Exam questions Flashcards

1
Q

1: Hematopoesis

10.000 blood cells, how many leucocytes (number), how many of them are lympocytes and granulocytes in %

A

0,15% Leucocytes -> 15 cells

66% granulocytes
30% lymphocytes

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2
Q

1: Hematopoesis

What is non symmetric cell division? In which context of hematopoesis is it important?

A

Stem cells can divide non symmetric to form another stem cell and 1 differentiated cell (progenitor)

That makes self renewal of the stem cell population + differentiation possible at the same time

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3
Q

4: Complement and inflammation

Classical pathway of the complement system?
Trigger?
Name an example and it’s role.

A

Trigger: Antigen bound IgM or IgG that makes Fc part of antibody accessible and for binding of C1q, cascade is activated

Example and role
Invasion of bacteria leads to antibody secretion (IgM and IgG isotype) that result in activation of classic pathway, role is clearance of pathogen via formation of Membrane attack complex, opsonitation, analphylatic reaction and help for B cells (C3b/C3d)

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4
Q

1: Hematopoesis

What are commited myeloid progenitors?
Give 3 examples. what cells can these progenitors differentiate to?

A

Common myeloid progenitor cell differentiate into commited myeloid progenitors. These are cells that already commited on a special lineage

Examples
meg-CFC: megakaryocytes or platelets
eo-CFC: eosinophilic granulocytes
Mast-CFC: mast cells / basophilic granulocytes
G-CFC: neutrophilic granulocytes
M-CFC: Monocytes/Macrophages/DCs/..

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5
Q

7: Immunological memory

Please explain the term hypermutation. Which molecule in which cell is mutated? Which property of the molecule is altered?

A

T helper signal promotes somatic hypermutation of B cells in the CDR encoding parts that are responsible for antibody specificity

Multiple B cell clones arises with different affinities for antibodies that results in affinity maturation

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6
Q

2: Innate immune cells

Please explain the term extracellular traps (NETs) Which cells? Which property does it consist of? Which function does it have? Provide details about their composition and function.

A

NETs (neutrophillic extracellular traps) consists of fibres (chromatin and antimicrobial peptides) that are released from neutrophils that undergo cell death (NETosis).

Works as physical barrier to prevent further infection + helps recruiting other immune cells

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7
Q

7: Immunological memory

What is cytokine memory?

A

Cytokine memory refers to the ability of memory T and B cells to express the same cytokine profile like after the 1st exposure, this is possible to due the histone modification and DNA methylation of cytokine genes that leads to a specific profile once being reactivated

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8
Q

11: Mucosal immunity

IgA can be in 2 formations. Which ones and how do they differentiate in their function? One has a special function. which?

A

monomeric form:
forms immune complexes and binds to CD89, activates APCs, induced cellular immune response

dimeric form with j chain and secretory component: neutralization of antigen on mucosal surfaces, prevents attachement and movement of microbes and transport antigens from lamina propria into lumen

Special function of dimeric IgA: mucosal immunity functions

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9
Q

7: Immunological memory

FDCs
What are FDcs, in which organ do they occur? Which substructure? What would be the outcome if FDCs would be impaired? Function of FDCs

A

Folicular DCs cells occur in the geminal centre of lymphoid tissue, these cells lead to an increased antigen exposure via immune complexes to B cells that supports the germinal centre reaction.
The also support interaction between T helper cells and B cells that support activation, somatic hypermutation, affinity maturation and clonal expansion

Impairing would result in an inefficient germinal centre reaction with less functional B memory and long-lived plasma cells and less high affinity antibodies

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10
Q

5: adaptive immunity B cells

What ar natural antibodies? Which molecule do they bind, by which B cell subset are they produced? What induced it’s production?

A

Natural antibodies are antibodies with no prior exposure to an antigen, against conserved PAMPs of different pathogens (carbohdrates, lipids, …) that are germline encoded, activated by B-1a subset. Induced by commensal bacteria, enviromental antigens such as pollen, dust or genetics

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11
Q

? 2 or 4 maybe

What are defensins? Name 2 cellular sources

A

Defensive are small peptides that support antimicrobial functions e.g. disrupting cell membrane of pathogens

Neutrophils produce alpha and beta defensins

Epithelial cells produce mainly beta defensins

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12
Q

11: Mucosal immunity

What would happen if oral tolerance fails completely?

