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Immunology Flashcards

1
Q

Describe the components of the immune system.

A

Fixed elements: The lymphoid organs

Mobile elements: immune cells and soluble humoral components

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2
Q

What are the fixed elements?

A

They are the lympoid organs

  • Primary: bone marrow and thymus
  • Secondary: the spleen and lymph nodes, muscoal tissues ( peyer patches)
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3
Q

Describe the Hemopoesis slide

A
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4
Q

Where are the following cells made/ where do the reside?

Lymphoid progenitor

B cell precuror

T cell precursor

B lympocytes

T lymphocytes

NK cells

A
  • made in BM where stem cells reside
  • made in BM and stays in BM
  • made in BM but goes to thymus and replicates in thymus
  • bone marrow
  • thymus
  • made in bone marrow
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5
Q

What cells are made from granulocyte colony stimulating factor (G-CSF)?

A
  • MYLEOBLASTS
  • these furter differentate into neutrophils, basophils and eosinophils which occur in the bone marrow
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6
Q

What is produced under monocyte colony stimulating factor (M-CSF)?

A

myeloid progenitors differentiate into monoblasts which further differentiate into blood monocytes and dendritic cells which occurs in the bone marrow.

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7
Q

Monocytes can migrate into various tissues and differentiate into ____ and ____.

A

monocytederived dendritic cells and tissue macrophages

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8
Q

HEMOPOIESIS – DEVELOPMENT OF BLOOD CELLS ask to know

A
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9
Q

Describe the of Blood Cells and Their Identification

A
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10
Q

Granulocytes contain what? What does the latter do? What is another word for granulocytes?

A
  • contain granules with mediators prepared to discharge upon activation of those cells.
  • they are also called polymophic nuclear cells –> refering to the shape of their cells as they have 3-5 compartments.
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11
Q

What are CD molecules?

A
  • cell surface markers useful for identification and characterization of leukocytes when the cells can’t be differentiated based on microscopic morphology
  • assigned an arbitrary number
  • numbered up to 363
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12
Q

The presence or absence of a specific Ag on the surface of particular cell population is denoted with ____ or ___ respectively. Varying cellular expression levels are also marked as ____ or ___.

A

+

-

high

low

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13
Q

T cell CD marker

A

3,4,8

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14
Q

B cell CD marker

A

19, 20

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15
Q

NK cell CD marker

A

56

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16
Q

Macrophage/ monocyte CD marker

A

14

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17
Q

Phagocytes

A
  • Phagocytes include neutrophils and macrophages.
  • Then primary function is to ingest and destroy MICROBES and get rid of damaged tissues (scavenger function)

-Activated phagocytes also secret cytokines which promote and regulate immune responses.

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18
Q

Phagocytes Steps

A

• STEPS in functional responses of phagocytes:

– recruitment of the cells to the sites of infection

– recognition of and activation by microbes

– ingestion of the microbes by the process of phagocytosis

– destruction of ingested microbes

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19
Q

Neutrophils

A
  • have 3-5 connected lobules
  • Neutrophils comprise the majority of white blood cells (40–70%).
  • mediate the earlierst phases of the inflammatory rxn
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20
Q

Why are neutrophils named granulocytes?

A

-Neutrophils are named granulocytes because of the prominent cytoplasmic granules which contain:

• peroxidase • lysozyme • degradative enzymes • defensins

-Neutrophils can produce inflammatory mediators - cytokines, prostaglandins, and leukotrienes.

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21
Q

How long do neutrophils live in the blood and inflamatory tissue after they enter in it?

A
  • In the blood, neutrophils live for hours or a few days. And the die by apoptosis.
  • After entering inflammatory tissues, neutrophils function for 1 to 2 days and then die.
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22
Q

Leukocytosis

A

• Leukocytosis is defined as an elevated WHITE BLOOD CELL (WBC) count greater than 11,000 cells/mcL in nonpregnant adults.

