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Immunology > Innate immunity 1 > Flashcards

Innate immunity 1 Flashcards

1
Q

4 ways to describe innate immunity

A
  • not antigen specific
  • fast
  • no memory
  • phylogenetically ancient
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2
Q

The adaptive immunity is designed to discriminate __________ while the innate immunity is designed to discriminate ___________.

A
  • adaptive:substance A from substance B
  • innate: dangerous from self

-if an innate receptor is activated, it is automatically a dangerous substance, whether it is self or nonself

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3
Q

What 2 main things does the innate immune system do with danger?

A
  • try to fix the problem (kill, eat, wall off, repair)
  • communicate the danger to other components of the immune system ( to other innate cells, non-immune cells, to the adaptive immune system)
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4
Q

Humoral vs. cellular face of innate immunity

A

H: cytokines, complement
C: neutrophils, macrophages, dendritic cells, NK cells, Eosinophils/basophils/mast cells..etc

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5
Q

Define cytokines. Give 2 broad categories of them with examples.

A
  • Soluble factors produced by immune cells to communicate in an autocrine, paracrine, or endocrine manner
  • Inflammatory: TNFa, IL-6, IL-12
  • Anti-inflammatory: IL-10, TGFb
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6
Q

Innate vs. Adaptive immunity cytokines

A
  • Innate: cytokines produced by macrophages and NK cells mediate the early neutrophil dominated inflammatory reactions to microbes and promote their elimination
  • Adaptive: cytokines stimulate proliferation and differentiation of antigen-stimulated lymphocytes and activate specialized effector cells; important in fine tuning lymphocyte responses
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7
Q

Complement is a multi-component host defense system consisting of more than 35 proteins that participate in a highly regulated fashion to provide many of the effector functions of humoral immunity and inflammation. What are the 3 effector functions?

A
  • opsonization
  • lysis
  • chemotaxis to recruit other immune cells
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8
Q

Opsonization by the complement component ______; recruitment of other inflammatory cells by complement components _________; lysis of pathogens by activation of _______.

A
  • C3b
  • C3a and C5a
  • MAC:membrane attack complex
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9
Q

What are the 3 complement pathways that can be activated?

A
  1. classical: triggered by antibodies that bind pathogen
  2. alternative: “always on”, but held in check by regulatory factors
  3. Mannose binding lectin: triggered by mannose found on the surface of pathogens
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10
Q

Active _______ is the central event that turns on complement no matter which pathway is the starting point.

A

-C3b

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11
Q

The classical pathway is activated by _________ which turns on C1a which does what? Describe the rest of the cascade.

A
  • surface bound IgM which turns on C1a
  • C1a cleaves C4 to active C4b which cleaves C2 to active C2b. C4b2b cleaves C3 to make C3b which initiates activation of the rest of the cascade
  • eventually reach C9 and drill pore into cell
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12
Q

The alternative pathway works because C3 is constantly being cleaved into C3b by hydrolysis. Normally this C3b is ___________. What happens, though, int he presence of bacteria or other pathogens?

A
  • inconsequential because it is inhibited by factors found on our own cells
  • in presence of bacteria or other pathogens, this C3b can bind to their surface and in combination with Factor B can initiate the complement case of C5-C9
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13
Q

What needs are bypassed by the alternative pathway of complement activation?

A

-surface antibody and the C1,4,2 steps

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14
Q

Mannose Binding Lectin (MBL) binds to ______, a carbohydrate found on the surface of pathogens and in combination with __________ which when organized into multimolecular complex can cause what?

A
  • mannose
  • Mannan-binding lectin Associated Serine Proteases which cleave C4 and C2 and activate complement in manner identical to classical pathway except no antibody binding occurs
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15
Q

Opsonization as a result of complement activation

A
  • complement receptors bind to complement fragments to enhave phagocytosis
  • coat with C3b
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16
Q

Osmotic lysis

A
  • outcome of complement activation

- membrane attack complex (MAC) punches holes in bacterial membrane, allowing extracellular fluid in and osmotic lysis

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17
Q

Chemotaxis

A
  • outcome of complement activation

- C3a, C4a, and C5a are potent signals calling for the influx of neutrophils and macrophages

18
Q

MBL works in conjunction with ________ to activate complement pathway.