A

If oral tolerance fails completely, chronic inflammation will occur:

Normally harmless stimuli like commensals or food proteins will inhibit DC maturation, these immature DCs will lead to differentiatiin of regulatory T cells to induces supression of other immune function.

If oral tolerance fails, even harmless stimuli lead to differentiation of effector TH1/2 cells and a high inflammation resulting in tissue damage.

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13
Q

?

What function does the extracellular matrix have for migratory immune cells?

A

Extra cellular matrix components are important for lymphoid tissue architecture

provides barrier and routes for migration

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14
Q

3: Innate immune system: pathogen recognition

What is the evolutionary ancestry of ILR/NF-kappyB?

A

The Spätzle/Toll/Cactus gene casette in drosophila

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15
Q

3: PRR

Name a receptor that is germ-line encoded and one that’s not + function of these receptors

A

Germ line encoded:
TLR4: recognition of gram- bacteria (LPS) or fungi surface molecules

non germ line encoded:
TCR: binding of specific antigen bound to MHC molecule for activation resulting in cell killing (CD8+) or B cell help (CD4+)

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16
Q

?

Different homing capacities of naive T cells an memory T cells. Name a receptor that is differently expressed in these cells.

A

CCR7 more in naive T cells: lymph node associated

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17
Q

5: Adaptive immunity B cells

What is the difference between constitution of pre-BCR and BCR? What is the pre-B cell doing if the pre-B cell receptor is triggered? Provide at least two direct consequences resulting from activation of the pre-B cell receptor.

A

The difference is that pre-BCR has a surrogate light chain that is expressed as a precursor of the rearranged light chain

so BCR consist of a somatically rearranged light chain

If the pre-B cell receptor is triggered , differentiation and proliferation is induced.

+ it induces the rearrangement of the light chain gene segments (VDJ) for a unique heavy AND light chain

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18
Q

5 Adaptive immunity B cells + ?

What is anergy? Name 2 cell types that can become anergetic. How and when is anergy induced? What would happen if this mechanism istnt available?

A

Anergy is the functional unresponsiveness of T and B cells to antigens. This mechanism is useful to prevent autoreactivity towards self antigens (autoimmunity). Induced when B or T cell react against self antigen for central tolerance (bone marrow B cells, thymus T cells) + peripheral tolerance

If this mechanism is not available this would result in loss of T and B cell tolerance to a certain degree

(there are other tolerance mechanisms like deletion, B receptor editing or T regulatory dells),

probability result in autoimmune disease

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19
Q

6 Adaptibe immunity T cells

Which coreceptor does the TCR have for MHC recognition?

A

CD4 (MHC II) or CD8 (MHC I)

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20
Q

Adaptive immunity B cells

Somatic recombination is not existant: What happens to an individual who gets infected? How would an immune response differ from that to a normal person? If the person survives, would the immune response of reinfection differ from that of a normal person?

A

This can lead to death because:

The adative immune response would be impaired, APCs would find to fitting T and B cells because there is no variability due to impaired somatic recombination. No functional B and T cells can develope and the infection can´t be cleared.

It is necessary to treat the person with antibiotics/antivirals, probably also cytokine and antibody therapy to induce a immune response

Immune response of reinfection would differ. The healthy person would have memory T and B cell that lead to fast adaptive immune response (high IgG levels) and probably fast clearance. For the unhealthy person it can even be more dangerous than before, cause there is no memory + the immune system is even more susceptible due to prior illness.

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21
Q

?

What does immune priviliged mean? Name 2 tissues / organs.

A

Examples: Brain, eye

Sites with limited immune response (limited access leucocytes) so inflammation is limited and does not lead to damage of tissue

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22
Q

?

Memory: Name 4 examples in which immunization is helpful. What is it good for?

A

Immunization helps to eradicate diseases that would kill many people (e.g. Polio, Measles, BCG,…)

It helps to prevent susceptible groups through herd immunity

It helps to protect newborn that get antibodies through maternal placenta or breast milk

It helps to protect against reinfection after 2nd exposure

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23
Q

Adaptive immunity B cells

TI-1 antigen
Which molecule resemble typical T cell independent TI-1 antigens? Which receptors are involved in TI-1 B cell activation at low or high antigen concentration? How does antigen concentration influence the B cell response?

