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Phase 2 - Immunology (ICS) Flashcards

1
Q

What is the purpose of the immune system

A

To distinguish between self and non-self and protect self from non-self

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2
Q

What is the immune system made up of

A

Cells and soluble factors

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3
Q

Characteristics of the innate system

A

First line of defence
Barrier to antigen
Instinctive
Present from birth
Non-specific
Slow response
No memory

Independent of lymphocytes (but does include phagocytes and monocytes/macrophages)

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4
Q

Characteristics of adaptive system

A

Specific
Aquired/learned (from initial exposure to specific non-self)
Has memory to specific antigens
Quicker response second time onwards

Dependant on lymphocytes
Antibodies

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5
Q

Which cells are involved in the innate immune system

A

Neutrophils
Eosinophils (mainly functions in parasitic reactions)
Basophils (mainly functions in allergic infections)
Monocytes (kidney shaped nucleus - only found in blood) - release cytokines and produce complement components
- become macrophages when they leave blood and enter tissues

Mast cells - involved in allergic reactions, lots of histamine involved (from blood but reside in tissue)
Dendritic cell - major antigen presenting cells (present to macrophages and t cells) - found in epithelium

(Things like skin, tears, mucocilliary escalator are all part of innate response)

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6
Q

Which cells are involved in the adaptive system

A

Lymphocytes
* T cells
- T regulatory cells
- T helper cells (CD4)
- Cytotoxic T cells (CD8)
- Cytokine production
* B cells
- Plasma cells (antibody production)

Monocytes (only found in blood) - release cytokines and produce complement components

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7
Q

Cell components of the immune system

A

Lymphocytes
- T cells
* T regulatory cells
* T helper cells (CD4)
* Cytotoxic T cells (CD8)
* Cytokine production
- B cells
* Plasma cells
** Antibody production

Phagocytes
- Mononuclear cells
* Monocytes/ Macrophages
** Cytokine production
** Complement production
- Polymorphonuclear cells
* Neutrophils
* Eosinophils
* Basophils

Other cells
- Mast cells
- Natural killer cells
- Dendritic cells

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8
Q

What do soluble factors (humoral componant) of the blood consist of

A

Complement
Antibodies (aka immunoglobulins)
Cytokines
Chemokines

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9
Q

What is complement and what does it do

A
  • 20 proteins produced by the liver
  • mostly exist in an inactive state
  • activated via cascades
  • there are 3 activation pathways
  • only activated for the immune response
  • They have 3 modes of action:
  • Direct lysis
  • Attracting leukocytes to site of infection - chemotaxis (works by releasing chemotaxes - C3a, C5a)
  • Opsonisation (coating invading organism to increase the chance of them being phagocytosed)
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10
Q

Makeup of antibodies

A

Consists of 2 heavy chains and 2 light polypeptide chains
- Has a Fc region which is the same on all antibodies
- Has a Fab region (variable region) which is specific to the target and is where the binding site is located
- Can exist as free in solution or membrane bound to B cells

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11
Q

Functions of antibodies

A
  • bind to specific antigens
  • acts as adapter to link microbe to phagocyte
  • Neutralise toxins by binding to them
  • Activate complement (classical pathway)
    • Increase opsonisation and stimulate phagocytosis
    • agglutination, precipitation
      (-> cell lysis + chemoattraction)
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12
Q

Type of antibodies in blood

A

IgG
- most abundant - 75% of antibodies found in serum (small, can get almost anywhere - can CROSS PLACENTA)
- HIGHLY SPECIFIC

IgM
- large molecule (PENTAMERIC)
- only found within blood
- HIGHEST CAPACITY to ACTIVATE COMPLEMENT
- not super specific

IgA
- two versions: normal or DIMER
- dimer is in secreted substances e.g. saliva
- MUCOSAL
- MAIN Ab in COLOSTRUM and neonate gut

IgE
- BOUND to MAST cells and BASOPHILS
- involved in ALLERGIC reaction and HELMINTH infection
- production can be driven by eosinophils
- LEAST ABUNDANT in blood

IgD

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13
Q

What are cytokines and name the four main ones

A

Proteins secreted by immune and non-immune cells

  • Interferon
  • Interleukin
  • Colony stimulating factor
  • Tumour necrosis factor
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14
Q

What are interferons, where are they released from and what do they do?