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23
Q

What is the most common type of leukocytosis

A

NEUTROPHILIA is the most common type of leukocytosis because neutrophils are the most abundant granulocyte in blood circulation.

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24
Q

Leukocytosis is a ____, particularly caused by ______.

A
  • common sign of infection
  • extracellular bacteria
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25
Q

The normal reaction of bone marrow to infection or inflammation leads to an increase in the number of white blood cells, predominantly neutrophils and less mature cell forms _______

A

left shift

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26
Q

Leukopenia

A

is a reduction in the circulating WBC count to less than 4000/mcL.

-is usually characterized by NEUTROPENIA, a reduced number of circulating neutrophils

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27
Q

Neutropenia is

A

often caused by cancer chemotherapy or radiation therapy.

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28
Q

Decribe the ways neutrophils kill bacteria

A

1) PHAGOCYTOSIS: they use phagocytosis to engulf them. Pathogens in phagosomes are killed by reactive oxygen species or antibacterial proteins.
2) DEGRANULATION: antibacterial proteins are also released from the neutrophil granules into the extracellular milieu and kill pathogens extracellularly.
3) neutrophil extracellular traps: NETS: Composed of Core DNA elements to which histones, proteins and enzymes are relalsed from neutrophils granuels are attached. They immobilze pathogens and preventing them from spreading but also facilitate phagocytosis.

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29
Q

Do Neutrophils Live or Die After NET Formation?

A

-neutrophils continue their activities after NET formation.

they just have a net hanging out

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30
Q

MONOCYTES vs Macrophages

A

MONOCYTES are the main type of “mononuclear” phagocytes in the blood, whereas MACROPHAGES (MO) reside in the tissues.

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31
Q

DENDRITIC CELLS

A

similar functional characteristics with Mf and are the most efficient of the antigen-presenting cells (APCs).

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32
Q

MATURE MONOCYTES are released into the blood circulation.

A

Monocytes account for 3- 8% of white blood cells in the blood.

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33
Q

Normally blood monocytes ______. But if they enter the tissue _______.

A
  • a few days before undergoing apoptosis
  • a few days before undergoing apoptosis
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34
Q

Define Monocytosis and explain why it can occur.

A

• MONOCYTOSIS , an increased number of monocytes in the blood

can occur in response to: • chronic infections • autoimmune disorders • certain cancers • sarcoidosis (a proliferation of resident Mf can occur in tissues)

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35
Q

Monocytopenia

A

a low number of monocytes in the blood, can occur in people receiving chemotherapy

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36
Q

The Embryonic Origin of Resident Macrophages

A
  • when developing your hematopoetic progentiors emerge from hte yolk sack and diff into different macrophages in the tissues. These are called tissue resident macrophages
  • the tissue resident macrophages fulfill tissue specific function
  • after development you cant make these anymore, they regenerate on there own
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37
Q

Monocyte-Derived Inflammatory Tissue

A
  • Monocytes migrate into tissues where they differentiate into INFLAMMATORY macrophages
  • they are involved in: inflammatory reactions and 2. tissue remodeling that repairs “collateral damage” produced by hypersensitivity reactions.
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38
Q

Dendritic Cells (DCs)

A
  • are professional APC cells
  • BROADLY DIVIDED to myeloid (mDCs) and plasmacytoid DCs (pDCs)
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39
Q

mDC

A
  • derived from monocytes similar to tissue Mf. mDCs are responsible for capture, processing, and presentation of antigens on their surface to T cells.
  • langerhan cells are these, but they reside in the epidermise of the skin
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40
Q

pDC cells

A

IFN-producing DCs that circulate through the blood and peripheral tissues. The developmental origin of pDCs is uncertain

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41
Q

Mast Cells vs Basophiles

A

-mast cells:

found in tissue, are larger, are oval, cell border is bumpy, lives for months

  • basophils:
  • smaller, round, lobated nuclear shape, fewer than mast cells, cell border appears smooth, lives for a few days, found in blood (.5-1%)
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42
Q

Mast Cells and Basophiles have what in common?

