Abilash - Principles year 1 > immunity > Flashcards

immunity Flashcards

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1
Q

innate defences

A

surface barriers:
* Skin
* Mucous membranes

Internal defences:
* Phagocytes
* Natural killer cells
* Inflammation
* Antimicrobial proteins
* Fever

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2
Q

adaptive defences

A

humoral immunity - B cells

cell mediated immunity - T cells

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3
Q

naturally acquired immunity

1.active

  1. passive
A
  1. pathogen enters body naturally, innate and adaptive defences respond and provide long term defences
  2. antibodies passed from mother to foetus via placenta, breast milk to provide immediate short term defences
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4
Q

Artificially acquired immunity

1.active

  1. passive
A
  1. antigen enters through vaccination, innate and adaptive defences respond and provide long term defences
  2. antibodies from immune individuals injected to provide short term Protection.
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5
Q

what are the polymorphonuclear leukocytes

A
  • neutrophils
  • eosinophils
  • basophils
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6
Q

what are the antigen presenting cells

A
  • dendritic cells - skin + tissues
  • monocytes - precursor to tissue macrophage
  • macrophages - tissues
  • ( B cells - adaptive)
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7
Q

what are neutrophils

A
  • most abundant phagocytes
  • first line of defence
  • granules containing cytotoxic molecules, antimicrobial enzymes are released
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8
Q

how do neutrophils digest

A
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9
Q

eosinophils funtion

A
  • type of leukocytes that is produced in people with parasitic infections
  • activate mast cells to release histamine
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10
Q

basophils function

A
  • release anticoagulant heparin into blood to prevent blood coagulation
  • bind to IgE to protect against allergens
  • resident to GI tract
  • has heparin and histamine in granules
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11
Q

mast cells function

A
  • release histamine - causes dilation of small blood vessels, increases vascular permeability and contracts smooth muscle
  • Develop rapid hypersensitivity reactions including production of IgE antibodies in response to an antigen, binding of IgE to Fc receptors of mast cells, cross-linking of the bound IgE by the antigen and release of mast cell mediators
  • heparin and histamine in granules
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12
Q

monocytes function

A

-Make up 2-10% of white blood cells
-Immature in blood (1-2 days)
-Produced in bone marrow, travel to tissues, mature, enlarge and become tissue macrophages
-Roles inphagocytosis,antigen presentationand cytokine production
-Much more powerful phagocytes than neutrophils
-Can phagocytise as many as 100 bacteria
-Can engulf large particles such as malarial parasites
-Can survive after phagocytosis for months
-kidney shaped nucleus

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13
Q

Macrophages function

A

-Effector cells of innate immune system found essentially in all tissues
-Develop from monocytes and are most robust phagocytic cells
-Performantigen presentationand canactivate memory cells
-Free macrophages wander through tissue spaces, for example alveolar macrophages
-Fixed macrophages are permanent residents of some organs such as microglia (brain)
-Source of IL-1

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14
Q

natural killer cells

A

-non phagocytic, large granular cytotoxic lymphocytes
-kill cells by inducing apoptosis in cancer cells and virus infected cells

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15
Q

necrosis vs apoptosis

A

necrosis - is accidental cell death occurring due to uncontrolled external factors causing inflammation

Apoptosis - is programmed cell death where the cell actively kills itslef

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16
Q

function of antigen presenting cells

A

-is an innate immune cell that detects antigens and activates the adaptive immune response

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17
Q

what are dendritic cells

A

-Main antigen-presenting cells(APCs) of the immune system
-Role in activatingT helper cellsandmemory cells

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18
Q

function of MHC (major histocompatibility complex) class 1 and 2

A

-they help APC to present cells

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19
Q

when do immature dendritic cells mature

A

once they are in the presence of inflammation the cytokines stimulate them and become mature and migrate to lymph nodes

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20
Q

how do dendritic cells contribute to the development of HIV

A

They bind to HIV and transfer it to the lymph node where it contributes to the development of the infection by transferring the virus to CD4 T helper cells

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21
Q

what are cytokines

A

Small proteins – secreted by cells of the immune system

Signalling molecules released by neutrophils, macrophages, TLRs, NK cells and lymphocytes

