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Immunology > Immune Structures & Mucosal Immunity > Flashcards

Immune Structures & Mucosal Immunity Flashcards

1
Q

What are the primary lymphoid organs?

A

-Bone marrow
-Thymus

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2
Q

What are primary lymphoid organs?

A

Sites where B & T cells are made & mature

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3
Q

Where do B cells develop & mature?

A

Bone marrow

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4
Q

Where do T cells develop & mature?

A

-Develop = bone marrow
-Mature = thymus

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5
Q

What are the secondary lymphoid organs?

A

-LNs
-Spleen
-MALT

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6
Q

What are secondary lymphoid organs?

A

Sites where B & T cells move to once developed & matured
–> here = can recognise antigen - so are activated - to fight infection/cancer

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7
Q

Which of the secondary lymphoid organs are capsulated, & what does this mean?

A

-LNs
-Spleen
–> have CT ‘bag’ around them - controls movement in & out (& contain things inside)

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8
Q

What is the secondary lymphoid organ that is non-capsulated, & what does this mean?

A

MALT
–> no controlled movement in & out (antigens move freely in to activate B & T cells)

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9
Q

How is the spleen different from other secondary lymphoid organs (LNs & MALT)?

A

-Filters blood (NOT LYMPH - as has no lymphatic drainage system - where ‘stuff’ enters)
–> antigens & lymphocytes enter via blood
-PALS (periarteriolar lymphoid sheath) = where imm cells are
-(no cortex or medulla - has red pulp & white pulp instead)

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10
Q

What type of infections will spleen respond to?

A

Systemic infections

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11
Q

Entry & exit from spleen?

A

-Splenic artery = antigens & lymphocytes enter
-Splenic vein = out

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12
Q

Which organ has the greatest number of lymphocytes that flow through it?

A

Spleen

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13
Q

Describe structure of spleen.

A

Capsule w/ extensions - trabecula
->
Red pulp (RBC ‘graveyard’) - w/ vascular sinusoids
->
marginal zone (boundary between red & white pulp)
->
white pulp:
-(marginal zone - w/ primary lymphoid follicles)
-PALS (periarteriolar lymphoid sheath)
-primary follicle

Splenic artery (in) & vein (out)

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14
Q

What are the 2 distinct regions of the spleen?

A

-Red pulp
-White pulp

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15
Q

What cells are in red pulp?

A

-Macrophages
-RBCs
-Few lymphocytes

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16
Q

Role of red pulp?

A

-Filter out old/damaged RBCs
–> the phagocytosis of these RBCs (macrophages)

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17
Q

Cells in marginal zone?

A

Dendritic cells

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18
Q

What is the periarteriolar lymphoid sheath (PALS)?

A

-Part of white pulp surrounding arteries - forms sheath of lymphocytes around artery
= contains mostly T cells (respond to antigens/pathogens entering here)

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19
Q

What is found in marginal zone of white pulp?

A

Mostly B cells & primary lymphoid follicles (for initiating imm resp)

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20
Q

What is needed in secondary lymphoid organs for an immune response?

A

B cells & T cells come together - form follicles (where response occurs) - as otherwise there will be relatively distinct B & T cell zones

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21
Q

What are the 3 key features of ALL secondary lymphoid organs?

A

-Lymphoid follicles (primary & secondary)
-Germinal centre

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22
Q

What is the process of immune response occurring in spleen?

A

2 = Dendritic cells & T cells interact (T cells spend time in PALS but come from blood)
3 = dendritic cells activate T cells (as dendritic cells phagocytose antigen - APC)
4 = T & B cells come together –> T cells provide survivor signals & signals to inform B cells what to be (differentiate into)
-Primary follicle = where T & B cells come together
-B cells = prolif & make anitbodies
5 = forms secondary follicle
-Germinal centre = where the specific B & T cells are
-Cuff around germinal centre = from the inactivated B & T cells

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23
Q

What is a primary follicle?

A

Collection of cells - where not much happening (in terms of immune resp)

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24
Q

What is a secondary follicle?

A

Collection of cells which are activated & begin imm resp
-Has a germinal centre (active part)

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25
Q

Where are LNs found?

A

Junctions of lymphatic vessels

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26
Q

What do LNs do?

A

Trap pathogens & antigens entering lymphatic system (from tissues)

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27
Q

Structure of LNs?