A
  • play a role in allergic and anaphalytic reactions
  • contain basophilic granules with: histamine, serotonin, heparin, cytokines and chemokines
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43
Q

Mast Cells, Basophils, and Eosinophils do what?

A
  • They protect against helminthes and responsible for allergic reactions.
  • These cells share the common feature of having CYTOPLASMIC GRANULES filled with various inflammatory and antimicrobial mediators.
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44
Q

Mature mast cells do not ______. Instead, the MAST CELL PRECURSORS migrate via the blood circulation from the bone marrow into various tissues where they ______.

A
  • mature in blood
  • differentiae and mature locally
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45
Q

Mastocytosis: define it and give Sx

A
  • pathologic increase in mast cells within tissues
  • People affected by mastocytosis are susceptible to itching, hives, and anaphylactic shock, caused by the release of HISTAMINE from the abundant mast cells.
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46
Q

When mastocytosis is localized to the skin its called?

A

CUTANEOUS MASTOCYTOSIS

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47
Q

URTICARIA PIGMENTOSA

A

common form of cutaneous mastocytosis.

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48
Q

Eosinophils

A

most promient feature are their LARGE SECONDARY GRANULES containing four basic proteins

  • SMALL GRANULES contain histamine, peroxidase, lipase, and major basic protein.
  • BASIC PROTEINS are involved in anti-parasitic defense mechanisms as toxins directed against helminths.
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49
Q

Eosinophilia

A

peripheral blood eosinophil count > 500/mcL

  • common cause of it is: allergic or atopic disorders
  • other common causes are: infections and tumors
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50
Q

Natural Killer (NK) Cells

A
  • NK cells are granular lymphocytes which function is the IMMUNE SURVEILLANCE, a process that purges the body of infected cells and precancerous cells.
  • NK cells arise from BONE MARROW PRECURSORS and diff in the bone marrow
  • NK do not generate immunity and do not posses antigenic specificity
  • part of adaptive immunity, but because of BROAD SPECIFICITY for Ags, NK cell functions like a cell of innate immunity.
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51
Q

There are two major types of lymphocytes

A

B and T cells

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52
Q

The development and maturation of T cells occurs in

A

Thymus

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53
Q

When a mature T cell is Ag-stimulated, it gives rise to the development of

A

Cell mediated immunity

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54
Q

The development and maturation of B cells occur in the

A

-bone marrow and spleen

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55
Q

When a B cell is activated, it leads to the development of

A

Humoral immunity- involves the production of soluble effector molecules (Immunoglobulins)

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56
Q

Cell-Mediated Immunity (CMI) is by responses of _______ which often function in concert with ______ and ____ in elimnation of pathogens causing an infeciton.

A
  • t lympocytes
  • ag presenting cells
  • phagocytes
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57
Q

CMI mediates host _______ against ______ such as ____ and _____ where they are inaccessible to cirulating Ab.

A
  • defese
  • intracellular microbes
  • virus
  • some bacteria
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58
Q

CMI function is the _____ that eliminates the reservoirs of infection.

A

-killing of infected host cell

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59
Q

Some T lymphocytes (called T helper cells) also help ____ to make _____ and there by contribute to the eradication of _____.

A
  • b cells

high affinity abs

-eradication of extracellular microbes

60
Q

In humoral immunity, B lymphocytes ___________.

A

secrete Abs that prevent infections and eliminate extracellular microbes.

61
Q

In CMI, T helper cells activate ________________.

A

Mf to kill phagocytized microbes, or cytotoxic T lymphocytes (CTLs) to directly destroy infected cells.

62
Q

Hypothesis of Clonal Selection

A

All immunocompetent individuals have many distinct lymphocytes, each of which is specific for a different Ag.

  • When Ag is introduced into an individual, lymphocytes with receptors for this Ag seek out and bind Ag and are triggered to proliferate and differentiate giving rise to clones of cells specific for the Ag.
  • The cells from the clones or their products specifically react with the Ag to neutralize or eliminate Ag.
  • Some Ag-specific cells late in the immune response is responsible for the ‘memory’ involved in adaptive immunity.
63
Q

Explain the functional role of epithelial barriers.