A
  • type of cytokine
  • IFN alpha and beta produced by infected cells
  • IFN gamma produced by activated T cells
  • induces antiviral resistance in uninfected cells
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15
Q

What are interleukins, where produced and function

A

type of cytokine
Product of many cells
around 35 diff types

Pro (IL1) or Anti inflammatory (IL10)
Can cause:
- Cell division
- Cell differentiation
- Cell secretions

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16
Q

What are colony stimulating factors and what do they do

A

type of cytokine
Directs division and differentiation of bone marrow stem cells
- can have specific interleukins for specific leukocytes

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17
Q

What is tumour necrosis factor, where is it released and what does it do?

A

Type of cytokine
- TNF alpha and beta

  • released by macrophages
  • proinflammatory (especially TNF alpha)
  • mediate cytotoxicity
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18
Q

What are chemokines

A

Leukocyte cheoattractants

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19
Q

What is the innate system composed of

A

Physical and chemical barriers
Phagocytic cells
Blood proteins
- Complement

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20
Q

What happens during an inflammatory response to physical trauma

A

Coagulation
Leukocyte recruitment - acute inflammation
Kill pathogens
Clear dead cell
Prolifereation of cells to repair
Remodel extracellular matrix - remove clot

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21
Q

What is inflammation, what does it result from

A
  • series of reactions that brings cells and molecules of immune system to sites of infection and damage
  • can result from tissue damage and/or infection
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22
Q

What are the 3 key processes of inflammation and subsequent hallmarks of inflammation?

A

Increased blood supply
Increased vascular permeability
Increased leukocyte transendothelial migration (Extravasation)

Hallmarks of inflammation:
- red
- swelling
- heat

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23
Q

Which cells are associated with recognising non-self?

A

In blood:
- Monocytes
- Neutrophils

In tissues
- Macrophages
- Dendritic cells

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24
Q

What happens at sites of inflammation which results in extravasation occuring

A

Macrophage releases TNF when it needs help
- coats endothelial cells, makes them sticky

neutrophils roll on these sticky endothlelial cells
- when neutrophil hits chemokines present on endothelial surface it becomes activated
- firm attachment bonds form due to intergin
- chemokine gradient causes extravasation

  • helps macrophage
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25
Q

What occurs when sensing non-self

A

Pattern recognition receptors (PRRs) recognise Pathogen associated molecular patterns (PAMPs) on bacteria
- Lectin to recognise sugars, scavenger receptors for identifying lipids on bacteria

Multiple ways for leukocytes to bind to bacteria

Phagocytes engulf - Proteolytic degradation -
forms a phagolysosome
Some fragments of bacterial peptide gets combined with MHC to present the antigen on the phagocyte surface

Macrophages can take in around 50 microbes at a time

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26
Q

Why is adaptive immunity necessary?

A

Microbes can evade innate immunity
- Decoy proteins
- some bacteria can live within macrophages
* Intracellular viruses and bacteria can hide from innate immunity

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27
Q

What occurs in cell mediated immunity

A
  • Cells connect with each other to activate each other
  • Requires intimate cell contact
  • antigen presenting cells connect to T cells
  • T cells connect to B cells
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28
Q

What substance does cell-mediated immunity require

A

Major histocompatibilty complex (MHC)
- is the thing that allows cells to present antigens

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29
Q

Characteristics of MHC

A

Class I
- Intracellular antigen presentation (EG with viruses)
- Present in all cells
- Leads to activation of Cytotoxic T cells
* Kill infected cell

