiss –> differn to macrophages

  • mononuc phago sys
    fx: engulf, secr, present (APC)
89
Q

Macrophages and neutrophils destroy microbes through a _________

A

2-step process:

1) engulfment and 2) killing.

90
Q

Antimicrobial Molecules

A

ROS

NADPH Oxidase

MPO (myeloperoxidase)

reactive N sp (iNOS)

proteolytic enz, lysozyme

91
Q

Chronic Granulomatous Disease (CGD)

A

mut: NADPH oxidase

recurr infection with catalase

granulomas: inab to kill phagoed bac

92
Q

macrophages

A

PRR: M1 (classic activ macrop) - inflam, microbe kill

  • IL-6
  • TNF-alpha
  • IL-1beta
  • CSCL8
  • IL-12

M2 (alt activ macrop) - activ by IL-4/IL-13 (absense strong TLR sig)

APC: adaptive imm response

93
Q
A

Dendritic Cells: link b/w innate and adaptive imm

myeloid precursors in bone marrow –> peripheral tiss in immature cells

capture antigen –> lymph –> present to naive T cells

94
Q

conventional DC (cDC)

A

capture antigens in peripheral tiss –> present to adaptive immune cells in lymph node

95
Q

plasmacytoid DC (pDC)

A

circ in perip blood –> recruit to inflam site –> activ –> prod interferon type 1

96
Q

mast cells

A

degranulation (s):

  • histamine - vasodil/inc permea
  • TNF-alpha
  • tryptase/chymase - proteolytic enz = kill bac, inactiv toxins
  • amine

eicosanoids (min)

  • LT, PG

cytokines/chemokines/GF (hours)

97
Q
A

Natural Killer Cells: CD16/CD56

  • do not expr antigen receptors like those expr by T and B lymphocytes

from common lymphoid progenitor

recog targ cells by ansense of MHC class 1 mol (self healthy cells)

2 pathways

  • perforin/granzyme
  • fas/fasL
98
Q

NK Cell Receptors

A
99
Q

Antibody-Dependent Cell-Mediated Cytotoxicity (ADDC)

A
100
Q

NK Cell Cytokines

A

IL-12: Stimulates the production of IFNγ from NK cells

IL-15: Important for the development and maturation of NK cells

Type I Interferons: Enhance the killing function of NK cells

101
Q

Lymphocytes with Limited Antigen Receptor Diversity

A

These cells have features of both the innate and adaptive immune systems, but are considered part of the innate system

102
Q

Complement (C’) System

A

made by liver –> present in blood, lymph, extracel fl

zymogens: proteolytic enz circ in inactive forms

activation via cleavage –> amplication –> less activated to large # effecgtor mol

103
Q

C-activation

A

cleave C prteins –> effector fx –> next pathway

104
Q

c-fixation

A

bindg active serum complement –> antigen-antibody pair/ microb surf

105
Q

Convertase/esterase

A

alt c-prot = proteolytic enz for another c-cmpt

106
Q

hemolytic units (CH50)

A

quant complement activity

dilution that lyses 50% stand ab-coated RBC

107
Q

The three main functions of complement

A
108
Q

3 pathways of complement activation

A

alt: early innate response to infection
lectin: innate but needs more time
classic: antibodies –> antigen: humoral adaptive immunity

109
Q

central to all c’ pathways…

A

cleave C3 –>

  • sml C3a
    • chemo-attactant: effector cells, mast cells –> vasoactive chem
  • lg C3b
    • opsonin: conval bind

C3 activates alt pathway but is later in other pathways

110
Q

Alternative Complement Pathway

A
111
Q

alt pathway of C’: important cmpts

A

C3:

  • C3b = opsonin - bind patho surf
  • C3a = stim inflam
  • C5 convertase

fac B:

  • Bb = serine protease: active enq of C3 and C5 convertase

fac D:

  • serine protease - cleaves fac B when it is bound to C3b

properdin:

  • stab C3 convertase (C3bBb) on microbe surf
112
Q

lectin pathway

A

init: absense of antibody
req: bind lectins (MBL: mannose binding lectin) –> microbe polysacc
* acute phase prod prod by liver during inflam

innate immunity: init by microb prod

113
Q

Activation of the lectin

pathway:

A

bind MBL to microbe –> brkdown C4 & C2 to a & b frag

  • C4b & C2a: coval bind to microb surf = c4b2a complex = C3 convertase = brkdwn C3
    • C3b =
      • opsonin
      • bind c4b2a –> C5 convertase = init last steps of C’ activ
114
Q

claassical complement pathway

A

init: bind antibody –> antigen

  • adaptive immune response
  • C1 bind Fc parts of IgG/IgM
115
Q

Activation of the classical complement pathway:

A

C1 binds 2 adj Abs –> activ –> cleave C4 & C2 to a & b frag

  • c4b2b = bind to surf = classical pathway C3 convertase = brkdwn C3
  • c3b:
    • opsonin
    • binds c4b2b –> C5 convertase = last steps of c’ activ
116
Q

end result of 3 pathways of c’activation

A

microbe acquires coat of C3b = opsonin

117
Q

anaphylotoxins in decreasing order of potency

A
118
Q

C9

A

final protein in c’ activation pathway

pore in cell memb (MAC - memb attack complex)

  • allows water and ions to enter = cell rupture
119
Q

Complement Deficiencies

A

C3 = usu fatal - recurr, server bac infections

C5-C9 = requ for assemble MAC

  • inc suscept to Neisserial infections: thin cell walls - esp suscep to lytic actions of complement
120
Q

why is host not dmged by c’ and microbes are?

A

mammals have reg protesin that inhib c’ activ: microbes lack

reg can be overwhelmed if coated with lg enough amts of antibody

121
Q

DAF

A

decay accelerating factor

disrupts C3 convertase in all 3 pathways

122
Q

MCP

A

memb cofactor protein

proteolysis C3b to inactive frag: med by factor I

123
Q

C1 inhibitor

A

C1 IHN

stops classic path activ: interfere with C1q

124
Q

Hereditary Angioedema

A

C1 INH deficiency: C1 esterase inhibitor

excessive C1 activation and subsequent activation of kinin sys

unpred/recurr episodes periodic swelling in subQsubmucosal tiss

125
Q

clinical symp of inflammation

A

redness: dil bv, inc blood flow

heat flow: dil bv, inc blood flow

swelling: accum fl/inflam cells
pain: stretch/distortion tiss by inflam fl, release of pain-inducing inflam mediators

loss of fx: swell/pain inhibit mvmt

126
Q

in the innate immune response, the priniciple course of cytokines are…

A

macrophages, mast cells, dendritic cells: activated by recog of microbes

127
Q

Major Proinflammatory Cytokines

A

TNF, IL-1, and IL-6

128
Q

local effects of proinflammatory cytokines

A

vasodil: marginalization fo leuko

activ endothelium: adhesion mol for stickyy

inc endothelium permea: diapedesis/extravasation

129
Q

Systemic Effects of Inflammatory Cytokines

A
130
Q

pyrogens

A

IL-1, IL-6 and TNFa: can induce fever

higher temps:

  • slow patho growth
  • actively sequester iron - lim bac growth
131
Q

acute phase proteins

A

prod by liver in response to inflam cytokines: induced bby IL-1, IL-6, TNF

  • MBL: recog microb carbs = coat for phago, or activ lectin c’ pathway
  • c-reactive protein: binds PC –> coats for phago by macrop
    • expr receptor for CRP –> can trigger classical c’ path
132
Q

Septic Shock:

A

very high lvls TNFa prod in response to sys bac infection

133
Q

IL-8

A

major chemotactic factor for neutrophils

134
Q

IL-12

A

prod by macrophages and dendritic cells:

  • activ NK cell
  • induce differen of CD4 T cells into Th1 cells
  • end prod: IFNg
135
Q

•Type I Interferons (IFN)

A

major innate cytokine for viral infecftions

  • secr by viral infect cells/various lueko
  • Interferon-alpha (IFN-α)
  • Interferon-beta (IFN-β)

fx: protect surr cells from being affecting

136
Q

RIG-1

A

Host cells are alerted to the presence of a viral infection by the recognition of viral PAMPs (here dsRNA), by pattern recognition receptors

137
Q

biological actions of type I IFN (5)