A

can activate B cell without help of T cells, usually antigens with repeated structures like LPS or peptidoglycan, …

Activation of B cells is mediated by BCR and TLR

low concentration supports activation by TLRs to promote proliferation and antibody secretion

high concentrations lead to stronger B cell response including memory cell generation and class switching

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24
Q

3: Innate immune system: pathogen recognition

Different recognition of gram+ and gram- via which receptor?

A

TLR 4 (LPS of gram-) and TLR2 (Lipid of gram+)

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25
Q

1: Intro

Name 2 immunodeficiencies and examples for each of them

A

Primary
- genetic diseases
- Severe Combined Immunodeficiency like ADA that leads to high amount of infection in 1st year due to absense of functional T or B cells
- Bruton’s Agammaglobulinemia:
X recessive mutation in Bruton’s Tyrosine kinase where bacterial infection in the first year occur due to absence of antibodies / functional B cells, can be cured with Ig therapy

Secondary
- aquired through disease or therapy
- AIDS induced by HIV
- Glucocorticoid induced Immunodeficiency that suppresses cytokine and t cell proliferation genes

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26
Q

1: Hematopoiesis

Explain hematpoietic hierachy. How do cells clones at beginnign and end of hierachy differ?

A

hematopoietic hierarchy refers to the different stages of blood cell development, starting with HSCs and progressing through various progenitor cells to mature blood cells.

Cells at the start (stem cells) can self-renew + differentiate into 2 main types of progenitor cells, common lymphoid progenitor and common myeloid progenitor cell, these cells can still differentiate into several types of cells.

Master transcription factors will lead to commitment to a specific cell colony / lineage (committed progenitors)

After differentiation to mature hematopoietic cells these cells lost the ability to differentiate into other cell lineage, also proliferation is limited + mature cells have specific effector functions

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27
Q

1: Hematopoiesis

Colony stimulating factor: general function, where are these molecules expressed and what is their function there?

A

Colony stimulating factors are differentiation factors that lead to differentiation into specific progenitor cell or also mature cells

Expressed by various different cell types, one example stromal cells in the bone marrow that offers a microenvironmental niche for differentiation on a local level

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28
Q

Name 2 distinct cell types of adaptive and innate immunity and their functions

A

Innate
- Macrophages for antigen presentation and phagocytosis, inflammation, …
- NK cells for cell killing

Adaptive
- B cells to secrete antibodies (plasma cells), generate memory (memory B cells, long-lived plasma cells)
- T cells to kill infected cells (CD8+) or T helper cells (CD4+) that help B cells to survive, proliferate, …

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29
Q

1: Hematopoiesis

Which cytokine is produced in kidney dependent on oxygen level?

A

EPO
EPO is a systemically regulated factor with a negative feedback mechanism: EPO leads to more RBC mass that strenghtens oxygen production, once oxygen is high enough, low/no EPO production

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30
Q

Mucosal immunity (last slides)

Which CD4+ T cell subpopulation produces IFN-Gamma and what is the function?

A

IFN-Gamma is produced by TH1 effector cells that activate B cells to produce IgG for complement activation and other immune functions

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31
Q

What are pattern recognition receptors? Name 2 examples and their respective ligand

A

PRR are receptor that bind conserved antigens shared by a broad range of microorganisms to induce a proinflammatory immune response

TLR 4: LPS
TLR 5: Flaggelin
FC receptor: Fc part of antigen bound antibody

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32
Q

Name 4 hallmarks of inflammation and 4 clinical paramters of inflammation.

A

Hallmarks
Redness
Swelling
Heat
vascular permeability

Clinical parameters
increased white blood cell count
fever
pain
CRP protein

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33
Q

Name 3 types of complement activation and their initial trigger (upstream complement)

A

Lectin: Mannose recognized by MBL
Classical: Fc part of antigen binding antibody IgM and IgG
alternative: spontaneous hydrolysis of C3 and binding of factor B

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34
Q

Which requirement has to be fullfiled, so that IgGs and IgMs are capable of activating the complement system?

A

They need to be bound to an antigen, otherwise the Fc part of the antibody is not accesible and can’t be bound by the C1q

35
Q

Explain why it is stated that macrophages have a dual role in inflammation. Name functions which are associated with the 2 roles.