Class II
- Extracellular antigens
- Result from phagocytosis
- Only found on antigen presenting cells
- Leads to T helper cells
* Help B cells make antibodies to an extracellular pathogen

(class II are the ones you think of with typical antigen presentation after phagocytosis, class I is intracellular and helps activate cytotoxic t cells)

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30
Q

Process of cell mediated immunity

A

Phagocytic cells present antigens via the Major Histocompatibility complex (class II)

T cell receptors recognise and bind to the Major Histocompatibility complex, and the antigen it is associated with

Leads to:
- Division
- Differentiation
- Effector Functions
- Memory

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31
Q

Stages of T cell activation

A

Starts with naive t helper cells
- becomes activated

  • CD8 cells (when combined with MHCI/peptide) become Cytotoxic T cells (Tc)
  • these release perforins and granulysin and directly kill cells
  • CD4 cells:
  • in the presence of high levels of IL-12 - becomes Th1 helper cells
    ** makes macrophages more active and helps kill intracellular pathogens
  • at a modereate level of stimulation (by IL-12?) - becomes Th2 helper cells
    ** activates B cells
    ** Helps antibody production in humoral response
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32
Q

What is humoral immunity. Explain the process which occurs.

A

The immune response that occurs from the activation of B cells

Process of activation:
- B cells identify antigens via binding to their membrane-bound antibodies
- B cells present this antigen on MHC II
- Th2 cells (primed by binding to antigen-presenting cells) bind to B cells presenting the specific antigen
- Th2 secrete cytokines
- Triggers B cells to clonally expand and differentiate
- Differentiate into:
* Plasma cells
* B memory cells

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33
Q

What are characteristics of B cells

A

B cells express membrane-bound Immunoglobulin (IgM or IgD)

Each B cell can make 1 antibody type – specific to one epitope of an antigen (epitope is the specific site where the antibody can bind)

Born with all possible antibodies complementary to every possible epitope

Anti-self antibodies (antibodies that react to anything that is self) are killed during development

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34
Q

What is an epitope

A

The specific site on an antigen where an antibody can bind

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35
Q

What type of PRRs are there

A

Secreted and circulating PRRs
Cell associated PRRs (more traditional receptors)

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36
Q

What do PRRs (pattern recognition receptors) do

A

They recognise patterns that are typically associated with non-self

Examples:
- LPS (lipopolysaccharides)
- gram-positive/gram-negative bacteria
- dsRNA
- CpG motifs

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37
Q

Types of secreted and circulating PRRs

A
  • Antimicrobial peptides secreted in lining fluids, from
    epithelia, and phagocytes.
  • Defensins, cathelicidin
  • Lectins and collectins: carbohydrate-containing
    proteins that bind carbohydrates or lipids in microbe
    walls. Activate complement, improve phagocytosis.
    Surfactant is also involved
  • Mannose binding lectin (deficiency syndromes),
    surfactant proteins A and D
    E.g. Pentraxins. Proteins like CRP (non-specifc marker of infection - used to recognise clinically - has some antimicrobial action) can react with the C protein
    of pneumococci, activate complement, and
    promote phagocytosis.
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38
Q

Cell associated PRRs

A
  • Receptors that are present on the cell membrane
    or in the cytosol of the cells.
  • Recognise a broad range of molecular patterns
    TLRs are main family
    Activate proinflammatory pathway
    Interferon for dealing with viruses
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39
Q

Membrane bound PPRs

A
  • Family of receptors that may participate in
    pathogen recognition and particularly in pathogen
    phagocytosis, the C-type Lectin receptors
  • Mannose receptor on macrophages (fungi).
  • Dectin-1, Dectin-2. Widespread on phagocytes,
    helps recognise beta glucans in fungal walls.
    Scavenger receptors on macrophages (non-specific)
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40
Q

Examples of intracellular pathogens

A
  • Viruses multiply in the cytoplasm of cells
  • Bacteria such as Salmonella burst out from the
    phagolysosome and multiply in the cytoplasm of
    macrophages
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41
Q

What are giant cells

A

Large multinucleated cells formed by fusion of various cells like macrophages, epithelioid cells, monocytes etc.

