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BII > Roger Booth > Flashcards

Roger Booth Flashcards

1
Q

What is the disease called when you don’t have T cells?

A

Severe combined immunodeficiency (SCID)

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2
Q

Recurrent infections with extracellular bacteria indicate what type of immundeficiency?

A

IgM and IgG, complement or pgagocytosis

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3
Q

Recurrent infections with intracellular bacteria indicate what type of immundeficiency?

A

T cells and macrophages

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4
Q

Recurrent infections with viruses indicate what type of immundeficiency?

A

T cell, IgG, IgA, IFN

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5
Q

Recurrent infections with paracites indicate what type of immundeficiency?

A

IgE, eosinophils, mast cells, T cells

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6
Q

When will congenital immunodeficiencies be recognised in new borns?

A

After 4 months when the transferred immunity from the mother decreases.

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7
Q

What do Th1, Th2 and Th17 cells do?

A

Th1 - IgG and IgM, cytotoxic T cells, acute viral and bacterial infections.

Th2 - IgG and IgE, mucisal immunity, chronic infections, especially paracites

Th17 - mucosal immunity and promote inflammatory response

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8
Q

What is the outcome from the modern environment relative to the primitive environment?

A

Less expose to antigens means less ability to control pathogens -> less Treg stimulation and more inflammation -? allergies and hypersensitivities

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9
Q

How does the immune system interact with the autonomic nervous system?

A

Nerves of the ANS can innervate the secondary lymphoid organs which can control lymphocyte activation and downstream responses.

Hormones of the endocrine system also can interfere with T cells, B cells and APCs

Cytokines of the immune cell also influences the nervous system.

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10
Q

What cytokines can influence the nervous system and what do they do?

A

IL-1, IL-6 and TNF -

Fever, - IL-1
Sleep wake cycles -
Promote illness behaviors

IL-1 acts on the vagus nerve branches, can be secreted by astrocytes and glial cells
IL-1 has neurotransmitter activity.

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11
Q

What do sympathetic nerves do in the lymph node?

A

The sympathetic NS branches into the paracortical region where T cells are and release norepinephrine that communicates with T cells

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12
Q

What are the most common bacteria that contaminate devices and what features allow them to do that?

A

Staphylococcis epidermis
Staphylococcus aureus
Escherichia Coli

Adhesive proteins (MSCRAMMS)
Polysaccharide intercellular adhesion (PIA)
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13
Q

What factors favor bacterial adhesion to devices?

A

Duration that it’s in.
What the device is made of
How often the device is used
Surface of the device (smooth or irregular)

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14
Q

What is myasthenia gravis?

A

An autoimmune condition where antibodies bind to and remove acetylcholine recpetors from postsynaptic receptors. Causes ptosis and diplopia

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15
Q

What receptors promote phagocytosis?

A

PAMP receptors - weak but common
Fc region of antibodies
C3b of complement

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16
Q

What are specific PAMPS?

A

Danger signals

Cell wall components - - LPS and peptidoglycans

Bacterial metabolic products

Heat shock proteins - released by stressed cells

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17
Q

What are acute phase proteins?

A

Stimulated by inflammation - in the blood
Released in the acute phase
Involved in complement and activation the adaptive immune response
Come from liver

Promote resolution and repair of lesions
Limit tissue injury

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18
Q

What does complement do?

A

Vascular permeability
Opsonisation - C3b
MAC formation
Chemotaxis - C5a

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19
Q

What are the MHC I and II subtypes and structures?

A

MHC I: HLA-DP, DQ and DR
MHC II - HLA-A, B and C

MHC I: alpha and beta subunits
MHC II: Alpha subunit and B2 microblobulin

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20
Q

What happens to people who have deficiences in TAP proteins?

A

Low HLA-A, B and C expression. Can’t generate CD8 T cell responses. Few CD8 T cells
- have poor immunity against viruses. Recurent URTIs

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21
Q

What are the different selectins?