A

Can be understood in 2 ways:

Macrophages one one side induce a proinflammatory response by phagocytosis and invading pathogens and expression of pro inflammatory cytokines, so macrophages are very helpful for initial inflammatory response

One the other hand they play a big rule in sensing antiinflammatory responses by phagocytosis of apoptotic cells and expression of antiinflammatory cytokines to reduce inflammation at later stages of infection

They play also a crucial rule in inducing the adaptive immune response by antigen presentation via MHC molecules

36
Q

Explain what alpha/beta abd gamma/delta T cells are. Do they belong to the innate or adaptive immune response?

A

alpha/beta T cell belong to adaptive immunity, alpha/beta because their receptor consists of a alpha and a beta chain, these T cells recognize antigens on MHC molecules

Activation leads to differentiation into CD8/CD4 effector cells with different functions

gamma/delta T cells as cells from innate immune system can activate other cells and express cytokines in an TCR independent manner (stress induced, …)

37
Q

Explain differences between type 1 and type 4 hypersensitivity reaction. Name one allergen at least for each condition + other cells and molecules. Which trigger is required for a type 1 reaction, which is not present in type 4? Name One example for each type.

A

Type 1 hypersensitivity due to antigens like pollen

The trigger required for hypersensitivity type 1 is the presence of IgE antibodies against the specific antigen, this leads to antigen/antibody binding that can activate mast cells to produce histamine

Histamine leads to hypersensitivity reaction including swelling, itching, …

Other cells involved are eosinophils that produce granules + IL4 and IL-13 that also activate IgE production by B cells

Type 4 is delayed type hypersensitivity, that is caused by CD4+ T cells, e.g. poison ivy triggers this hypersensitivity resulting in contact dermatitis. It also trigger macrophages + IFN-G production that also promotes T cell activation and inflammation

38
Q

What would be the consequence for immune system if expression of pre-B-cell receptor wouldnt be possible due to mutation?

A

If the pre-B cell receptor would not be present, no trigger would lead to further development and differentiation of the B cells, this would lead to non functional B cells and also impaired development of other immune response due to absence of specific antibodies

e.g. Brutons Agammaglobulinemia, primmary immunodeficiency, gen related

39
Q

How is it possible that B and T cell receptors show an enormous variety despite limited expression of functional genes from the genome?

A

During developement of B and T cells the cells undergoes different differwntiation steps that also include somatic rearrangement and mutation of the receptor / antibody gene segments that results in almost infinite amount of possible antigen binding sites.

Also hypermutation in the germ centre plays a rule to increase variability so memory B cells are even more variable and specififc to a specific antigen

40
Q

Explain affinity maturation. Which property of which cell? Which tissue/substructure?

A

Affinity maturation happens in the germinal centre reaction (secondary lymphatic tissue) after somatic hypermutation that leads to altered B cell receptors with higher/lower/same affinity

Affinity maturation refers to the interaction of these B cells that interact with antigen via FDCs or also T helper cells. Only the B cells with high affinity to present antigen will maturate and proliferate

41
Q

Mucosal immunity

Which impact have commensals on immune modulation? Provide 2 examples how. Under which condition they become dangerous?

A

Commensals help to modulate immmune system by:

  • inducing oral tolerance by production of TFG-ß, … to inhibit DC cell maturation
  • blocking TLR signalling by activating PPAR-y that removes NF-kappa B from nucleus or by blocking degradation of I-kappaB, preventing NF-kappaB translocation from nucleus
42
Q

11: Mucosal immunity

What is a M-cell? Location? Which cell type they belong to? Function?

A

M cell is a specialized epithelial cells located at the Payer’s patches of epithelium.

They have membrane ruffles and can phagocytose or endocytose antigens, transport them in vesicles and release into lumen so DCs can bind to antigen

43
Q

Mast cells: which pathogen? which immune disorder? Soluable factor and receptor inducing mast cell activation?

A

Mast cells can be activated by pathogen like bacteria, viruses and parasites but also by harmless stimuli like pollen antigen.

If IgE is present against specific antigen, these bound antibodies bind to Fc receptor of mast cells to activate mast cells that support several inflammation mechanism and also promote recruitment of other cells

44
Q

What determines L. major infection outcome? Which immune response is protective? Which is not?