Found at site of chronic inflammation/oother granulomatous conditions

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42
Q

Primary Lymphoid organs

A

Bone marrow - origin site

Thymus - T cell maturation site

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43
Q

Secondary lymphoid organs

A

Lymph nodes - site of dendritic cell, B and T-cell interactions

Spleen - removes RBCs and Ab-coated bacteria

Muscosal associated lymphoid tissues e.g. GUT ASSOCIATED LYMPHOD TISSUE (GALT) - has most plasma cells in body
* includes PAYER’S PATCHES

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44
Q

Tertiary lymphoid organs (TLOs)

A

Transient germinal centres

Usually ectopic lymph node-like structures formed during chronic infection, GvHD, autoimmunity.
- e.g. in MS, TLOs form in brain - produce anti-myelin antibody -> demyelination

45
Q

What occurs at lymph nodes

A

Dendritic cells enter via afferent lymphatics
- present Ag to naive CD4 cells in PARACORTEX.
-> become effector cells or memory cells
- cells exit via efferent

Site of interaction between innate and adaptive cells

46
Q

What do lymphoid follicles (like Peyer’s patches) mainly consist of

A

B cells

47
Q

Diff parts of the spleen and their function

A

Red pulp - mechanical filtration of RBCs

White pulp - active immune responses through humoral/cell-mediated.
* Primary follicle - rich in B cells
* Marginal zone
* Periateriolar lymphoid sheath (PALS) - rich in T cells

Also stores RBCs, lymphocytes etc - can be released in hypovolaemia/-oxia - and clear old plts from circulation

48
Q

Types of PRRs

A

Membrane bound
- Toll-like Receptors (TLRs)
- C-type Lectin Receptors (CLRs)

Cytoplasmic
- NOD-like receptors
- RIG-I-like receptors

49
Q

What are PRRs and what do they do

A

Germline encoded Pattern Recognition Receptors (evolutionary conservation)

Detects Pathogen-Associated Molecular Patterns (PAMPS) and Damage Associate Molecular Patterns (DAMPS)

50
Q

Types of TLRs

A

Typically:
- TLRs detecting genetic material are located on ENDOSOME WITHIN CELLS
- TLRs detecting other bacterial material - CELL SURFACE

TLR 5 - Five for Flagellin (flagellated bacteria)

** TLR 2 - detectes LIPOTEICHOIC ACID (peptidoglycan wall of gram +ve)
- Two for TB - DETECTS MYCOBACTERIA

** TLR 4 - LPS on G-ve

TLR 9 - Nine for Non-methylated CpG (cytosine-guanine) - found in bacterial/viral DNA
TLR 3/7/8 - viral RNA

51
Q

NOD 1/2 function

A

activate NF-kB pathway -> APOPTOSIS

activated via CARD domains on NODs

52
Q

Function of dendritic cell

A

Phagocytic

PROFESSIONAL ANTIGEN PRESENTING CELL (MHC II)
- can even CROSS-PRESENT

53
Q

Which chemokine receptor guides DCs to secondary lymph organs

A

CCR7

54
Q

Differences in function of Dendritic cells once mature

A

Increased Co-stimulatory molecules
INCREASED MHC II expression
INCREASED secretion of PRO-INFLAM CYTOKINES
INCREASED CCR7 expression

Increased Glycolysis

DECREASED PHAGOCYTIC capacity

55
Q

How do plasmacytoid dendritic cells repond to viral infection

A

Release IFN alpha and beta

56
Q

Which interleukin is particularly associated with acute inflammation

A

IL-8 - attracts Neutrophils!!