Affect the behaviour of other cells

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22
Q

what are interferons

A

Interferons are cytokines which are produced in response to viral infection

Protein kinase R (PKR) pathway is triggered by dsRNA and interferon

Produce an ‘anti-viral state’ in target cells

Acts on cell that produces it, as well as neighboring cells

Shuts down protein synthesis machinery of cells, thus preventing viral replication

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23
Q

Steps for phagocyte mobilisation

A
  1. Leukocytosis: release of neutrophils from bone marrow in response to leukocytosis-inducing factors from injured cells
  2. Margination: endothelial cells of capillaries in inflamed area project cell adhesion molecules (CAMs) into vessel lumen that attach to passing neutrophils, causing them to slow and roll along, clinging to vessel wall
  3. Diapedesis: neutrophils flatten and squeeze between endothelial cells, through capillary walls, moving into interstitial spaces
  4. Chemotaxis: inflammatory chemicals act as chemotactic agents that promote positive chemotaxis of neutrophils toward injured area
  5. As attack continues, monocytes arrive later 12 hours after leaving bloodstream, they are transformed into macrophages
    These “late-arrivers” replace dying neutrophils and remain for cleanup prior to repair
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24
Q

what is the complement system

A

-series of over 30 proteins

-when foreign material is detected it initiates a
cascade of reactions that amplify the signal

-cooperates with other host defences to generate inflammation and remove the pathogen