A

The different subtypes of T cell effector cells:

TH1 immune response is protective via macrophage activation and cell mediated protection
TH2 immune response leads to chronic infection / dissemination via inhibition of TH1 response

45
Q

How is it explainable that graft rejection occurs in MHC dependent manner, if foreign antigens preseneted by foreign MHC molecules cannot be recognized by recipient T cells?

A

Mechanism is called allo-reactivity

foreign MHC molecules can be recognized by T cells as non-self antigens, by reaction against the MHC peptide binding groove

46
Q

Name 2 innate T cells and their function

A

gamma/delta T cells: TCR independent activation and activation of other immune cells + cytokine expression

NK cells: killing of infected cells via activation by APCs

47
Q

?

What is the difference between primary and secondary lymphatic tissue? Name 2 example and explain function.

What is tertiary lymphatic tissue?

A

primary lymphatic tissues are where immune cells, such as T and B lymphocytes, mature and differentiate.

secondary lymphatic tissues are where these mature immune cells encounter and respond to foreign antigens.

Tertiary lymphatic tissue develops in response to chronic inflammation / infection

Primary
Bone marrow: maturation and differentiation of blood cells
Thymus: maturation and differentiation of T cells

Secondary
lymph nodes: T cell activates
MALT: Antigen presentation to DCs
spleen

48
Q

Draw Multiple Leucocyte Extravasation and name the steps and important point.

A
  1. Rolling: leucocytes roll along endothelial blood vessel tissue via unspecific binding
  2. Tight binding of adhesion molecules like ICAM-1 or Intergrin to cell receptors
  3. Diapedesis supported by PECAM-1
  4. Migration to site of infection
  5. Activating through APCs
  6. Effector functions
49
Q

Give approximate half life of neutrophils and 5 mechanims of pathogen control.

A

half life: 6-10 hours in blood after 10-15 days maturation in bone marrow

Pathogen control via degranulation, ROS, NET formation, APCs and phagocytosis

50
Q

Complement classical pathway
trigger, 1st and final molecule

A

Classcial: Fc part of antibody IgG or IgM is accessible for C1q due to antigen binding, final molecule is membrane attack complex

51
Q

Asthma: which hypersensitivity class? What molecule causes pathogenicity? what determines allergen specificity? What is the effector molecule?

A

Hypersensitivity class 1, caused by different environmental antigens like pollen, dust mites, cold spores,

Specificity by IgE binding to allergen, if present, this leads to mast cell activation that induces histamine secretion and inflammation

52
Q

Which molecule mediates graft rejection?

A

MHC molecule mediated graft rejection

53
Q

Explain term MHC haplotype

A

MHC genes that are inherited together on a single chromosome from one parent, one haplotype from each parent, polymorphic MHC I and II genes are highly variable for each person

54
Q

What is central and peripheral tolerance? Name cells that play a role.

A

Central tolerance:

Checking for auto reactivity of immature T (thymus) and B (bone marrow) cells that would lead to autoimmunity

via T regulatory cells, deletion, B cell receptor editing, anergy

Peripheral tolerance:

Checking for auto reactivity for mature T and B cells in peripheral tissue

Mechanisms include regulatory T cells, anergy, deletion, + expression of inhibitory molecules on surface

55
Q

Name 3 function of antibodies during immune protection against pathogens.

A

Neutralization of pathogen / toxins, …

Opsonization of pathogens / PAMPs

Activation of complement system (classical)

Memory response induction

Antibody dependent cell mediated cytotoxicity to activate NK cells

56
Q

1: Hematopoiesis

Name 3 locations where hematopoiesis occurs and when?

A

First prenatal months: yolk sak
after some month (still prenatal): liver and spleen
some months before birth - life-long: bone marrow

57
Q

Why is the developement of T and B cells more complex than other cells?

A

clonal distribution of antigen receptors as a resut of somatic rearrangement

need for self tolerance, antigen receptor can’t recognize self antigen

different microenviromental niches for different differentiation steps

maturation into memory cells in germinal centre reaction with hypermutation + affinity maturation

58
Q

Memory immune responses are stronger, faster and optimized compared to primary response. How is that possible? What has changed compared to before the first encounter?

A

After 1st exposure the development of adaptive immunity takes some days, so pathogen has a higher chance to lead to a disease

But 1st exposure will result in the development of high affinity antibodies and long lived plasma cells and memory cells due to hypermutation and affinity maturation

During 2nd exposure these antibodies and cells support a very quick and specific response.