57
Q

Major components of neutrophil phagolysosme

A

ALPHA-DEFENSINS

LACTOFERRIN

58
Q

What is resp burst? What happens in resp burst

A

Killing mechanism of neutrophils (oxygen dependant)

  • Electrons pumped into phagolysosome by NADPH OXIDASE
  • Combine with O2 to make SUPRAOXIDE IONS
  • ions combine with PROTONS to make PEROXIDE (bacteriacidal)
  • peroxide can also be CHLORINATED by MYELOPEROXIDASE to make HYPOHALOUS ACID (bactericidal)
59
Q

Process of neutrophil extravasation

A
  1. E-selectin (an adhesion molecule on the capillary endothelium), is activated by IL-1 and TNF-α from damaged cells and binds to the glycoprotein CD15 on neutrophils in blood.
  2. This causes neutrophils in the blood to slow down and roll along the endothelium lining.
  3. ICAM-1 on endothelium (induced by LPS, IL-1, TNF-α) binds to integrin on neutrophil; the neutrophil stops.
  4. Diapedesis: neutrophil squeezes through endothelium (holes caused by C3a, C5a, chemokines, histamines, prostaglandins, leukotrienes (causing smooth muscle contractions in the bronchioles))
60
Q

How do eosinophils deal with parasitic infections

A

Release CATIONIC GRANULES (e.g. MAJOR BASIC PROTEIN)

Release ROS
(eicosanoids, leukotrienes, elastase among other molecules)

61
Q

Function of mast cells. Site. And relation to Ig?

A

Plays important role in ALLERGIC reactions + PARASITIC infections
- MAIN source of HISTAMINE

Found in MUCOSAL SURFACES

IgE binds to antigens and presents Fc region to activate mast cells

62
Q

What do activated mast cells release and what do those substances do

A

HISTAMINE
- increase VASC PERMIABILITY
- SMOOTH muscle CONTRACTION

Cytkines:
- !L4, IL13 - promotes Th2 DIFF and IgE PRODUCtion
- TNFa - TISSUE INFLAMMATION

Lipid Mediators
Leukotrines
PROSTAGLANDINS
- collectively -> vasc perm, SM contract, MUCUS secretion, are CHEMOATTRACTANTS

63
Q

What is required for cells to develop in into mast cells

A

Stem cell factor (a cyotkine + growth factor)

64
Q

What is Antibody-dependant Cellular Cytotoxicity. What occurs in ADCC?

A

Independant mechanism that does not require complement and uses only 1 CELL TYPE (typically NAT KILLER CELLS)

(Typically) IgG binds to SURFACE ANTIGENS on infected/cancerous cells (or VIRAL PROTEINS during VIRAL REPLICATION).

NK have CD16 Fc receptors and CROSS-LINK with antibody Fc region.
- triggers DEGRANULATION of LYTIC agents -> CELL APOPTOSIS

65
Q

What do NK cell lytic granules contain

A

PERFORIN and granzymes
- induce apoptosis + cell lysis

66
Q

How do NK cells differentiate between self and non-self

A

By PRESENCE of MHC 1
- CANCER cells typically DOWNREGULATE MHC 1

NK has INHIBITORY RECEPTORS activated by MHC I. If not enough MHC present - NK activate + try to kill cell

67
Q

What stimulates cytotoxic T cells to attack tumour cells

A

The cytokines produced by NK cells
(also specifically they kill cells with endogenous antigens)

68
Q

Which cells are professional antigen presenting cells

A

Macrophages
B-cells
Dendritic cells (most potent - go to 2ndry organs - aid adaptive response)

69
Q

What do professional APCs do

A

Present EXOGENOUS Ag in context of MHC-II
- processed in ER

70
Q

How are endogenous proteins presented? By which cells?