A
  • skin and mucous membrane provide a barrier (has sebum: made of lactic acid and fatty acids, which reduce skin pH to 3-5 to ihibit microbe growth)
  • mucous membranes contain antimicrobal substances and are covered by cillia which trap it in mucous and propel them out
64
Q

Innate DEFENSE BARRIERS include

A

(1) anatomic barriers (2) physiologic barriers (3) inflammatory barriers phagocytic barriers (4) phagocytic barriers.

65
Q

Define inflammation:

A

• Inflammation is a COMPLEX REACTION that results from any injury, including an invasion by microorganisms.

66
Q

INFLAMMATION has a _____ but it can also cause substantial ____ and ___.

A
  • protective function
  • tissue damage
  • disease
67
Q

What are the 5 cardinal signs of inflammation

A
  • tumor (swelling)
  • rubor (redness)
  • calor (heat)
  • dolor (pain)
  • loss of function
68
Q

inflamation steps

A

1) blood supply increases to help carry immune cells to affected are
2) infected area becomes red and warm
3) swelling occurs
4) immune cells are recruited
5) wbc release subtances that attack the bacteria and contine the process of inflamation
6) inflamatory mediators (bradkin, prostaglandins, leukoteines, histamine, cytokines) produce by immune cells stimulate the nerves and cause pain
7) body rxns include chills, fever, muscle aches

69
Q

Fever due to inflamation is what?

Why does a fever help?

A

It is important to understand that fever is not directly caused by pathogenic factors.

Rather, bacterial constituents trigger production of the pyrogenic cytokines TNF, IL-1, and IL-6 in macrophages which are potent inducers of fever response controlled by the hypothalamus.

-beneficial to host in that most pathogens replicate poorly in elevated systemic temps.

70
Q

PAMP

A
  • how innate immunity recognizes self from nonself
  • pamps are unique to particular classes of pathogens
  • pamps often required for survival of pathogens so that PAMPs cannot be altered, suppressed, or hidden from the surface by pathogens
  • no structural similarity with self Ags.
71
Q

Examples of pamps

A
  1. Porins

2. Lipoproteins

3. Lipopolysaccharides

  1. Lipoteichoic acid
  2. Teichoic acid
  3. Mannoproteins

7. b-glycan

  1. Lipoarabinomannan
72
Q

Decribe the mannose receptor

A

It is a PRR: recognizes glycan with a terminal mannose.

  • found in bacteria, fungi and viruses
  • no glycans with a terminal mannose are found in humans
73
Q

General Properties of PRR

A
  • Germ-line encoded refers to sequences that are found in gamete producing cells.
  • A nonclonal distribution of receptors on innate immune system cells means that all cells have receptors with identical specificities.
74
Q

Which toll like receptors are found on the cell surface?

A

1,2,4,5,6

75
Q

Which are found inside and what do the regonize?

A

TLR 3,7,8,9

recognize intracellular patogens

76
Q

TLR chart

A

… SLIDE 20

77
Q

TLR function

A
  • when bound they stimulate the expression of cytokines and other mediators involved in the inflamatory and antimicrobal functons
  • activate TF: NF-kB and IRF
78
Q

NF-KB

A

promotes expression of various cytokines and endothelial adhesion molecules that play important roles in inflammation.

79
Q

IRF

A

which stimulate production of the antiviral cytokines IFN-a/b called type I interferons.

80
Q

Answer the following questions:

Which TLR are for bacteria?

Which are for viruses?

which are for fungi?

A

Bacteria …..TLRS 1,2,4,5,9

Viruses…….TLRs 3,7,8,9

Fungi………..TLRs 2, 6

81
Q

Which TLR does not activate MyD88 ?

What does that TLR activate?

