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BS2032 > Immunology > Flashcards

Immunology Flashcards

1
Q

Why havent we eliminated all diseases?

A

Antibody vaccines work well and easy to design
Not all pathogens are controlled by antibodies
Not all pathogens maintain the same antibody targets over time
Kinetics, location and interplay between pathogen and host

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2
Q

Hoffmann, Beutler, Steinman

A

Activation of the immune system (2018 Nobel)

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3
Q

Alison and Honjo

A

Inhibition of negative regulation of immune system (2011 nobel)

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4
Q

Innate Cells

A

Respond to changes in tissues and invading objects - initiate the immune response

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5
Q

Intracellular - Type 1 immunity

A

Macrophage, Dendritic cell, Neutrophil

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6
Q

Extracellular - type 2 immunity

A

Eosinphils, Basophil, Mast cell

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7
Q

Macrophages

A

Phagocytosis and activation of bactericidal mechanisms

Antigen presentation

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8
Q

Dendritic Cells

A

Antigen uptake in peripheral sites

Antigen Presentations

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9
Q

Neutrophils

A

Phagocytosis and bactericidual mechanisms

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10
Q

Eosinphil

A

Killing of antibody-coated parasites

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11
Q

Basophils

A

Promotion of allergic responses and augmentation of anti-parasitic immunity

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12
Q

Mast Cell

A

Release of granules containing histamine and active agents

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13
Q

Why do we have an immune response

A

Toll-like receptors on machrophages respond to specific markers, such as flagellin, on foreign bodies and elicit a response.

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14
Q

Immune system protects against 4 types of pathogens

A

Extracellular bacteria, parasites and fungi
Intracellular bacteria and parasites
Viruses
Parasitic worms

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15
Q

Dendritic immune response

A

Immature dendritic cells reside in peripheral tissues
Dendritic cells migrate via lymphatic vessels to regional lymph nodes
Mature dendritic dendritic cells activate naive T cells in lymphoid organs such as lymph nodes

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16
Q

Creation of lymphocytes

A

Common lymphoid progenitor - Bone marrow
Naive differentiated lymphocyte - Thymus or bone marrow for maturation
Circulation
Naive lymphocyte experiences antigen - Lymph node
Circulation
Lymphocyte becomes an activated effector cell - Inflamed tissue

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17
Q

B Cells

A

Make specific antibody which binds to a specific antigen

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18
Q

T Cells

A

Have specific receptors which bind to specific antigens in context of presenting molecules
The epitopes recognised by T-Cell are often buried
Antigen must be broken into peptide fragments
Epitope peptide binds to a self (MHC - Major Histocompatibility Complex) molecule
T-cell receptor binds to a complex of MHC molecule and epitope peptide

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19
Q

MHC Class 1

A

Expressed in all cells of body - CD8 T cells

20
Q

MHC Class 2

A

Expressed in dendritic cells and macrophages (professional antigen presenting cells) - CD4 T cells

21
Q

Production of lymphocytes

A

A single progenitor cell gives rise to large number of lymphocytes each with a different specificity
Removal of potentially self-reactive immature lymphocytes by clonal deletion
Pool of mature naive lymphocytes
Proliferation and differentiation of activated lymphocytes to form a clone of effector cells (after a lag which requires an innate response to control the disease whilst the cells expand)

22
Q

Postulates of the clonal selection hypothesis

A

Each lymphocyte has single type of receptor with a unique specificity

Interaction between a foreign molecule and a lymphocyte receptor capable of binding to that molecule with high affinity leads to lymphocyte activation

The differentiated effector cells derived from an activated lymphocyte will bear receptors of identical specificity to those of the parental cell from which that lymphocyte was derived

Lymphocytes bearing receptors specific for ubiquitous self molecules are deleted at an early stage in lymphoid cell development and are therefore absent from the repertoire of mature lymphocytes

23
Q

B Cell production

A

B-cell precursor rearranges its immunoglobulin genes
Immature b-cell bound to self cell-surface antigen is removed
Mature B cell bound to foreign antigen is activated
Activated B-cells give rise to plasma cells and memory cells

24
Q

B-Cell - Viruses

A

B cell binds to virus through viral coat protein
Virus particle is engulfed and degraded
Peptides from internal proteins of the viruses are presented to the T-cell which activates the B cell (antigen recognition induces expression of effector molecules by t-cell which activates b cell)
B-Cell activation by antigen and helper T-Cells
Antibody secretion by plasma cells
Leads to neutralistation/Opsonisation/Complement activation

25
Q

T helper cell and b cell interaction

A

Helper T cell adheres to the b cell and begins to synthesise IL-4 and CD40 ligand
Helper t cell reorients its cytoskeleton and secretory apparatus towards the b cell
IL-4 is released and is confined to the space between the b/t cell

26
Q

T-dependent antigen

A

Requires t-cells to activate B-cell

27
Q

T-independent antigen

A

Requires danger signal but can be activated without T-helper cell -
Ti-2 antigens alone can signal production of IgM ab in b-cells
Activate dendritic cells release a cytokine, BAFFS, that augment production of Ab against TI-2 antigens and induces class switching