This response is already stronger because the frequency of antigen specific adaptive immune cells is much higher

Also more optimimized due to several reason based on memory: cytokine memory, class switch of antibodies after 1st exposure (IgG), antibodies with higher affinity, …

59
Q

Name 2 antibodies produced by B-1 cells. Which antibodies are never produced by B-1 cells and why?

A

B-1 cells:
- IgM antibodies, often referred to as natural antibodies.
- IgA antibodies, which are predominantly found in mucosal secretions

NEVER IgG antibodies, production of IgG antibodies requires T cell-dependent activation of B cells, which is not a common for B-1 cells.

60
Q

Please explain differences in immune recognition of viruses and extracellular bacteria and consequences for the subsequent immune effector functions initiated after infection with these 2 distinct agents.

A

Extracellular bacteria can be recognise by PRRs on the surface of innate immune cells, that activates inflammatory response, recruitment of other immune cells, …

Also B cells can be activated to produce antibodies that help neutralising, opsonising the bacteria for lysis, macrophage activation, further inflammatory responses, …

Viruses are intracellular, which means they need to be recognised with different cells, effector molecules, …

Viruses can be recognised intracellularly by PRR such as TLR3,7,8,9

DCs help promote inflammatory response by MHC class I molecules that activate CD8+ cells to kill infected cells, activation of T helper cells can also support B cells to produce antibodies against the virus that

61
Q

Macrophages secrete following cytokines: IL-1ß, IL-6 and IL-12. Please name the local effects.

A

IL-1ß: promotes inflammatory immune response by inducing cytokine production and migration of immune cells via increasing vascular permeability

IL-6: induces proliferation and differentiation of B cells to produce specific antibodies

IL-12: TH1 response including IFN-G, further activation of macrophages, …

62
Q

11: Mucosal immunity

Briefly explain function and constitution of Waldeyers ring.

A

Waldeyers ring is lymphatic tissue consisting of tonsils and adenoids that from a ring around entrance of gut and airways (MALT)

helps to prevent infection from the airway and gut route with different immune cells like M cells, DCs, …

63
Q

CD11c as marker for DCs is part of receptor important for activating these cells. Wich receptor?

A

CR4 activated by complement factor C3b

64
Q

KO mice are generated exhibiting genetic deletion of surrogate light chain. Which effect do we expect for T, B and myeloid cells. Are there differences between each cell type? If yes, why?

A

For myeloid cells we don’t expect direct consequences, but indirect ones as non functional B cells lead to a non functional adaptive immune system including memory T and B cells, antibodies, ….

T cells are not directly affected, but interaction between T and B cells plays a big role in generating a memory immune response, …

Non functional adaptive immunity will have an effect on myeloid cells because the adaptive immune system alters function and mode of innate immune system by expression of cytokine, effector cells, complement activation, …

65
Q

Please explain the molecular rearrangement that allows class switch without changing antigen specificity.

A

somatic recombination during B cell development leads to altering of the constant region gene segments that allows class switching with different effector functions

Antigen specificity is not affected (variable region)

66
Q

1: Hematopoiesis

Hemeatopoisesis slowly declines after birth. Which change of bone marrow contributes to this effect?

A

There is a gradial reduction of red active bone marrow tissue and more inactive fatty tissue that results in decrease of hematoiesis, but expansion can be observed when an increased need for hematopoiesis is observed

67
Q

Explain microenviromenntal niche in the contect of hematopoiesis.

A

There are some differentiation factors like EPO that are systemically regulated and lead to differentiation of progenitor cells into mature cells.

But microenviromental niches are very important for complex anbd spatial seperated differentiation: Microenviromental niches like stromal cells (cell cell contacts, cytokine profile) lead to differentiation into hematopoetic lineages locally

68
Q

Provide a rough time scale for:
- t cell mediated killing of infected cells
- IL-12 production
- NK cell mediated killing of infected cells

A

Provide a rough time scale for:
- t cell mediated killing of infected cells: (adaptive immunity needs time to devloe: a few days
- IL-12 production: probably also within hours (released by APCs) ?
- NK cell mediated killing of infected cells: within hours ?

69
Q

NK cells and epithelial gamma/delta T cells both belong to class of innate lymphocytes. Which class of antigen are recognized by NK cells? Which molecules on APCs are important to present antigens to NK t cells and epithelial gamma/delta T cells?

