Chapter 6 pt 1 Flashcards

1
Q

location of dendritic cells

A

in epithelia, lymphoid organs and most tissue

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2
Q

role of NK cells

A

early protection against many viruses and intracellular bacteria

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3
Q

innate lympohid cells

A

look like lymphocytes but have features of innate immunity

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4
Q

plasma proteins

A

complement
mannose binding lectin
CRP
lung surfactant

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5
Q

complement system innate and adaptive

A

innate by alternative and lectin path

adapative uses classical pathway by recognizing microbes coated with Abs

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6
Q

TLRs signal via NF-Kb and what else

A

Interferon regulatory factors which stimulates the production of antiviral cytokines (type 1 interferons)

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7
Q

NLR signal via what and can play a role in what

A

inflammasome pathway

gout
obesity associated type 2 diabetes
atheroscelrosis

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8
Q

inflammasome pathway

A

1) NLRP3 recognizes pathogenic bacteria or extracell ATP
2) recruit adapter protein (X2) and inactivated caspase-1 (X2)
3) caspase-1 becomes activated and cleaves Pro-IL1B to IL-1B
4) IL-1B secreted and causes accute inflammation and fever

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9
Q

where is C-type lectin receptors located and on which cells

what does it detect

A

on PM of macrophages and dendritic cells

detects fungal glycans and elicit inflammatory reactions

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10
Q

G protein coupled receptors that recog microbes are on what cells
and recognize what microbes

A

neutrophils macrophages and most leukocytes

recognize bacterial peptides containing N-FMEt

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11
Q

B lymphocyte functions

A

neutralization of microbe with Abs
phagocytosis
complement activation

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12
Q

helper T cell function

A

activation of macrophages
inflammation
prolif and diff of T and B cells

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13
Q

what is clonal selection

A

when a lymphyocyte is exposed and responds to one antigen it undergoes this and proliferates
-all the “clones” recognize the same antigen

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14
Q

lymphocyte diversity: enzymes that are recomb

A

RAG-1 and RAG-2

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15
Q

majority of lymphocytes in blood and tissue are

A

T lymphocytes

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16
Q

TCR 2 types

A

95% are made up of a and B polypeptide chain

small population are yd

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17
Q

what do yd TCR receptors recognize

  • where do they aggregate
  • assistance or no assistance MHC proteins
A

Lipids, peptides, and small molecules
without assistance from MHC proteins
aggregatie at epithelial surfaces

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18
Q

NK T cells recognize what dsiplayed by what

A

glycolipids displayed by MHC like molecule CD1

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19
Q

which is more prevelenat CD4 or CD8

A

CD4: 60%
CD8: 30%

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20
Q

innate lymphoid cells produce what cytokines

A

IFN-y
IL-5
IL-17
IL-22

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21
Q

functions of innate lymphoid cells

A

early defense against infections
recognize and eliminate stressed cells
provide cytokines that influence differntiation of T lympocytes

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22
Q

what are innate lymphoid cells

A

populations of lymphocytes that lack TCRs but produce cytokines similar to T cells
NK cells are first defined

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23
Q

what happens in the bone marrow

A

production of all blood cells and where B lymphocytes mature

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24
Q

what is the main fnct of peripheral lymphoid organs

A

concentrate antigens, APCs, and lymphocytes in same spot

-optimizes interactions amoung these cells

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25
Q

dendritic cells and LN

A

dendritic cells pick up and transport antigens of microbes from epithelia and tissue via lymphatic vessels to lymph nodes. migrate to T cell zones and present them to T cells

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26
Q

in the spleen antigens are trapped by ____ and ___

A

macrophages and dendritic cells

recognize bloodborne antigens

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27
Q

where are 1/2 of the body’s lymphocytes

what types of cells are many of these

A

in the mucosal tissues, many are memory cells

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28
Q

what do B cell receptors recognize

A

proteins, polysaccharides and lipids

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29
Q

process of antigen presentation and prolif of T cells

A

APC presents to naive T cell with costimulation and cytokines
naive T cell expresses high affinity IL-2R and secretes IL-2 (autocrine)
causes prolfieration into effector and memory cells

30
Q

which T helper subset is involved in IBD, psoriasis and granulomatous inflammation

A

Th1

31
Q

which t helper subset is involved in IBD, psoriasis, and MS

A

Th17

32
Q

type 1 hypersensitivity Abs produced and others released

A

IgE
vasoactive amines
mediateors from mast cells

33
Q

type II HS Abs released

A

IgG and IgM bind to antigen on target cell

-phagocytosis or lysis of target

34
Q

type II prototypical disorders

A

autoimmune hemolytic anemia
goodpasture syndrome
unmatched blood transfucsion

35
Q

type III HS disorders

A

SLE, some glomerulonephritis, serum sickness, arthus reactions

36
Q

type IV HS disorders

A

contact dermatitis, MS, T1DM, tuberculosis`

37
Q

type 1 HS reactions (2)

A

immediate: vasodilation, vascular leakage, SM spasm, glandular secretion
- minutes after exposure, subsides in few hours

late-phase reaction
without additinal exposure to antigen
last several days
infiltrate tissue with BEN monocytes and cd4+ T cells

38
Q

besides IgE what else are mast cells triggered by

A
complement components (C5a and C3a)
chemokines (IL-8)
drugs (codeine and morphin)
adenosine
melittin (in bee venom)
physical stimuli (hot, cold, sunlight)

8 DAMP coochie

39
Q

Th2 cells nad IL-4

A
stimulates class switching of B cells to IgE 
promotes development of additional Th2 cells
40
Q