28
Q

Primary Ab repertoire is generated by three processes

A

Primary IgM - V(D)J recombination - Constant region IGM - bone marrow early development
Somatic Hypermutation - mutations in heavy and light chains of variable region (increasing affinity)
Class switch - change in constant region of molecule to others of different function

29
Q

Neutralisation

A

Toxin binds to cellular receptor
Endocytosis of toxin-receptor complex
Dissociation of toxin to release active chain which poisons cell
Ab protects cell by blocking binding of toxin

30
Q

Blocking

A

Virus binds to receptor cell surface
Receptor-mediated endocytosis of cirus
Acidification of endosomes after endocytosis triggers fusion of cirys with cell and entry of viral dna
Ab blocks binding virus by binding to receptors and block fusion event

31
Q

Opsonisation

A

Pentameric IgM mol binds to antigen on bacterial surface and adopt stale form
C1q binds to one bound IgM
Binding of C1q to Ig activates C1r which cleaves and activates the serine protease C1s

32
Q

Targeted cell killing

A

Ab binds to antigens on surface of target cells
Fc receptors on NK cells recognise bound Ab
Cross-linking of Fc receptors signals the NK cell to kill the target cell
Target cell dies by apoptosis

Useful in cancer

33
Q

CD4-T cell

A

APC stimulates effector CD4 T cell to induce CD40L and IL-2

Stimulation of APC through CD40 increases B7 and 4 IBBL which costimulates naive CD8 T cells

34
Q

Protein in granules of cytotoxic t cells

A

Perforin - Aids in delivering contents of granules into the cytoplasm of target cell
Granzymes - Serine proteases which activate apoptosis once in the cytoplasm of the target cell
Granulysin - Has antimicrobial actions and can induce apoptosis

35
Q

Mucosal tissues

A

Large immune tissue

Consits of two immune systems of distinct compartments - the epitheium and lamina propria

36
Q

T-Cells and the Mucosa

A

T-cells enter the Peyer’s patches from blood vessels and are directed by the homing receptors CCR7 and L-selectin
T-cells in the Peyer’s patch encounter antigen transported across M cells and become activated by dendritic cells
Activated T-cells drain via mesentric lymph nodes to the thoracic duct and return to the gut via the bloodstream
Activated T-cell expressing alpha4:beta7 intergrin and CCR9 home to the lamina propria and intestinal epithelium of small intestine

37
Q

Location of T-cells is driven by integration of multiple signals

A

Gut-homing effector T-cell bind MAdCAM-1 on endothelium

Gut epithelial cells express chemokines specifc to gut homing T-cells

38
Q

Mucosal barrier can allow antigen to pass by a variety of pathways

A

Non-specific transport across epithelium
FcRn-dependent transport
Apoptosis-dependent transfer
Antigen capture

39
Q

Effector cells within the mucosa

A

Lymphocytes called intraepithelial lymps (IELs) lie within epithelial lining of gut
Are CD8-positive T-cells

40
Q

Effector cell response

A

Virus infects
Infected cells display viral peptide to CD8 IEL via MHC class 1
Activated IEL kills infected epithelial cells by perforin/granzyme and Fas-dependent pathways

41
Q

Immune mediated responses due to stress/damage

A

Epithelial cells undergo stress as aresult of infection/damage or toxic peptides and express MIC-A/B
NKG2D on IEL binds to MIC-A,B and activates IEL, CD8a:a homodimers also bind to TL
Activated IEL kills the stressed cell via perforin/granzyme pathway

42
Q

IgA

A

Unique to mucosal lumen
Secreted can bind and neutralise toxins and pathogens
Can neutralise antigens internalised in endosomes
Can export toxins and pathogens from the lamina propria while being secreted

43
Q

Salmonella

A

Can enter and kill M cells, kill macrophages and epithelial cells, can invade lumen and phagocytic cells
Chemokines and cytokines produced by macrophages recruit neutrophils out of blood vessels and activate them
Dendritic cells loaded with bacterial antigens acquired directly or from macrophages to the mesenteric lymph nodes via afferent lymphatics and provoke an adaptive immune response
If defenses fail Salmonella can enter bloodstream and cause systemic infection

44
Q

Shigella

A

Shigella penetrate gut epithelium through M cells
Shigella invade basal surface of epithelial cells and spread to other epithelial cells
Shigella cell-wall peptides bind and oloigomerise NOD1 activating NFkB pathway
Activated epithelium secretes CXCL8 recuriting neutrophils

45
Q

Clostridium difficile

A

Colon is colonised by large number of commensal bacteria
Ab kill many of these bacteria
C. difficile gains a foothold an dproduces toxin causing mucosal injury
Neutrophils and RBC leak into gut
Connective tissue degredation leads to colitis and pseudomembrane formation

BS2032 (2 decks)

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