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micro immuno exam 1 > antibacterial immunity > Flashcards

antibacterial immunity Flashcards

1
Q

Different pathogens trigger

A

distinct immune response and effector mechansims

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2
Q

Parts of Innate Immunity

A

Macrophages, Neutrophils, Complement system

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3
Q

Parts of Adaptive Immunity

A 
B cells and Antibody (IgG) 
T cells (Indirect help by helper CD4 T cells)
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4
Q

How neutorphils and Macrophages remove antigen

A

Phagocytosis

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5
Q

High Affinity receptors by the Phagocyte

A

Mannose receptor
Mac-1 Integrin
Scavenger receptor

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6
Q

Receptor that binds mannose on microbe cell wall mediated cell-microbe binding and initiating phagocytosis

A

Mannose receptor

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7
Q

Bind Microbes opsonized with complement proteins

A

MAc-1 Integrin

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8
Q

Binds Microbes in a non-mannose specific manner

A

Scavenger receptor

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9
Q

What region on the antibody binds to the Fc region of the phagocyte

A

Constant region

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10
Q

How Activated Macrophages and neutrophils can better kill pathogens

A

Reactive Oxyten Speices

Reactive Nitrogen INtermeidates (NO)

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11
Q

Conversion of Molecular oxygen into ROS

A

respiratory Burst

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12
Q

Strong activation of macrophages and neutrophils can do what

A

Hurt host tissue by release of lysosomal enzymes ROS and NO

-can;t differentiate between host and infected tissue

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13
Q

Macrophages fight what

A

Extracellular pathogens

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14
Q

How do macrophages remove antigens

A

Phagocytosis and production of ROS and RNI

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15
Q

What do macrophages do with antigen

A

take up soluble antigens and process and present it to T cells

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16
Q

Who helps MAcrophages

A

Helper CD4+ T cells via IFN_gama secretion

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17
Q

What do macrophages secrete

A

Pro-inflammatory cytokines and chemokines that induce inflammation and immune chemotaxis

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18
Q

Migrate towrads site of inflammation within an hour of tissue injury in response to chemotactic factors (IL-8, IFN-gama, C5a)

A

Neutrophil

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19
Q

how neutrophils kill extracellular pathogens

A 
phagocytose microbes(ROS and RNI)
also oxygen independent mechanisms via degranulation
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20
Q

Release of granules

A

Degranulation

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21
Q

What granules do neutrophils release

A

Defensisns
Myeloperoxidase
Neutrophil extracellular traps

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22
Q

Action of Neutrophil extraceullar traps

A

Neutrophil dies and releases DNA to trap incoming bacteria

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23
Q

Roll of Complement in Immunity against Extracellular microbes

A

Serves as opsonin and enhances phagocytosis
Serves as chemokine and activates leukocytes to site of inflammation
Forms membrane attack complex and mediates lysis of microbe

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24
Q

B cells fighting extracellular microbes

A

Produce antibodies for neutralization, opsonization, and memory

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25
Q

B cells express what to present antigens to T cell from extracellular

A

MHC II

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26
Q

How to activate B cells in a T cell independent maner

A

Bacterial products

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27
Q

How Antibodies can protect cells

A

blocks binding of microbe to receptor or toxin

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28
Q

B cerll roll in immunity against extracellula

A

Secrete antibodies

  • Neutralization
  • Opsonization and Fc receptor mediated phagocytosis
  • Phagocytosis of C3b-coated bacteria
  • Inflammation
  • Bacterial Lysis
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29
Q

CD4+ cells in fighting extracellular microbes

A

inflammatory cyokines (IFN and TNF) and helper procution of cytokines (IL-4, IL-5, and IL-10)

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30
Q

IFN and TNF cytokines cause

A

Activate macrophage and promate phagocytosis, bacterial killing, an inflammation

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31
Q

CD4+ T cell that make inflammatory cytokines

A

Th1 cells

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32
Q

CD4+ T cells that produce IL-4, IL-5 and IL-10 are

A

B cell growth fator, which activates B cell and promote antibody procution

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33
Q

CD4+ T cells that make B cell promoting cytokines

A

Th2 cells

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34
Q

Evation of immune system by extracellular bacteria

A

Antigenic Variation
Inhibit complement activation
Resist phagocytosis
Scavenging of ROS

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35
Q

What normally responds to Intracellular pathgoens

A

Cell mediated rather than antibodies

36
Q

Cells from innate immune response intracellular pathogen

A

Dendritic cells, Natural Killer, MAcrophage/neutrophils

37
Q

Cells from adaptive Immune response intracellular

A

CD4+ and CD8+ T cells

38
Q

Roll of Dendritic cells against Intracellular pathogesn

A 
Present Ag to T cells, and travel to lymph notes for naive T cells
Produce cytokines (IL-12) to regulate differention of DC4+ T cells(promote Th1 or Th2)
39
Q

