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Pathology 2 > 4.6 Immunopath 1 > Flashcards

4.6 Immunopath 1 Flashcards

1
Q

Host defense

A

Inate immunity – barriers + inflammation, Adaptive immunity –humoral + cellular

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2
Q

innate immunity

A

barriers–>epithelia–> mechanical barriers + secretory products, inflammation–> cells + complement

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3
Q

cells of innate immunity in inflammation

A

neutrophils, macrophages, NK cells, DCs

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4
Q

innate immunity

A

no specificity, linked to adaptive immunity, molecular pattern recognition receptors (eg. Toll like receptors) which recognize molecules unique and critical to microbes (proteins we don’t have), or cellular stress proteins (like heat shock proteins)

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5
Q

innate immunitiy recognizes

A

pathogen related molecular patterns (microbes) or Danger associated molecular patterns (stress proteins) and recognition results in leukocyte activation, opsonization, and direct microbial killing

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6
Q

adaptive immunity

A

humoral immunity –> B cells/Plasma cells, Cellular immunity –> T cells, there is crss talk btw these two branches

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7
Q

Adaptive immunity is

A

specific, and macrophages and DCs are also involved (along with innate)–>APCs

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8
Q

Cells of the Adaptive Response

A

T cells –CD8 and CD4 (Th1,2,17), Bcells–Plasma cells

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9
Q

where do you find B and T cells

A

they are anatomically separated until they need to interact

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10
Q

what makes up the majority of circulating lymphocytes

A

T cells (60-70%)

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11
Q

Where are T cells found

A

paracortical areas of lymphnodes and in the arteriorlar sheaths of the spleen

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12
Q

What are T cells programmed to do

A

each t cell is programmed to recognize a single antigenic component via its T-cell receptor

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13
Q

what are non variable accessory molecules associated with TCR

A

CD3 – they help transduce the signal after binding –CD3 is occasionally found on NK cells

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14
Q

what are the signals involved with Tcells and APCs

A

Signal 1–>CD4/8 and MHC II/I, TCR, CD3, Signal 2–> CD28–CD80/86

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15
Q

TCR

A

each receptor specific for a single antigenic determinant, diversity through gene rearrangement via RAG 1 and 2, remember all cells have TCR genes but they are only rearranged in a T cell

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16
Q

CD4 and CD8 on T cells

A

markers and functional surface proteins that separate T cells into 2 distingce populations: CD4–helper and CD-8–killer

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17
Q

of CD3 positive cells

A

CD4 cells represent 60%, CD8 cells represent 30%

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18
Q

CD4s further divided into

A

Th1, Th2, Th17 by cytokine markers

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19
Q

Th1

A

induced by IFN gamma and IL12, cytokines produced are IFN gamma, actions–Macrophage activation, IgG production, Host defense against–intracellular microbes, role in disease–immune mediated chornic inflammatory diseases (often autoimmune)

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20
Q

Th2

A

induced by IL4, cytokines produces are IL4, 5, 13, Actions: IgE production eosinophil activation, Host defense against –helminthic parasites, role in disease–allergies

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21
Q

Th17

A

Induced by TGFbeta, IL6, 1, 23, Cytokines produced IL 17, 22, Actions: Recruit monocytes and neutrophils, host defense against –extracellular bacteria, fungi, role in disease–immune mediated chronic inflammatory diseases (often autoimmune)

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22
Q

B Cells make up

A

10-20% of peripheral circulating pool

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23
Q

B cells are found in

A

lymphnodes and spleen infollicles, in submucosa of GI tract

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24
Q

on stimulation B cells turn into

A

plasma cells, the Ab factories

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25
Q

B cell receptors

A

unique receptors, surface IgM and IgD ab is the ag binding moiety

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26
Q

B cell non variable accessory molecules

A

Ig alpha and Ig beta (CD79 a and b) similar to CD3 molecuels that help transduce the signal

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27
Q

B cells have receptors for

A

complement, Fc, and CD40

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28
Q

Bcells have abundant

A

C’2 receptors (CD21) which is the receptor for EBV

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29
Q

B cell markers

A

CD19, CD20, CD22

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30
Q

B cell activation

A

B cells are activated by a number of ag but mostly require T-cells for a robust response (especially protein ag), some ag are T independent

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31
Q

T cells secrete

A

stimulatory cytokines for b cells, and express the ligand for CD40.