A
  • TLR3 (does not activate MYDD88 an adaptor protien)
  • TRIF (an adaptor protien)
82
Q

Steps for TLR 4 activation

A
  • PAMP binds
    1. MyD88 binds to TLR 4 and activated IRAK 4 to phosporylate TRAF6 (adaptor protein) which phosporylates IKK
  • 2.a IKK phosporylates IkB which then degrades it and relsease NFkB
  • 2.b activates mapk
  • NF-Kb can then work in the cell and release cytokines
83
Q

4 things can happen when you bind to TLR

A
  • INFLUENCE ADAPTIVE RESPONSE
  • direct bacterial death
  • tissue death: apoptosis of host cells and spetic shock
84
Q

NOD-Like Receptors (NLRs) and Inflammasome

A
  • NLRP 3 is a intracellular sensor to pathogenic bateria, extracellular ATP, bactieal products, crystals, k efflux and ROS
  • when it senses that, it with an adaptor and caspase 1 form an inflamasone in the cytosol of cells
  • NLRs act as SCAFFOLDING PROTEINS that assemble signaling platforms triggering activation of NF-kB and mitogen-activated protein kinase (MAPK) signaling pathways.
  • the inflamasone activates caspase 1
  • and these then activate 1L -1B and IL- 18 WHICH ARE potent pro inflamatory cytokinse which drives inflamation
85
Q

NLRP3 INFLAMMASOME IN GOUT

A
  • IL-1β as a key regulatory proinflammatory cytokine in gout
  • NLRP3 inflammasome complex is stimulated in response to the MSU “danger signal” because of terrible food intake

monosodium ureate is built up in joints bc of bad food intake

86
Q

_______ therapy is used to treat gout patients.

A

Anti-IL-1

87
Q

DAMPS

A

DAMPs are endogenous DANGER MOLECULES that are released from damaged or dying cells.

DAMPs induce potent inflammatory responses by activating the innate immune system during NON-INFECTIOUS INFLAMMATION.

DAMPs activate the innate immune system by interacting with PRRs.

These DAMPs are recognized by Mf via TLRs which trigger an inflammatory response.

88
Q

Necrosis generates DAMP BY WHAT MECH?

A
  • NECROSIS is a “dirty” form of cell death characterized by swelling and rupture of cell membrane (cell lyse) which causes inflammation. It occurs in response to exteranal toxic factors.
  • WHEN necrosis occurs, everything is relased out that is usually not present in the extracellular fluid
  • this will bind to PRR and activate the innate immune system which will cause the pathways similar to PAMPS to occur
89
Q

Apoptosis and DAMP

A
  • Apoptosis is a clean way of death: because apoptotic bdoies are forming
  • this causes little damp to be released
  • cells will be removed via phagocytes
90
Q

HMGB1

A

DAMP: high mobility gorup box 1

-activates NF-kB via • via TLR2/TLR3 signaling

91
Q

URIC ACID

A

damp

-Activates NF-kB • via NLRP3

92
Q

HSP

A

damp

-Activates NF-kB • via TLR2/TLR4

93
Q

All DAMPS

A

stimulate production and release of TNF-a and IL-1.

94
Q

explain how damps cause auto immune diseases

A

microbial/sterile stimuli > tissue injury > necrosis and release of DAMPs > DAMPs recognition by PRRs of innate immunity > activation of the innate immune system > infective/sterile inflammatory response > activation of adaptive immunity

95
Q

DAMPS cause what auto immune dz

A

multiple sclerosis

type 1 diabetes

systemic lupus erythematosus

rheumatoid arthritis.

96
Q

PRR triggered repsonses in phagocytes

A
  • N-formyl methionyl peptide (fMet) is a constituent of prokaryotes but not eukaryotes (its a pamp) by 7 alpha transmebrane receptors
  • Can use toll like receptors and mannose receptors to initiate killing of microbes
  • causes migration to tissues and CAN initate phagocytiosis
97
Q

Functions of Macrophages in Innate Immunity

A

. RESPOND TO DANGER SIGNALS – PAMPs and DAMPs.