A

-Reticular - mesh-like (so can trap pathogens & antigens so can hold here & to be processed & presented for imm resp)
-Bean-shaped
-Enlarged when is infection - imm resp occurring
-LOTS of lymphocytes, macrophages, dendritic cells
-Cortex
-Paracortex
-Medulla

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28
Q

Why are macrophages needed in secondary lymphoid organs?

A

Lots of cells die - so can phagocytose (cells die intentionally - not fit for purpose)

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29
Q

Why are dendritic cells needed in secondary lymphoid organs?

A

Phagocytose antigens & pathogens - APCs - activate T cells –> B cells

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30
Q

How does lymph enter & exit LNs?

A

Afferent lymphatic vessels = in
Efferent lymphatic vessels = out

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31
Q

What is filtered out by LNs (to stay in LNs)?

A

-Antigens/pathogens
-Dendritic cells
–> both from tissues

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32
Q

What is the subcapsular space of LNs?

A

= space between capsule & cortex - allows transportation of lymphatic fluid
so….
= where the lymph containing lymphocytes, dendritic cells, macrophages, possible antigens & pathogens - enters into from afferent lymphatic vessel

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33
Q

What leaves in efferent lymphatic vessel from LNs, if an infection is detected?

A

Antibodies + LOTS of lymphocytes (prolif of lymphocytes in LNs)

34
Q

What is the process of the immune response occurring in LNs?

A

1 = antigen + dendritic cells enter via afferent lymphatic vessel in lymph
-resident dendritic cells reside in paracortex of LN
(x2 sources of dendritic cells)
2 = Dendritic cells & B cells (in follicle) become APCs –> activate T cells (Th)
3 & 4 & 5 = B cell becomes APC & activated if antigen bound is the right one
–> all B cells will phagocytose antigen - only one = correct (comp to BCR)
–> activated B cell makes IgM
–> B & T cells interact - primary follicle to secondary follicle (w/ germinal centre) - B cells activated here
–> B cells prolif if activated & T cells too if activated - T cells ‘help’ B cells
–> get T cell differentiation - to ‘right’ T cell type for this response
–> B cells differentiate = plasma cells = antibodies produced

35
Q

What are lymphoid follicles?

A

-Visible nodules
Number of lymphoid follicles in secondary lymphoid tissue - collection of mostly B cells, macrophages, follicular dendritic cells

36
Q

What are germinal centres?

A

-When activated B cells & their associated Th move into lymphoid follicles & proliferate = GC
-Once form GC, follicle goes from
primary lymphoid follicles –> secondary lymphoid follicle

37
Q

Describe the formation of germinal centres.

A

-B cells come across antigen
-B cells move to T & B cell border - to be activated by T cells (via signals)
-B cells now - prolif = plasmablasts (Bl) OR germinal centres (blue)
-B cells can move from light to dark zones of GC - to undergo somatic hypermutation & class switch recombination
-B cells can leave GC - as high-affinity memory cells (M) or plasma cells (P)

38
Q

Where are lymphoid follicles seen?

A

ALL secondary lymphoid organs/tissues

39
Q

Describe this image.

A

Whole thing = germinal centre with light & dark zones

Darker = clonal expansion & somatic hypermutation
Lighter = class switching, selection & differentiation
—> both zones = B cell proliferation

Mantle zone = outer cuff/area surrounding germinal centre - of Th & inactive B cells (as these don’t have specific BCR to antigen)

40
Q

What are GCs specialised microenvironments for?

A

-B cell prolif
-Somatic hypermutation

41
Q

Structure of GC & surrounding areas?

A

-Inactive B cells pushed to edge = mantle zone
-Central active B cells
-Th surround B cells (in cuff)

42
Q

What is the desired outcome for GCs?

A

High affinity tight binding antibody produced (to antigen) correct class for area of body infection is in & for that particular pathogen - so get correct resp

43
Q

Why is affinity of binding of antibody to antigen important?

A

More likely to neutralise antigen

44
Q

Describe process of naive B cell going from primary follicle to secondary follicle (GC) to producing high affinity B antibodies (plasma & memory cells)

A

-Naive B cell in primary follicle
-Receives antigen via BCR
-Proliferation/clonal expansion of B cell
-Somatic hypermutation
-TFH & follicular DC enter primary follicle
-If get improved affinity BCR/antibodies:
-TFH recognises B cell via BCR = x3 signals from TFH to B cell = activates B cell - forms secondary follicle w/ germinal centre
-TFH provides cytokine to B cell - instructs which antibody to make (class switching of B cell)
-B cell differentiates = memory OR plasma cell
-Plasma cell - secretes high affinity antibodies = via affinity maturation

BUT - is somatic hypermutation leads to lower affinity BCR/antibodies = apoptosis of B cell - as TFH won’t recognise & provide survival signals = no secondary follicle & germinal centre made

??? Is secondary follicle & germinal centre formed immediately as B cell proliferates (clonal expansion) ???