A

-MASPs

19
Q

Pros and cons of complement pathway

A
  • positive amplification via cascading of proteins allows for rapid amplification of a small signal
  • need a lot of control; negative regulation via a number of mechanisms
20
Q

2 main ways complement activation is regulated

A
  1. complement activation is localized due to the covalent binding of activated complement proteins to surfaces; complement only works when it becomes surface bound; therefore, the availability of surface limits complement activation–only when pathogen surfaces are present
  2. our own cell surfaces are filled with molecules that inhibit complement–so if it binds out own cells, it is inactivated
21
Q

Neutrophils aka ________. How long do they take to develop? What drives their production?

A
  • polymorphonuclear cells or granulocytes (PMNs)
  • 14 days to develop in BM and 6 hr half life in peripheral blood
  • Cytokine G-CSF drives their production
22
Q

________ are the first line of innate defense.

A

-neutrophils

23
Q

Neutrophils come from bone marrow precursors. So when the BM is revved up and trying to spit out neutrophils, immature neutrophils called ________ are sometimes seen in the blood. What can their presence signify?

A
  • band cells

- since infections often result in an attempt to make more neutrophils, the presence of bands often signifies infection

24
Q

In the olden times, having a lot of band cells in one’s blood smear would be stated has being ______ shifted.

A

-left

25
Q

Neutrophil granules

A

-granules filled with toxin (ROS, proteases, etc)

26
Q

Role of neutrophils, but why this is also bad.

A
  • phagocytose viruses, bacteria, fungi within the tissues
  • first line defense in infection and very effective, but also very toxic and result in tissue damage which is why it is nice to have an adaptive immune system for a more surgical strike
27
Q

There are many different receptors for phagocytosis, all of which get the pathogen into the cell where it will ultimately end up in a __________ where what happens?

A
  • phagolysosome

- ROS (bleach) and NO will kill the pathogen

28
Q

3 general killing pathways of neutrophils

A
  1. Oxygen independent: granule contents
  2. Oxygen dependent: MPO independent
  3. Oxygen dependent: MPO dependent (myeloperoxidase-ROS)
29
Q

Functions and origin of macrophages

A
  • arise from monocytes in the peripheral blood
  • primarily function to eat: pathogens, damaged tissue, dead cells
  • produce cytokines and can present antigen to T-cells
  • phagocytosis, cytokine production, APC
30
Q

Macrophage receptors to respond to pathogen

A

-CD14 and TLR-4

31
Q

Dendritic cell function

A
  • like macrophages, these cells eat their surroundings
  • however, these cells are uniquely poised to present antigen efficiently** main role is to sample antigen in peripheral surroundings to present to T cell in LN
  • high levels of MHC I and II
  • produce cytokines that are good at activating T cells
32
Q

Natural Killer (NK) cells

A
  • lymphoid derived, but still innate cell type
  • mediate cell death via release of toxic granules
  • kill cells that lack MHC I
  • large producer of cytokines IFNy
33
Q

Do NK cells have antigen receptors?

A

-No, remember their main role is to kill cells lacking MHCI

34
Q

What types of cells lack MHC I?

A
  • virally infected cells

- malignant cells

35
Q

NK cell activation

A
  • NK cells have sets of activating and inhibitory receptors that balance eachother out and result in the NK cell remaining quiet
  • inhibitory receptors are normally turned on my MHC I, but when it is missing, only activating R are on and without the counterbalancing inhibiting R, the NK cells carries out effector action of killing the cell
36
Q

Do NK cells kill viruses directly?

A

-no, just the cells they invade

37
Q

Difference between eosinophils and neutrophils

A

-similar size but E have larger and orange granules, fewer lobes, and much less frequent

38
Q

Eosinophils are important for what immune responses?

A
  • parasitic infections

- allergies

39
Q

3 major types of mediators in eosinophils

A
  1. granule components (MBP)
  2. cytokines
  3. eicosanoids
40
Q

What is the least common cell in the blood?

A

-basophils

41
Q

3 major types of mediators of basophils

A
  1. lipids: LTC4
  2. cytokines: IL4, IL13
  3. Granule components: histamine, proteases, etc

Immunology (13 decks)

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