  1. REGULATE EXTRAVASATION of blood cells into the tissues.
  2. Degradation of foreign material, bacteria, and cell debris by PHAGOCYTOSIS and TISSUE REPAIR by secreting various enzymes - elastase, lipases, collagenase, lysozyme, and others.
  3. Play a key role in tissue inflammation via production of INFLAMMATORY MEDIATORS: 1. Cytokines and chemokines 2. Reactive oxygen intermediates (ROI) 3. Nitric oxide (NO) 4. Prostaglandins 5. Cationic proteins and polypeptides (defensins)
  4. ANTIGEN PRESENTATION to effector T cells.
  5. IMMUNOMODULATION of the homeostasis in tissues.
98
Q

Mast cells functions:

A
  • regulate vascular permeability and recruitment of blood cells.
  • mast cells can modulate the behavior of these and other neighboring effector cells through the release of mediators (release histamine, proteases, seratonin, heperan, cytokines, chemokines and more)
  • they are activated by cytokines, chemokinse, c3a and c5a complement, pamps…
99
Q

Cytokines vs chemokines

A
  • cytokines are small proteins that are secreated by many cells
  • they mediate inflamation, immunity and hematopoesis
  • they can be pro or anti inflamatory

CHEMOKINES: are small proteins which are chemoattractants. They are important for trafficking of immune cells

100
Q

What cell is the prinple source of most cytokines?

What does IFN gama activate?

Which cytokines are anti inflamatory?

A
  • macrophage
  • macrophages
  • IL10, TGF B
101
Q

What does IL 12 do?

A

activates NK cells which makes IFN gamma

-also induces differentiaon of CD4 T cells into Th1 cells

102
Q

What 3 cytokines have systemic effects

A

TNF-a, IL-1, and IL-6 results in the SICKNESS BEHAVIOR SYNDROME which includes lethargy, depression, anorexia, fever, cognitive impairment, hyperalgesia, & decreased social interaction.

103
Q

Complement system c3a role

A

inflamation and chemotaxis

104
Q

c3b role

A

phagocytosis and formation of c5 convertase

-Surface-bound C3b serves as an opsonin (‘tag’) and increases phagocytosis by phagocytic cells

105
Q

MAC

A

Membrane attack pathway: a supramoleculer organization of molecules that contain c5b, c6, c7, c8 and c9 which leads to cell lysis

C5B fragment is repsonsible for initiating the self assembly of MAC

106
Q

Acute phase protiens definition and action

A
  • proteins whose concentrations rise during the acute phase
  • The proinflammatory cytokines IL-6, IL-1, and TNF-a are the major signals responsible for induction of the acute phase response
  • act on hepatocytes in the liver inducing them to secrete APR protiens at higher levels
107
Q

C reactive protein and mannose binding protein are _____ and they do what?

A

Acuet phase protein, fixes complement, opsonizes

108
Q

Alpha acid glycoprotein is __ and does what

A

it is an acute phase protein and it is a transport protien

109
Q

serum amyloid P component is __ and does what?

A

It is an acute phase protein and it is an amyloid compeonet precursor

110
Q

What allow more accureate lab dections of inflamation?

A

high blood concentrations of CRP (c reactive protiens) and serum amyloid A (SAA)

111
Q

Neutrophils and Monocytes enter through which mechanism?

A

post-capillary venules except parenchymal tissues (liver, lungs, kidney) where all blood cells enter through capillaries

-they enter the tissue through POST C

112
Q

Neutrophils and Monocytes

A

eliminate infectious pathogens, clear dead tissues, and repair the damage.