REMEMBER BCR IS AN ANTIBODY!!!

45
Q

What is somatic hypermutation?

A

-‘making better antibodies’
-Of BCR
-Further mutations to immunoglobulin genes
-Occurs after encounter antigen
-Induces point muts (swaps bases) - high rate
-Rearrange V, D, J sequences of heavy chain & V, J for light chains = diversities of specificities
–> B cells mutate their genes in GC
-Changes BCRs & soluble antibodies of B cell!!!

46
Q

Outcome of somatic hypermutation?

A

-Beneficial = higher affinity antibodies (select B cells w/ highest aff BCRs by interacting w/ T follicular helper cells = affinity maturation)
-Detrimental = lower affinity antibodies (will get apoptosis of B cell)

-Affinity = ability to bind antigen, recognise self prots

47
Q

Outcome of somatic hypermutation?

A

-Beneficial = higher affinity antibodies (select B cells w/ highest aff BCRs by interacting w/ T follicular helper cells = affinity maturation)
-Detrimental = lower affinity antibodies (will get apoptosis of B cell)

-Affinity = ability to bind antigen, recognise self prots

-BCRs & soluble antibodies change

48
Q

What is affinity maturation?

A

= process by which TFH cell-activated B cells produce antibodies with increased affinity for antigen
—> produce antibodies w/ increased affinity for antigen = via somatic hypermutation
-BUT muts = random

49
Q

What is the type of T helper cell in GCs?

A

-T follicular helper cells (in secondary follicles) - signal cytokines to B cells to cause B cell to differentiate

-(Activate & mature B cells)

50
Q

What happens after somatic hypermutation & affinity maturation of B cells?

A

-B cells move further into light zone (of GC)
= get 2nd signal from Th so…
-Class switching of antibodies - due to cytokine release from TFH
-B cell differentiates = plasma/memory B cells

51
Q

What are isotypes?

A

The different classes of antibodies

52
Q

How are isotypes formed?

A

Class switching of B cells

53
Q

What is different about the different isotype?

A

-Different heavy chain constant region
-Different characteristics - binds to different Fc recs

54
Q

Purpose of isotype?

A

Useful against different infections at different anatomical sites

55
Q

What determines the isotype?

A

Constant region on heavy chain

56
Q

What determines antibody specificity?

A

Variable region

57
Q

5 types of antibody?

A

IgM = 1st made when encounter antigen
IgA = secrete at mucosal sites
IgD = B cell rec can release? Soluble? - basophils
IgE = parasite responses & allergies
IgG = many purposes - high affinity - crosses placenta

58
Q

Which antibodies are important components of MALT?

A

IgA
IgD

59
Q

Why are mucosal surfaces at risk of infection?

A

Are open to outside world

60
Q

What do mucosal surfaces have to protect from infection?

A

-Barrier functions
-Local immunity

61
Q

What are the second line of defence if mucosa are breached?

A

-LNs to drain
-MALT
-Constantly active innate + adaptive immune cells in ep & lamina propria (CT)

62
Q

Role of MALTs?

A

Defend body against pathogen entry via mucous membranes

63
Q

What is found in MALT (cells)?

A

Plasma B cells (more than spleen, LNs, BM together)

64
Q

2 types of MALT?

A

-BALTS (bronchus)
-GALTS (gut)

65
Q

What does GALT include?

A

-Peyer’s patches (SI)
-Isolated lymphoid follicles (throughout intestine)
-Lamina propria imm cells
-Appendix
-Palatine tonsils
-Adenoids
-Lingual tonsils
–> all drain to mesenteric LN

66
Q

What are the 3 types of tonsils?

A

-Palatine
-Pharyngeal
-Lingual

67
Q

Structure & components of tonsils?

A

-Nodular
-Meshwork of reticular cells, macrophages, granulocytes & mast cells
-B cells organised into follicles & GCs - T cell cuff surrounds
(Have GCs + follicles too!)

68
Q

Role of tonsils?

A

-Provide lymphoid tissue at intake of pathogen in food - protect from what we consume
-Defence against potential antigens entering via nasal & oral ep

69
Q

What are inductive sites of MALTS?