Roll of Natural Kiler cells

A

Kill virus infect cells and tumor

40
Q

NK cells secrete

A

Cytokines (IFN-gamma) for macrophages and Th1 development

41
Q

What regulates NK activation

A

signals from activating and inhibitory receptors

42
Q

How NK cells can kill cells

A 
Directly(if no MHC class I) it will kill it
Secrete IFN-gamma to recruit macrophages
43
Q

How CD4+ T cell helps with Phagocytic killing

A

Secretes IFN-gamma to kill bacteria in phagolysosome

44
Q

CD4+ T cell activating CD8+ T cell results in

A

Killing of infected cell (MHC class I)

45
Q

Th1 or Th2 for intracellular

A

Th1 to produce IFN-gamma and TNF-alpha and promote cell mediated immunity (help to CD8+ T cells and Macrophages)

46
Q

What do CD8+ T cell recognize

A

MHC I

47
Q

CD8+ cells secrete

A

Perforin and granzymes to directly lyse/ kill infected cells

IFN-gamma and TNF-alpha

48
Q

What phagocytes can CD8+ T cells kill

A

Those that have engulfed microbes

49
Q

A non-specific response to infection/injury that is characterized by enhanced accumulation of immune cells and plasma proteins

A

Inflammation

50
Q

Is Inflammation normal

A

Yes

51
Q

Why Pain receptors are stimulated during inflammation

A

Due to protein and fluid leak from damaged cells

52
Q

FIrst stage of wound healing

A

Inflammation

53
Q

Accute inflammation is involved with

A

Innate

54
Q

Why chronic inflammation

A

Stimulus stays and addaptive is there

55
Q

Cause of CHromic Inflammation

A

Persistance infection
Immune mediate inflammatory disease
Toxic agents

56
Q

Cells of accute inflammation

A

Neutrophils, monocytes/macrophages, mast cells, eosinophils and basophils

57
Q

Cell of Chronic Inflammation

A

MOnocytes/macrophages, T cells, Neutrophils

58
Q

Proinflammatory cytokines

A

Tumor Necrosis factor (TNF

Interleukin (IL-1beta and Il-6)

59
Q

Inflammatory mediates for vaosdilation

A

Histamine, Bradykinin, leukotrientes

60
Q

What released histamine

A

Mast cells due to interaction with microbes(compliment or IgE (allergy

61
Q

Prostoglandins are dervied from

A

Inflammatory mediators from cell membrane

62
Q

C5a is involved in

A

Monocytes/neutrophil recruitment for inflammatory

63
Q

c3a and c5a can trigger what in mast cells

A

Degranulation

64
Q

Cyotkines for stopping inflammation

A

IL-10, Tranforming Growth Factor (TGF-beta)

65
Q

How to stop cronic inflammation

A

Glucocorticoids, immunosuppressant, anti-leukotrienes

66
Q

the general process of leukocytes movement from blood to tissue

A

Migration/recruitment

67
Q

Low affinity adhesion molecules involved in early stage of leukocyte capture

A

Selectins

68
Q

Adhesion molecules invovled in later stage of leukocyte migration(high and low affinity)

A

Integrins

69
Q

what determines the type of Chemokine

A

Location of N terminal cystein residue

70
Q

1st step of

A

Tethering/rolling, slows down leukocyte within post-capillary venule

71
Q

Mediates Tethering/rolling

A

Selectin

72
Q

Where selectins are found

A

Plasma membrane adhesion molecule

73
Q

Selectins recognizes

A

Sialylated carbs

74
Q

Affininty of selectins

A

low

75
Q

Where are P selectins are store

A

Store in cytoplasmic granules to be expressed imediately

76
Q

When E elected expressed

A

2 hours after due to Cytokines

77
Q

Selecton on the Leukocyte

A

L-selectin

78
Q

Step 2

A

Integrin Acitvation

79
Q

What happens during integrin activation

A

Chemokines act on Rolling leukocyte and integrins change to high affinitny to stop leukocyte

80
Q

what makes Chemokines

A

Leukocytes, epithelial cells, and fibroblasts

81
Q

Upregulation of Chemokines

A

Microbes and proinflammatory cytokines

82
Q

Chemokine effect on integrins

A

Change to high affininty and cluster together to touch epithelium

83
Q

Step 3

A

Adherence

84
Q

Once leukocyte contant and stops

A

becomes flat due to change of cytoskelleton

85
Q

Step 4

A

Migration (diapedesis)

86
Q

To enter into tissue the leukocyte must

A

rearrange cytoskelton
Tight junctions loosen
follow chemokines to final site of infection

micro immuno exam 1 (8 decks)

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