113
Q

Mechanism of entry into the cell of how neutrophils and monocytes enter

A

Neutrophil

1) Proinflammatory cytokines TNF-a and IL-1 produced by activated mast cells and tissue resident MO induce activation of endothelial cells (ECs)
2) Activated ECs increase surface expression of P selectin (PS) and E-selectin (ES) adhesion molecules
3) • PS and ES bind to their ligands (co-receptors) P-selectin glycoprotein ligand-1 (PSGL-1) and E-selectin ligand-1 (ESL-1), respectively, which are constitutively expressed on neutrophils. (this slows it down)
4) chemokine IL8 are released which bind to chemokine receptor which activate Leukocyte Function-associated Antigen 1 (LFA-1) and Very Late Antigen-4 (VLA-4) causing increase affinity and bind selectivity to ICAM AND VCAM1
5) then the they roll in due to the cheomkine gradient

Monocyte is the same but it uses Monocyte chemoattractant protein-1 (MCP-1) is the most important chemokine that regulates migration and infiltration of monocytes

114
Q

CLASSICALLY ACTIVATED M1 MO are induced by microbial products binding to

A

IFN-γ, and are MICROBICIDAL and PROINFLAMMATORY.

115
Q

ALTERNATIVELY ACTIVATED M2 Mf

A

induced by IL-4 and IL-13 and are important in TISSUE REPAIR and FIBROSIS.

AKA ANTI INFLAMATORY EFFECTS: WOUND REPAIR AND FRIBORIS

116
Q

Describe the role of PRR in phagocytosis

A
  • phagocyte binds with to receptors to the microbe
  • microbe is injested
  • phagosome and lyosome fuse
  • kille by ROS and NO via inducible nitic oxide synthase
117
Q

Respiratory burst

A
  1. oxygen dependent killing is by a product of repiratory burst that accomanies phagocytosis
  2. o2 consumption increased
  3. superoxide anion is made
  4. h2o2 production is increased
  5. single o2 is made
  6. hydrogen radials are mare (react with MOST ORGANIC MOLECUES THEY ENCOUNTER bc they are unstable)
  7. myloperoxidase catalyzes toxic peroxidation
  8. hypocholrite: product of myleoperoxidase enzyme is more animicrobal alone
118
Q

Anti viral innate immune response is mediated by

A

1) type 1 interferons (alpha and beta)
2) NK cells: which kill virus infected cells

119
Q

Type one IFN mechanism to kill viruses

A
  • Released by virus infected cells or plasmacytoid dendritic cells
  • Type I IFNs induce expression of proteins that interfere with virus replication in order to restrict and limit viral spread from cell to cell
  • Interferon-regulated double-stranded Protein kinase RNA-activated (PKR) prevents the recycling of guanidine diphosphate which in turns blocks viral RNA translation.
  • Type 1 IFN activates nuclease ribonuclease L which then mediates viral RNA degradation
  • Type 1 IFN activate NK cells to enhance cytotocitiy to elim infected cells
120
Q

NK cells

A
  • NK cells regonize lignands on infected cells or cells undergoing other types of stress
  • kills host cells and releasing intracellular pathogens for phagocytosis.
  • the activated NK cells will secret IFN gama (type 2 interferon)
  • this will actiavte macrophages to kill phagocytised microbes
121
Q

NK activiating receptors

A

killer cell immunoglobulin (Ig)-like receptors (KARS): recgonize stress associated molecules like MICA and MICB on surface of abnormal host cells

-activating recetpors of NK cells trigger activation of protein tyrosine kianse

122
Q

NK ihibitory receptors

A

KIPS, recognize class I MHC and activate protein tyrosine phosphatases (PTP) inhibit an activation signal.

123
Q

If insufficient ______ binding occurs, the NK cell will proceed to kill the target host cell.

A

KIR-MHC I

124
Q

Sufficient binding by _____ will override the ____ kill signal sparing the life of the host cell.