A

For slowing immune cells in the blood.

L-selecting - lymphocytes

P-selectin - platelets

E-selectin - leukocytes ( induced by IL-1 and TNF-alpha

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22
Q

What are the receptors involved in lymphocyte activation?

A

I-CAM-3 on the APC to LFA-1
TCR to MHC
CD4 0r CD8 to MHC
Checkpoint molecules

CD40L on CD4 T cells and CD40 on B cells

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23
Q

What are the function of IFN-alpha, beta and gamma?

A

They inhibit vital infections - interfere with viral replication.

Virus infected cells release IFNs which stimulate non-infected cells to cause them to change which prevents them from being infected

IFNs also stimulate natural killer cells to kill virus infected cells

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24
Q

What are the different classes of cytokines and what do they do?

A

1 .Innate cytokines - wound healing and immune stimulating

  1. Adaptive cytokines - lymphocyte stimulation
  2. Chemokines - recruit
  3. CFU - stimulate cell development
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25
Q

What are the regions of an antibody?

A

Conserved region and variable region. Light and heavy chains

CH2 - complement -binding region
CH3 - Fc region

26
Q

How do you treat a B cell deficiency in an infant (no antibodies)

A

Transfer serum

Bone marrow transplant

27
Q

What to Abs do?

A

Neutralisation: preventing attachment and entry of bacteria and toxins, immobilising bacterial flagella

Agglutination - clumping to assist phagocytosis (IgM) - depends of ratio of antigen to antibody

Opsonisation - Fc region

Activating complement - C5b -> MAC. C3a - > vascular permeability and chemotaxis (C5a too). C3b -> opsonisation. C5a ->

ADCC - NK cells and K lymphocytes

28
Q

What are the classical and alternative pathways for complement activation?

A

Classical: antigen-antibody complexes
Alternative pathway - pathogen surfaces
Different proteins - both cleave C3

29
Q

What are the differences between the antibodies?

A

IgM - pentimer, initial ab produced. Confined to circulation (too large) - 10% of AB pool. Good at agglutination and complement activation. Important defence against blood-borne infections such as bacteria.

IgG -small can gets out of the blood easy (extra vascular space). 70% of ABs. Good at neutrilisation, complement activation, and at enhancing phagocytosis, effective against viruses, also bacteria. Cross placenta.

IgA- Dimer. 15% of blood antibodies. Produced by mucosal immune system into seromucus to protect those surgaces, particularly in the gut and lungs.

IgD: small amounts - surface molecules on B cells (is a receptor)

IgE - small amounts - Binds to mast cells - paracytic and allergies

30
Q

How can CD8 T cells induce apoptosis and necrosis separately?

A

Apoptosis - production of TNF-alpha, and IFN-gamma

Necrosis - perforin and granzyme

31
Q

What antibodies does a mature B cell express?

A

IgM and IgD

32
Q

How is a antibody variable region created?

A

There are multiple Vh, Dh, Jh exons that recombine to create the variable region. Also a constant region.

Recombination is independent of antigen.

which happens once a cells has committed to become a B cell. Transcribed into RNA for VDJ and C.

Light chain is only V, J and C.

This recombination creates wide variation.

One way process. One Vh and Vl region per receptor. All constant regions are present initially.Mew is the first constant region which codes for the IgM antibody.

Convert from IgM to IgG by cutting out the constant regions. Retain V, D, J

33
Q

How does tolerance of B cell receptors occur?

A

Central tolerance.
Once variable region is developed. The cells is presented with self antigens that if the b cell binds it with high affinity it will be deleted.

Also peripheral tolerance - no costimulation

34
Q

How are T cell receptors created?

A

alpha and beta chains
Valpha, J alpha and C alpha

Vbeta, D beta, J beta and C beta (mixed in order). Random rearrangement.

Flow of differentiation is from the cortex to the medulla of the thymus.