IL-13 from Th2 cells

A

enhances IgE production

acts on epithelial cells to stimulate mucus secretion

41
Q

crosslinking of FceR1 receptor on mast cell downstream signaling

A

cytokine gene activation–>cytokines and chemokines secreted (late phase reaction)

signals activation of phospholipase A2 which leads to production of Arachidonic acid and PAF
-arachdonic acid forms PGD2 and LT B4,C4,D,4 (late phase reaction)

signals for degranulation
-histamine, proteases (immediate reaction)

42
Q

what are in the preformed mast cell granules

A

histamine: intense SM contraction, increased vascular perm, increased mucus secretion

enzymes neutral proteases (chymase and tryptase) and acid hydrolases

  • tissue damage
  • act on precursor proteins to make
  • kinins and C3a

proteoglycans
-heparin
chondroitin sulfate

43
Q

lipid mast cell mediators LT and prostaglandins and ___

A

LT C4 and D4: most potent vasoactive and spasmogenic agents known

prostaglandin D2
-intense bronchospasm and increased mucus secretion

PAF: platelet aggregation, release of histamine, bronchospasm, incresaed vascular permeability, and vasodilation

PB HIV

44
Q

mast cell cytokines produced

A

TNF, IL-1 and chemokines

  • leukocyte recruitment (late phase rxn)
  • inflammatory cells release additional waves of mediators and cause epithelial cell damage

IL-4
-amplifies Th2 response

45
Q

late phase reaction ____ recruited without what

A

leukocytes recruited without antigen

46
Q

what cells in late phase reaction damage tisue and via what

A

eosinophils via proteases, MBP, and eosinophil cationic protein

47
Q

how do you treat late phase reaction

A

with anti-inflammatory drugs

anti-histamine only good for immediate rxn

48
Q

people with increased atopy have higher what and more what

A

IgE levels and more Il-4 producing Th2

49
Q

non-atopic allergy

triggered by what
what cells

A

20-30% of immediate hypersensitivity rxns
triggered by non-antigenic stimuli like temperature extremes and exercise

no Th2 or IgE

thought due to mast cells that are abnormally sensitive to activation

50
Q

examples of disorders caused by immediate hypersensitivity

A
anaphylaxis 
bronchial asthma
allergic rhinitis, sinusitis
hay fever
food allergies
51
Q

type II HS Abs (2 types)

A

autoantibodies or antigbodies to exogenous antigens such as chemical or microbial proteins

52
Q

mechanisms of Ab mediated injury

A

1) opsoniztion of cells by Abs and complement components and ingestion by phagocytes
2) inflammation induced by Ab binding to Fc receptors of leukocytes and by complement breakdown products

3) antireceptor antibbodies disturb normal fnct of receptors
(graves disease and myasthenia gravis)

53
Q

Ab mediated cell destruction and phagocytosis in disease (type II HS)

A

Transfusion reactions
-cells from incompatile donor react with and opsonized by preformed abs in host

hemolytic disease of newborn (erythroblastosis fetalis)
-maternal IgG anti erythrocyte Abs cross placenta and cause destruction of fetal red cells

certain drug reactions
-drug acts as hapten by attaching to PM of red cells and Abs produced against the complex

54
Q

Ab mediated inflammation in disease (Type II HS)

A

glomerulonephritis, vascular rejection in organ grafts

55
Q

antigens for type III HS

A

can be endogenous or exogenous

56
Q

immune complex mediated diseases preferentially involve

A

kidney (glomerulonephritis)
joints (arthritis)
small blood vessels (vasculitis)

57
Q

immune complex disease pathogenesis

A

complement fixing antibodies (IgG and IgM)

-induce pathologic lesions of immune complex disorders

58
Q

complement proteins and immune complex disease

A

copmlement proteins detected at site of injury
consumption in active disease–> decreased serum levels of C3
-monitor disease activity

59
Q

T cell mediated hypersens damage

A

inflammation from cytokines produced by CD4+ T cells and cell killing by CD8+ T cells

60
Q

what are the diseases in type 4

A

one more round of IPC

diabetes type 1, MS, rheumatoid arthritis, IBD, psoriasis, contact dermatits

61
Q

IFN-y activated macrophages do what

A

enhance ability to phagocytose and kill microbes
express more MHC class II
secrete TNF, IL-1 and chemokines–>inflammation
produce more IL-12–>amplified Th1 response

62
Q

what cytokine from Th17 is produced to amplify Th17 response

A

IL-21

63
Q

classic example of DTH is what

A

tuberculin reaction

64
Q

tuberculous infection has what cells dominate after 2-3 weeks

A

macrophages, fuse to make epitheloid cells, and these surrounded by lymphocytes called granuloma

65
Q

granulomatous inflammation is associated with strong ____ cell activation and high level of cytokines like

A

Th1 cell

IFN-y

66
Q

CD8+ t cell mediated diseases

A

type 1 diabetes and graft rejection after organ transplantation

67
Q

Cd8+ cells plays role in what

A

reactions against virus (can cause cell damage) and killing of tumor cells

68
Q

gut microbiome due what

A
play important role in local and systemic immune functions
brain development (gut-brain axis)
metabolic functions
hormones and neurochem production
biofilm
69
Q

gut microbiome formed by

A

influence by mode of delivery
child diet
by 3-4 it is adult like
maintained and altered by dietary changes

70
Q

dysbiosis

A

alteration of body’s microbial community that decreases pop of good bacteria, and allows bad bacteria to flourish