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32
Q

B cell T cell interaction via CD 40

A

essential for secretion of IgG A E (hyper-IgM syndrome)

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33
Q

B cell signals

A

Signal 1– Ab-Ag w/ Igbeta &alpha, Signal 2–CD 21 - complement - Ag

34
Q

Antibodies

A

IgM, G (subtypes IgG1, IgG2), IgA, IgE, Each Ab is specific for a single antigenic determinant, diversity achieved through gene rearrangement (RAG1 and 2)

35
Q

how can you tell if you have B cell leukemia and not just an infection

A

the antiboides will all be the same in B cell leukemia bc the b cells are monoclonal

36
Q

IgM structure

A

like a star of 5 Abs

37
Q

IgG, D, E structure

A

a sing Y shaped structure

38
Q

Ig A structure

A

two Abs

39
Q

IgE

A

binds to receptors on mast cells, histamine released when Ag is bound, works with eosinophils to kill works, responsible for hay fever and anaphylactic shock

40
Q

IgA

A

secreted onto mucosal surfaces – if there is an IgA deficiency pt will survive and is often non symptomatic bc back up systems work well in this case

41
Q

how does the hep B vaccine work

A

first injection produces an IgM response that takes 3-4w to subside (need to wait till these Ab go down before you give the next dose to ensure that the initial Abs don_t eat up the 2nd dose of the vaccine), the second dose is small to produce a highly selective subset of ab with the higherst affinity, and the 3rd shot is to boost titer leves so you have Ab floating around that can respond if necessary. Need to check titers even if vaccinated to ensure that you have ab floating around and are protected

42
Q

The mononuclear Phagocyte System

A

monocytes, macrophages, Kupffer cells, microglia, mesangial cells, DCs, langerhans cells, major interaction in adaptive immunity is Ag presentation, Dendritic cells are professional APC especially for primary responses. Macrophages can present ag but usually recall Ags/ ones that you’ve seen before

43
Q

Monocyte becomes

A

a resident macrophage or an activated macrophage, remember they have the ability fo fine tune their functions so they can function without damaging self

44
Q

IFN gamma and LPS

A

alone they both produce a response (IFN>LPS), but together they are synergistic meaning when you have both you’ll have stronger responses even if at lower doses

45
Q

TLR2

A

ligand–lipoproteins, peptidoglycan, zymosan, LPS, GPI anchor, Lipoarabinomannan, Phosphatidylinositol dimannosied, Microbial source–Bacteria, Gram positive bacteria, Fungi, Leptospira, Trypanosomes, Mycobacteria

46
Q

TLR 3

A

Ligand–DS RNA, Microbial source –Viruses

47
Q

TLR 4

A

Ligand –LPS, HSF00, Microbial source–Gr neg bacteria, Chlamydia

48
Q

TLR 5

A

Ligand–flagellin, Microbial source–various bacteria

49
Q

TLR 6

A

ligand–CpG DNA, Microbial source–bacteria, protozoans

50
Q

Activated Macrophages

A

increased surface expressin of Class II MHC, increased phagocytosis, incresaed secretion of O2-, H2O2, proteases etc, increased secretion of cytokines (esp TNF, IL1, 12, 8, and sometiems IL 10), Secretion of NO, Increased killing of intracellular pathogens, increased ADCC, killing of some types of tumor cells

51
Q

ADCC

A

ab dep cellmediated cytotoxicity – monocytes activated, target cells coated with AB, they can kill (NK cells do this)

52
Q

slide 30??

A

Macs–classical IL12, Exposure to Steroids, IL4, or immune complexes IL10; T cells –IFN gamma and Th1, IL4 and TH2

53
Q

Dendritic cells

A

1 DC can present to many T cells due to all its dendrites

54
Q

Types of dendritic cells

A

interdigitating DCs (or just DC), Follicular DC

55
Q

Interdigitating DCs (or just DC)

A

located throughout body at portals of entry, Ag capture receptors, express same chemokine receptors as T cells recruited to T cell areas of lymphid organs, high levels of MHC II and costimulatory molecues so Ag presented to CD4 cells – only takes 15 seconds to get DC going to LN