A

NK cells detect altered MHC expression on cell surface, if no MHC is present or if there are too much stress induced ligand cell killing takes place

Antibodies binding an antigen also lead to activation of NK cell by binding of Fc part to CD16

70
Q

Which molecule can generate memory and why?

A

antigen because it leads to antigen specififc clonal selection of T and B cells that can further differentiate into memory T and B cells + long-lived plasma cells

71
Q

Why are beta lactam antibiotics not usefull against mycoplasma? Which work instead?

A

ß lactams against cell wall synthesis, mycoplasma no cell wall, other antibiotics targeting other functions or mechanims of mycoplasma to invade cells

72
Q

How do T cells remeber the cytokine profile they have?

A

Epigenetic modifications like DNA methylations and histone modifications lead to a distinct cytokine profile for each cell dependent on the functions and signals exposed to at the 1st exposure

73
Q

Differences between allergen / pathogen vaccination

A

Allergen vaccination target environmental antigen like dust mites, pollen, … by slowly desensitising the immune system over a long period with repeated injections of increasing doses of allergen

Pathogen vaccination (1 or few doses) results in protective memory immune response with memory T and B cells + high affinity neutralising antibodies that should protect from reinfection due to fast adaptive immune responses

74
Q

Receptor family of chemokines

A

homoestatic (CXCR4,5,CCR7) and inflammatory (CXCR1,2,3) chemokine receptor

75
Q

How can viruses interact with MHC? Give at least 3 examples.

A

MCH class 1: endogenous antigens processed by proteasome -> TAP -> ER -> surface
MHC class 2: exogenous antigens processed in endosome -> surface
MHC class 1: exogenous antigen by crosspresentation

they can also downregulate MHC molecules or mimmick them to modulate immune system to their owm benfits

76
Q

11: Mucosal immunity

Define oral tolerance

A

Oral tolerance is th state where oral antigen administration induces tolerance

Harmless stimuli like commensals and food proteins inhibit the maturation of DCs. Immature DCs recruit regulatory T cells that supress other inflammatory reactions

77
Q

Draw IgG. Which part is responsible for effector function and antigen binding? With what signalling molecules are activating and inhibiting Fc gamma receptors associated?

A

IgG, 2 heavy chains, 2 light chain, variable and constant region

effector function: constant region
antigen binding: variable region

+: SyK, FAK
-: SHP-1, SHIP-1 (not in the lectures?)

78
Q

Difference between SIRS and sepsis

A

sepsis: severe form of systemic inflammation as a result of blood infection that lead to organ dysfunction and severe conditions

SIRS (Systemic Inflammatory Response syndrome) where several condition can lead to a systemic inflammation.SIRS can occur with absence of infection

79
Q

MHCI and II: which cells expressed, Priming? What is cross presentation?

A

MHCI
all nucleated cells, endogenous proteins will be processed in cytosome via proteasome, TAP transporter into ER, then MHC I loading and presentation onto surface to activate CD8+ T cells

MHC II
proffesional APCs like B cells, macrophages and DCs, exogenous proteins be will processed in endosome by lytic enzymes, then MHC II loading in endosome and presentation onto surface to activate CD4+ T cell.

Cross presentation
Cross presentation could be helpful to activate T cell when there are less MHCI loading of endogenous proteins. Then also exogenous proteins can undergo processing to be loaded on MHC I molceule to activate CD8+ cells

80
Q

3 PAMPs of fungi

A

ß-glucan

mannans

chitin

81
Q

? Mucosal surface eine folie ganz bisschen

What happens to NF-kappaB and I-kappaB after phoshorylation of the latter?

A

Phosphorylation of I-kappa B leads to conformational change. I-kappa B can be degradaded to release NF-kappaB. NF-kappaB translocate into nucleus, binds to DNA to induce a proinflammatory response

82
Q

11: Mucosal immunity

Which forms of IgA exist? Which one is transported across membranes and how is it transported?

A

Dimeric and monomeric form exists, dimeric form can be transported across mucosal membranes

Polymeric Immunoglobulin receptor can bind sIgA for endocytosis into mucosal epithelial cell, then it can be released into lumen

83
Q

What describes the 4 groups of chemokines?

A

cysteine residues within chemokine leads to nomenclature / C,CC,CXC,CX3C