A

induce expr enz that block viral replication

induce chemokines to recruit more leuko

inc MHC class 1 expr & APC

inc cytotox of NK/cytotoxic T cells

activ dendritic cells/macrop

138
Q

final role of innate immune response

A

activ adaptive immune reponse

effective immune response req mech of BOTH innate and adaptive

139
Q

pneumococci

A

resist phago

cap polysacc inhib phago

140
Q

staphylococci

A

resis ROS

prod catalase –> brkdown ROS

141
Q

Neisseria meningitidis, Streptococci

A

resis alt c’ path

expr sialic acid –> inhib C3/C5 convertases

M protein blocks C3 fx

142
Q

Pseudomonas

A

resis antimicrobial peptides

synth mod LPS

143
Q

primary lymph organs

A

BM, thymus

B & T lymphocytes mature –> expr antigen recep –> commited specificity –> fx maturity

144
Q

secondary lymph organs

A

lymph nodes, spleen, MALT

init adaptive immune response

optimize interactions b/w lympo, APCs, antigen

145
Q

bone marrow

A

multipotent hematopoietic stem cells

  • origin of most mature circ blood cells
  • CD34+, c-kit+ markers

early B cell mature

plasma cell

146
Q

c-Kit ligand

A

sources: BM stromal cells

immature cell targets: MSCs

induces: all cell types

147
Q

IL-7

A

source: fibroblast, bone marrow stromal cells
targets: immaure lymphoid progenitors

induces : T lympho

148
Q

IL-3

A

source: T cell
target: immaure progenitors
induces: all cell pops

149
Q

GM-CSF

A

source: T cells, macrop, endothelial, fibroblast
target: imaure/commited myeloid progen, mature macrop
induces: granulocytes, monocytes, macrop activ

150
Q

M-CSF

A

sources: macrop, endothelial cells, BM cells, fibroblasts
target: commited progenitor
induces: monocytes

151
Q

G-CSF

A

sources: macrop, fibroblast, endothelial cells
target: commited granulocyte progen
induces: granulocytes

152
Q

fit-3 ligand

A

sources: BM stromal cells
target: HSC, DC, B cell progen
induces: classic and plasmacytoid DCs, B-cells

153
Q

Key Hematopoietic Cytokines in Bone Marrow

A

c-kit ligand (stem cell factor)

IL-7

IL-3

GM-CSF

M-CSF

G-CSF

fit-3 ligand

154
Q

common lymophoid progen cell

A

precursor: T, C, NK cells

most steps B-cell matur = in BM, final steps @ 2ndary lymph organs (esp spleen)

155
Q

common myeloid progenitor cell

A

makes: RBC, platelet, granulocytes, monocytes

most dendritic cells from monocyte lineage

156
Q

characteristics?

A

thymus: site of T cell mature

3rd pharyngeal pouch

2 compartments:

  • outer cortex: thymocytes
    • epith cells secr IL-7: GF for early T cell dev
  • inner medulla: mature T cells
    • epith cells remove self-reactive T cells

involution after puberty: decline new T cell prod

157
Q

DiGeorge syndrome

A

T-cell defic: gene mutation

also affects parathyroid gland –> hypocalcemia & heart dev

  • due to 3rd pharyngeal pouch origin
158
Q

•A 52 year old man who receives radiation therapy and cytotoxic drugs for treatment of cancer sustains significant damage to his bone marrow. Which of the following changes will most likely occur?

•

A.Decreased production of monocytes but not B lymphocytes

B.Decreased production of B lymphocytes but not T lymphocytes

C.Decreased production of neutrophils and monocytes but not B lymphocytes

D.Decreased production of B and T lymphocytes, monocytes, neutrophils, and red blood cells

E.Normal production of all red blood cells due to compensatory extra medullary hematopoiesis

A

Decreased production of B and T lymphocytes, monocytes, neutrophils, and red blood cells

159
Q

•In DiGeorge syndrome, the thymus fails to develop. Which of the following characterizes the immunodeficiency state in this syndrome?

•

A.Low numbers of neutrophils and monocytes in the blood.

B.Deficiency in antibody production in response to bacteria polysaccharides

C.Deficiency in cell mediated immunity in response to an intracellular infection

D.Normal T cell numbers, however, defective T cell activation

E.Deficiency in B cell maturation

A

A.Normal T cell numbers, however, defective T cell activation

160
Q

Peripheral Lymphoid Organs Function

A

collect/concentrate antigens

naive lympho mig here –>

  • try to recog antigens
  • concentrated here to init responses
161
Q

elephantiasis

A

Wuchereria bancrofti

Result of Interstitial Fluid Collecting and not Draining to the Lymphatics

162
Q

Different areas of the lymph nodes have distinct functional properties.

A
163
Q
A

Immuno Year 1 (4 decks)

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