A

Where lymphocytes are activated
(B & T cells primed by antigen - differentiate into effector cells)
- so where see follicles

70
Q

What are effector sites of MALTS?

A

Where lymphocytes act - where pathogen is
(B & T cells migrate to carry out effector functions to clear pathogens)
-In mucosa at surface of ep & in mucus (if anything breaks through)

71
Q

Example of lymphoid nodules in MALT?

A

Peyer’s patch - ileum (mostly) = lymphoid nodules in outer wall of ileum

72
Q

Peyer’s patch structure?

A

Nodules contain follicles - develop GCs (when exposed to antigens)

73
Q

How are GCs formed in Peyer’s patch (MALT)?

A

*Nodules = collections of primary follicles in underlying lamina propria - form GCs when detect antigen on intestinal ep layer
-M cells (@ inductive sites) - broad processes in contact w/ lumen & have invagination in their basal memb
-Invagination of M cells = contains T cells, B cells, DCs, macrophages
-M cells = endocytose antigen - from lumen of dig/resp/UG tract
-Antigen = transported & released into invagination of cell
-DCs = phagocytose antigen - in lamina propria
-DCs = activate T cells - in lamina propria
-T cells activate B cells - in lamina propria
-Immune cells diffuse across mucosa in ep layer & in lamina propria
These include:
• Goblet cells = produce mucus
• Plasma cells = secrete IgA & IgD
• Tc = eliminate infected ep cells

74
Q

What are the specialised cells found in inductive sites in MALTs?

A

Microfold (M) cells (type of ep cell)

75
Q

Role of M cells?

A

-Deep invagination/pocket (at basal surface) - where lymphocytes, dendritic cells, macrophages are found (in pocket) = inductive site - lymphocytes activated here - as is lots of phagocytes:
-Antigens endocytosed by M cells from lumen (of dig/resp/urogen tract)
-Antigen moved & released into basolateral pocket
-Antigen = phagocytosed by dendritic cells –> T cells activated –> then B cells (in lam propria)
-IgA made

76
Q

What are some other immune cells across mucosa - in ep layer & lamina propria?

A

-Goblet cells = secrete mucus (holds microbes away from body cells)
-Plasma cells = secrete IgA & IgD
-Tc = rapidly kill infected ep cells

77
Q

Role of IgA?

A

To ensure don’t get inflammatory response for every bacteria (as gut full of bact) - so doesn’t trigger inflamm - as can’t bind to Fc recs
-High avidity - can bind 4 antigens
-High affinity - binds well
-Neutralising antibody - sticks pathogens & stop prolif
-DOES NOT TRIGGER INFLAMMATION!

78
Q

Role of Paneth cells?

A

-Secrete antimicrobial peptide secreted into mucus - kill microbes that breached ep into mucus
-Mucus = toxic stuff of antimicrobial peptides - kills microbes that enter

79
Q

Summarise the general process in secondary lymphoid organs.

A

-Dendritic cell – phagocytosed antigen (phagosome, phagolysosome breaks down = peptide) – peptide presented on memb w/ MHC I = APC
-TCR binds to antigen (presented by dendritic cell)
-Costimulation – B7 from dendritic cell interacts with CD28 from T cell
-Dendritic cell produces cytokines – causes T cell to differentiate = specific effector cell – Tc or Th

-Antigen recognised by BCR - B cell uptakes antigen - phagocytosis (phagosome - binds to phagolysosome to break down – peptide taken) – peptide binds to MHC II – presented on memb – B cell = APC
-Naïve B cell into primary follicle
-B cell proliferates
-Somatic hypermutation = B cell changes BCR = better/worse affinity for antigen – some B cells die (apoptosis – if disadvantageous mutations)
-B cell moves to T/B cell border (as TFH & follicular DC have entered primary follicle)
1 - TCR recognises antigen on B cell - binds to antigen-MHC II complex on B cell (T & B cell interaction – in primary follicle)
2 - Co-stimulation – CD40 of B cell interacts w/ CD40L of T cell
3 - Cytokines – T cell produce = causes antibody class switching
-B cell now = activated (now changes to secondary follicle w/ germinal centre)
-B cell differentiates = plasma OR memory cells
-Affinity maturation = selected B cells
-IgM = 1st antibody secreted by plasma cell

80
Q

What are primary follicles, secondary follicles, germinal centres, mantle zones, PALS, marginal zone, red pulp, white pulp?

A

Immunology (6 decks)

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