-contains proteins C1-9 factors B,D,H and I

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25
main functions of complement system
-facilitates phagocytosis Generates activated complement proteins opsonising antigens (marking antigens for phagocytosis by attaching to the surface/coating a particle with opsonins allowing interactions with receptors on phagocytes) -lysis of pathogens lyses bacterial cell wall -inflammation Attracts more macrophages and neutrophils
26
What are toll like receptors
Phagocytes such as dendritic cells identify pathogens by recognising **pathogen-associated molecular patterns (PAMPs) using pathogen recognition receptors (PRRs) - toll like receptors are an example of PRRs.** Toll-like receptors (TLRs) link microbial products (PAMPs) to transcription factor activation in a signaling pathway
27
What is an epitope
The region of an antigen that interacts with an antibody
28
What are the 5 types of immunolgobulins
IgM IgG IgA IgE IgD
29
Where is the Fc and Fab region
30
IgM immunoglobulins characteristics
- have a pentameric structure - produced first during primary response - 3rd most abundant - marker of recent infection - activates complement has 5 complement bonding sites - too big to cross placenta
31
IgG immunoglobulins characteristics
- most prevalent antibody in serum 70% - crosses placenta from mother to foetus, protects newborn until can produce own antibodies - activates complement - secreted high quantities in secondary response (faster, more effective)
32
IgA immunoglobulin characteristics
- 2nd most common - most prevalent in secretions such as tears, saliva and mucous - monomeric in serum but dimeric with secretory component in lumen of GI and respiratory tract - resistant to digestion and can activate complement system - found in breast milk - localised protection on mucous membranes
33
IgD immunoglobulin characteristics
- monomeric structure - helps b cells mature - b cell membrane receptor
34
IgE immunoglobulin characteristics
- monomeric structure - triggers allergic responses, binds to basophils in blood and mast cells in tissues and release histamine which causes inflammation - associated with anaphylaxis - higher in people with asthma, hay fever and allergic disorders - least abundant - mediates type 1 hypersensitivity reactions
35
Antigens are spread via the…
Blood and lymphatic system to lymphoid organs such as spleen (blood) and lymph nodes (lymph)
36
Antibody secreting plasma cells initially secrete…
IgM immunoglobulins
37
When memory cells are exposed to the same antigen…
They convert to plasma cells and produce IgG
38
Affinity is the…
strength of the interaction between an epitope and antibody-antigen binding site or it is the association constant for binding (KA) KA= K1/K2
39
Valence is the…
number of epitopes/antigen binding sites. IgG is bivalent, IgM decavalent due to its pentameric structure. Grater the Ig valency, greater the amount of antigen it can bind. Antigens can also demonstrate multivalency because they can bind to more than one antibody
40
Avidity refers to…
refers to the accumulated strength of multiple affinities (affinity and valence)
41
Consequences of antigen-antibody binding
Neutralisation Agglutination Precipitation of soluble antigens Complement fixation
41
What does opsonisation mean
To make a foreign cell more susceptible to phagocytosis
42
Soluble innate immune molecules
Enzymes such as lysozyme - break bacterial cell wall, found in blood and tears Antimicrobial peptides Collections, ficolins and pentraxins - bind to pathogen and target for phagocytosis and activate complement Complement components - lyse bacteria, opsonise bacteria and induce inflammation
43
How does lysozyme disrupt peptidoglycan
Cleaves bond between the alternating sugars that make up peptidoglycan Most effective against gram positive bacteria
44
Actions of collectins, ficolins and pentraxins
* Soluble pattern recognition receptors * Act as opsonins that bind to pathogens and infected cells targeting them for phagocytosis * Activate complement through the classical pathway/lectin pathway
45
What is the complement system
A system of around 30 proteins that act in a sequence of activating another to defend against infection called the complement cascade Helps antibodies and phagocytic cells clear pathogens Part of Innate immunity bridges to adaptive
46
What are the 3 complement pathways
1. Classical 2. Alternative 3. Lectin
47
Which proteins make up the classical pathway
C1-C9
48
C1 structure
Has c1s, c1r, c1q Each c1q can bind to fc region of antibodies so each c1 can bind up to 6 antibodies C1r and c1s are both serine proteases which are hidden They are wrapped in calcium so if lack of calcium lack of c1
49
When c1q receptors bind to antibodies that are bound to antigens…
The c1 molecule twists exposes the c1r and c1s this activates c1 molecule which cleaves c4 into c4a and c4b and c2 into c2a and c2b C4b and c2b bind together on the surface of the pathogen forming c4bc2b=c3 convertase C3 convertase cleaves c3 into c3b and c3a
50
C3B is also called…
Opsonin - help phagocytes get a firm grip on bacteria, binds to antiphagocytic capsule
51
C3b binds to c4b2b complex to from c4b2b3b which is known as…
C5 convertase
52
C5 convertase cleaves c5 into C5a and c5b C5b then combines with
C6 c7 and c8, these 4 proteins then begin to penetrate the pathogen membrane
53
Role of c9
Form a channel through the pathogen membrane
54
The attachment of c9 c5bc6c7c8 form the…
MAC - membrane attack complex which creates a hole in the bacterial cell membrane
55
In the lectin binding pathway the difference from the classical pathway is..
Mannose binding lectin protein is used instead of c1 - they both have similar shapes It binds to mannose which is a sugar commonly found on bacteria membranes It cleaves c4 and c2 to produce c3 convertase and follows classical pathway
56
Four characteristics of adaptive immunity
**Self/non-self recognition** - T cells and B cells have ability to recognise one’s own cells versus a pathogen (invader) **Specificity** - lymphocytes are tailored to combat specific antigens due to the great diversity of B cells and T cells **Diversity** - There are potentially billions of different antigen receptors on B cells and T cells that recognize billions of different antigens **Memory** - Immune system is capable of “remembering” the pathogen once exposed
57
How do T-cells recognise self vs non- self
For mature T cell to develop without being self-reactive, it must go through both positive and negative selection A) T cell binds to antigen-MHC complex from infected cell causing cell death B) Positive selection: T cell in thymus that binds moderately to MHC complex and survives C) Negative selection: T cell that binds too strongly to MHC will likely be self-reactive and result in death
58
What is the membrane bound protein that inhibits the formation of MAC on host cells
CD59/Protectin
59
In alternative pathway c3…
gets cleaved very slowly without the presence of c3 convertase
60
Factor B binds to…
C3b and antigen membrane and is cleaved by factor D to form Ba and Bb Leaving c3bBb on the antigen membrane
61
What is the amplification step in the alternative pathway
c3bBb acts as c3 convertase and after this point it will follow the classical pathway
62
How is the alternative pathway regulated
C1 inhibitor Dissociates factor c3b form Bb which shuts down the alternative c3 convertase Factor H a cofactor for factor **I** which inactives c3b into ic3b ic3b is still a potent opsonin which cant propogate the alternative pathway
63
c3a and c5a act as...
1.chemotaxins - which attracts phagocytes 2.Anaphylatoxins - which degranulate basophils and mast cells to release proinflammatory molecules such as histamine and heparin - can cause contraction of smooth muscle, bronchial constriction, vascular permeabilty - c5a activates mast cells which stimulates inflammation
64
Complement deficiency conditions
65
Which leukocytes have bi-lobed nuclei
Eosinophils and basophils
66
Which leukocytes have multi-lobed nuclei
Neutrophils
Abilash - Principles year 1
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