A

Present in CYTOSOL (e.g. viral/cancer-related)
- processed in ENDOSOMES

Presented in context of MHC I
- found in ALL CELLS (EXCEPT RBCs)

71
Q

How do dendritic cells activate Tc cells

A

CROSS-PRESENTATION
- present EXOGENOUS antigens on MHC 1

72
Q

What is an immune synapse

A

When immune cells bind together

73
Q

What 3 things are essential for a response to occur at an immune synapse

A
  1. Binding of PRIMARY RECEPTORS (e.g. MHC II to TCR on t cells)
  2. Binding of CO-STIMULATORY MOLECULES (e.g. CD80 to CTLA4 - don’t need to know name detail)
  3. A robust release of APPROPRIATE CYTOKINES
74
Q

What happens if MHC binding to another immune cell occurs without any other stimulation

A

ANERGY
- lack of response - form of PERIPHERAL TOLERENCE

75
Q

What is the identifying co-stim molecule for all T cells. What is its main function

A

CD3 (protein complex - 1 gamma, 1 theta, 2 epsilon chains - probs don’t need this much detail)

Intracellular signelling -> activates T cell

76
Q

What co-stim type cells do T cells initaly start as? What do they change to in the thymus?

A

Initially NAIVE CD4+CD8+ double pos cells (have both).

Undergo THYMIC EDUCATION so they only have EITHER one or the other.

Also undergo VDJ recombination (also does same for Fab regions on Ab) to determine which EPITOPE their TCR (t cell receptor) will recognise - super specific to a certain antigen

77
Q

Which antigens are an exception the very specific nature of TCRs

A

SUPERANTIGENS - bind to alpha/beta chains of any TCR
- activates ~20% of T cell population (big response)

78
Q

What is a naive lymphocytes

A

Never encountered antigen

79
Q

How can Naive and Memory T cells be differentiated

A

nAive - has CD45RA

memOry - has CD45RO

80
Q

\what is the general marker for T cell activation

A

CD25 expression

81
Q

What are the 2 mechanisms by which Tc (CD8+) cells kill

A
  1. PERFORIN and GRANZYMES
  2. express Fas LIGAND
    - binds to Fas on target cells -> activates CASPASE CASCADE -> APOPTOSIS
82
Q

Perforin

A

PORE forming CYTOLYTIC protein
- alows SALT + WATER to enter cells -> CELL LYSIS

83
Q

What are granzymes and what do they do?

A

Serine proteases
- CLEAVE CASPASE PROTEIN (CPP-32)
-> ACTIVATE a NUCLEASE (CAD)
-> initiates DNA DEGRADATION + APOPTOSIS

84
Q

Th1 vs Th2

A

Th1 CELL-MEDIATED; Th2 HUMORAL

Th1 regulate MONOCYTES/MACROPHAGES, Tc, NK
- eliminate cellular antigens
Th2 regulate EOSINOPHILS, BASOPHILS, MAST CELLS, B CELLS
- increased IgE and IgG

they are ANTAGONISTIC to each other - T CELL POLARISATION

85
Q

Types of T helper cells (CD4+)

A

Treg (regulatory cells)

Th17

86
Q

Treg vs Th17 cells

A

Treg - PERIPHERAL IMMUNE TOLERANCE; Th17 - MUCOSAL MEMBRANE (stimulates INFLAMMATION)

Treg - principle cytokine = IL10 (mass ANTI-INFLAM action)
Th17 - IL17 (induces INNATE cells to make IL8 -> stimulates NEUTROPHIL production/recruitment)

87
Q

Which cytokine maintains Th17 populations

A

IL-23 (target for biologics)

88
Q

How can B cells be activated? What kind of response does each produce?