A
  • kir
  • kar
125
Q

How NK cells kill infected cells

A

1) NK cells release perforins which polyemerize and form a hole in virus infected cells
2) granzyemes form NK cells to enter the perfoin hole and activate apoptosis
3) dies by apoptosis
4) macrophage engulf and giest the dying cells

***** NEED ACTIVATING SIGNAL BY PHOSPHPRULATION***

126
Q

The Requirement of Two Signals in Lymphocyte Activation

A
  • Recognition of ANTIGEN by T lymphocytes provides signal 1 for activation of the cells.
  • Regulatory molecules expressed on Ag-presenting cells (i.e., dendritic cells and Mf) are called COSTIMULATORY MOLECULES and they provide signal 2 for T cells.
  • • In addition, CYTOKINES produced by innate immune cells provide signal 3 for potent activation of T cells.
127
Q

LAST SLIDE?? IGNORE

A
128
Q

What do potent vasodilators do?

A
  • cause contraction of nonvascular smooth muscle
  • increase vascular permability
  • cause pain
129
Q

TLR 1: TLR2

A
  • hetrodimer
  • ligands- microorgo recogized: lipopeptide -bacteria or GPI - parasites
  • found on plasma membrane
130
Q

TLR 2/6

A
  • lipoteichoic acid - gram positive bacteria
  • zymosan - yeast
  • -found on plasma membrane
131
Q

Inflammatory signs from biochemical actions of what?

List the latter

A

Vasoactive mediatiors

  • prostaglandings, lukotrienens, histamine (from mast cells)
  • bradykinin
132
Q

TLR 3

A
  • dS VIRAL RNA
  • viruses(west nile)
  • endosomes
133
Q

tlr 4/4

A
  • lipoplysaccharides
  • gram negative
  • plasma membrane
134
Q

tlr 5

A

flagellin

  • motlie bacteria that need a flaggela
  • plasma membrane
135
Q

TLR 7

A

single stranded viral RNA

  • virus (hiv)
  • endosome
136
Q

tlr 8

A

single stranded viral rna

  • viruses
  • endosomes
137
Q

tlr 9

A
  • unmetylated cpg rich dna
  • bacteria/ virus (herpes)
  • endosomes
138
Q
A
139
Q

TLR deffiency will lead to what?

A

succeptibility to infection by bacteria or virus

140
Q

How do you get inflamation with out an infection?

A

Damps

141
Q

What activate Mast Cells

what do mast cells release as effector molecules?

A
  • PAMPs
  • cytokines
  • chemokines
  • c3a and c5a complement

______
-histamine, protease, seatonin, heperain, cytokines IL-4, TNF

142
Q

How long does it take for mast cells to replenish granules?

A

Days

143
Q

Local effects of cytokines

A
  • activates vascular endothelum
  • lympocyte activation
  • recruitment of other wbcs
144
Q

Mast Cells minutes hours days

A

minutes: release cytoplasmic granules at site of infection via degranulation
- also produce eicanoids medaitors

second wave: they release de novo mediators like TNF and IL4

-mast cells have the ability to survive for prolonged periods after activation

145
Q

Complement System steps

A
  • C1 protein complex binds to immunoglobulins IgM or 2x IgG that is deposted on abctera and is active
  • C1 cleaves C2 and C4 (C1 can cleave many of these)
  • C4b can attach covalently to microbal surfaces
  • C2a Binds to c4b and then the c4bc2a c3 converase is formed
  • c3 convertase cleaves of c3a and makes c3b
  • c3b fragment can be deposited on the surface of the bacteria
  • surface bound c3b serves as an OPSONIN TAG and increases phagocytosis by pagocytic cells
  • c3b forms a complex with c3 convertase to give rise to c4 convertase
  • c5 convertase cleaves c5 into c5a and c5b
  • c5b fragment is repsonebile to make the self aseembly of MAC (LYTIC PATHWYA)
  • (c5 is a potent mediator for imflamatory responses)
  • the MAC is a supramolecular orgo which has c5b, c6,7,8,9
  • MAC creates a transmembrane channel that leads to lysis
146
Q

Rolling is ______.

Adhesion, crawling and transmigration is _____.

A
  • selectin dependent
  • integrin dependent
147
Q

What is the most powerful activator of macrophages to kill phagoccitized microbes?

A

ifn gama type 2

SFM (31 decks)

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