56
Q

Follicular DCs

A

in splenic and LN follicles, Fc and C3b receptors–capture Ab bound Ag, APC to B-cells and selection for inc affinity

57
Q

NK cells

A

aka the larger granular lymphocyte, have innate ability to kill virally infected cells and some tumor cells, 10-15% of circulating lymphocytes, CD3 negative but CD16 (Fc receptor) positive thus perfroming ADCC and CD56 positive, NK cells kill virally infected cellls that have low MHC I molecule, increased MHC I inhibits NK cells, NK cells recognize certain stress proteins not normally expressed on cells unless virally infected

58
Q

NK cells work by

A

secreting IFN gamma and TNF, IFN gamma activates macrophages and induces CD4 cells to differentiate toward TH1 responses, virally infected cells and newly formed tumor cells often have low MHC 1 molecules and certain stress/triggering molecuels on surface

59
Q

cytokines and chemokines

A

communication molecules of the immune response

60
Q

innate immunity cyto/chemo kines

A

TNF alpha, IL 1, 6, IFN alpha, beta

61
Q

Lymphocyte activation and growth cyto/chemokines

A

IL 2, 4, 5, 12, 15, TGF beta, IL 10

62
Q

Activation of inflammatory cells cyto/chemokines

A

IFN gamma, TNF alpha and beta, IL 17, 22

63
Q

Stimulation of hematopoesis cyto/chemokines

A

GM-CSF, M-CSF

64
Q

Leukocyte movement cyto/chemokines

A

CXC or C-C: IL8 and MCP1

65
Q

MHC

A

major histocompattibility complex, class I and II, major antigenic determinants on tissues, necessary for humoral and cellular immune responses,

66
Q

where are MHC genes coded

A

all coded from a small region on chromosome 6 called the MHC complex

67
Q

MHC function

A

MCH domains and peptides are highly polymorphic, many alleles in the population, major function is to display antigens, polymorphism associated with binding of different antigens, diversity ensures in whole population all ag can be presented (but not by all individuals), no 2 individuals have the same MHC haplotype so transplantation is a problem

68
Q

MHC I domains

A

alpha 2 alpha 1, alpha 3, beta2 microblobulin

69
Q

MHCII domaines

A

alpha1 beta1, alpha2 beta 2

70
Q

Class I MHC

A

present on all nucleated cells in body including platelets, a major transplantation barrier, HLA (human leukocyte antigetn), Three loci HLA-A, B, C, Binds and presents intracellular ag—mainly viruses that we are concerned about

71
Q

MHC I restricted functions

A

MCH has to bind self CD8 in order to kill, if it has nonself CD8 it won’t kill

72
Q

Why do we have MHC restricted functions

A

bc during a viral infection, the virus sheds proteins, those proteins coat cells. T-cells are not just going to kill a protein coated cell bc there would be no purpose in that. It wants to kill a cell that is infected. So to know it is infected the particles must be presented on MHC I.

73
Q

Class II MHC

A

on macrophages, dendritic cells, and some B-cells, major transplantation barrier, HLA-D region, subregions DP, DQ and DR, Major role – Processed exogenous ag presentation. Karatinocytes can start expressing class II but under most cases MHC II is only on APCs. binds CD4 T cells.

74
Q

Mac/DC stimulates T cells by producing

A

IL1 and IL12

75
Q

T cell stimulates Mac/DC bye producing

A

IFN gamma

76
Q

CD4 T cells self stimulate by

A

IL2

77
Q

CD4 T cells also produce

A

IL2 for B cell factors, and other T cell factors

78
Q

Macs/DCs also produce

A

TNF and other chemical mediators

79
Q

Costimulatory molecules on APC

A

B7 1 and 2 (CD80 and 86), CD40

80
Q

Costimulatory molecules on CD4 t cell

A

CD 28 and CD40L

81
Q

Why do we need MHC restriction and Costimulation

A

they help us select for clones that don’t react to self in the thymic epithelia and BM

82
Q

Diseases Associated with HLA

A

inflammatory diseases –Ankylosing spondylitis, HLA-B27 have 90 fold inc chance of disease, Metabolic genetic disease several metabolic genes map within HLA locus, Autoimmune disease MHCI and II associations

Pathology 2 (15 decks)

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