A
  1. Th2 cells - produce LONG-LIVED plasma cells
    • typically make IgG, E or A+
  2. Can be activated directly by ANTIGEN in absence of T cell help
    - makes SHORT-LIVED plasma cells (+ response)
    • typically these plasma cells have LESS AFFINITY and produce IgM
89
Q

What are the marker and the co-stimulatory molecule associated with mature B cells

A

Marker - CD20

Co-stim - CD19

90
Q

What processes do B cells undergo upon activation and where does activation occur

A

SOMATIC HYPERMUTATION and AFFINITY SELECTION (aided by dendritic + t cells)
- mainly in CORTEX OF LYMPH NODES

91
Q

What occurs in somatic hypermutation and affinity selection

A

somatic hypermutation:
- activation-induced cysteine deaminase (AID) introduces RANDOM MUTATIONS in Fab Ab region gene

Affinity selection:
- Dendritic cells present same antigen (testing AVIDITY)
- less avidity - neg selected
- greater avidity = Positively selected -> undergo CLASS SWITCHING and clonal proliferation

92
Q

What happens when B cells are activated in lymphoid follicles

A

They develop into germinal centres

93
Q

Where does complement bind during opsonisation

A

Fc region of antibody

94
Q

Which antibodies are in colostrum

A

IgA, M and G - but IgA is principle

95
Q

Which cell type raised in bacterial infection

A

Neutrophils
(esp if pyogenic)

96
Q

Which cell type raised in viral infections

A

Lymphoctes

(also raised in intracellular bacterial infections e.g. TB and some protozoa e.g. Toxoplasma)

97
Q

Define hypersensitivity

A

Undesirable response to antigenic, allergenic or self material.

This requires a pre-sensitized state of the host

98
Q

Types of hypersensitivity reactions

A

Type 1 - Anaphylactic

Type 2 - Cell bound

Type 3 - Immune complex

Type 4 - Delayed Hypersensitivity

Type 5 - Ab interferes with ligand binding (uncommon)

99
Q

Type 1 hypersensitivity reaction

A

FAST - within minuites

CROSS-LINKING of ANTIGEN to IgE on MAST CELLS + BASOPHILS
-> massive DEGRANULATION -> massive HISTAMINE RELEASE
** IL4 - KEY CYTOKINE - causes class switching to IgE, Th2 Polerisation

ANAPHYLAXIS + ATOPY (asthma, eczema)

100
Q

Type 2 hypersensitivity reaction

A

IgG/IgM binds to SELF ANTIGEN
-> CELL DESTRUCTION by membrane attack complex + cell mechanisma

AUTOIMMUNE

101
Q

Type 3 hypersensitivity reaction

A

IgG BINDS SOLUBLE ANTIGEN (free antigen + antibody combine) -> circulating IMMUNE COMPLEX

  • DEPOSIT in vessel walls esp in KIDNEYS
    -> inflam response
  • RBCs with COMPLEMENT RECEPTOR 1 bind to complement coated immune complexes and transport them to the liver and spleen for phagocytosis.

E.g.
- SLE
- post-strp glomerular nephritis

102
Q

Type 4 hypersensitivity reaction

A

Th1 mediated - ACTIVATED BY APCs
-> forms memory T cells
-> when reactivated -> activate macrophages
-> tissue damage

E.g.
- TB
- GvHD
-MS
- Guillain-Barre syndrome

103
Q

Type 5 hypersesitivity reaction

A

IgM/IgG bind to CELL SURFACE RECEPTORS
-> BLOCKS or STIMULATES ENDOGENOUS LIGAND BINDING

e.g.
- Graves
- Myasthenia gravis

104
Q

Main ways autoimmunity can develop

A
  • Incorrect THYMIC education
  • Tregs
  • CD4 activation against AUTOANTIGEN
105
Q

Features of autoimmunity

A
  • Often relapsing-remitting
  • Organ-specific vs Systemic
  • Damage to or destruction of tissues
  • Altered organ growth/function
  • Generation of autoantibodies
106
Q

What is the defining factor for developing AIDS

A

< 200 cells/uL of CD4 cells

107
Q

Which cytokine is the main activator of macrophages

A

IFN gamma

108
Q

What triggers classical complement pathway

A

Antibodies

109
Q

What triggers lectin pathway of complement system

A

when MANNOSE BINDING LECTIN (MBL - a protein which binds mannose sugars on pathogen surfaces) binds to mannose on bacteria

triggers cascade response

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