35
Q

How is T cell tolerance conducted.

A

alpha beta receptor developed.
Expresses both CD4 and CD8
Positive selection - can it recodnise MHC I or MHC II. Does Cd4 or CD8 bind. No recondition = death. (positive = keep; selection = binding)

Down regulate either CD4 or CD8 depending on what binds.

Negative selection: tested against some self peptides. Strong binding = remove. (negative = remove; selection = binding).

CD3 then expressed and T cell is exported.

Peripheral tolerance.

36
Q

What type of pathogen are antibodies most effective against?

A

Bacteria

37
Q

What happens in mucosal immuntiy?

A

Pathogen gets through the serum IgA that is in the mucosal tissues and then to the mast cells with the IgG expression. This triggers the release of granules that vasodilation and recruitment, complement products etc.

38
Q

What are the function of NK cells?

A

They have Fcreceptor binding of antibodies that allow them to do ADCC.

They have killeractivator and killer inhibitor receptors.

Activity enhanced by IL-2 and IFN-y. Are an early response, prior to T cell response.

39
Q

What is the order of immune response to a virus?

A

Virus: infected cells release IFN that reduces spread (also stimulate NK cells).

If down regulation of HLA then NK killing

Then CD8 T cells

Antibodies to prevent reinfection

40
Q

What are the functions of proinflammatory cytokines?

A

Induce acute phase proteins
Fever and behavioural changes
Tissue repair
Acivate T and B cells

41
Q

What is the function of IFNs?

A

Induce transient anti-viral state
Activate NK cells
Upregulate MHC expression

42
Q

What sort of vaccine uses T cells?

A

Protein antigens generate T cell dependent antibodies

Polysaccharide antigens - T cell independent antibodies

Live vaccines - antibodies and CD8 T cells

43
Q

What are the different types of antibodies?

A

Live attenuated vaccines - good memory development

Inactivated vaccines -
a) whole pathogen
b) protein-based vaccines - toxoids
Polysaccharide based vaccines - cell wall from bacteria
Conjugate vaccines
44
Q

Who is at risk with live attenuated vaccines?

A

Immunocompromised people - this places babies at risk because you don’t know if they will be immunocompromised until the mothers antibodies have gone

45
Q

What are the type of inactivated vaccines?

A

Killed whole pathogen

Component vaccine (subunit) - subunits or toxoids

46
Q

What are some component antigen vaccines?

A

Diptheria, tentus, hep B, pertussis, polio, haemophilus influenzae type B

47
Q

What is tetanus?

A

Clostridium tetani - an anaerobic spore forming gram-positive bacillis, penicillin-sensitive.

Spores everywhere -

symptoms 10 days after exposure - muscle rigidity - arching back, lock jaw

48
Q

Who is most at risk of tenanus?

A

Infants - neonatal tetanus - entry via the umbilicus of an unvaccinated mother.
Mortality (>90%)

Give all mothers of child bearing age the vaccine 3 doses.

49
Q

What are the disadvantages of passive immunity?

A

No long term protection
Risk of transmission disease
Expensive and poor access
Serum sickness

50
Q

What are the features of bordetella pertussis?

A

Gram negative bacilli

Highly contagious - sneeze or cough

Catarrhal phase - runny nose, conjunctival, malase (1-2 weeks)

Bad cough (1-10 weeks)

51
Q

What is the treatment for bordetella pertussis?

A

Erythromycin (macrolide)

May shorten illness - decrease infectivity

Was a whole cell killed vaccine but now component vaccine vaccine containing a number of virulence factors - many don’t get 3rd dose. Old people resivour for disease.

52
Q

What is polio?

A

A disease caused from poliovirus that destroys lower motor neurons resulting in paralysis

Was a live attenuated oral vaccine -intestinal immunity

Now component vaccine -

53
Q

What type of vaccine is the tetnus vaccine?

A

Vaccine against the tetanus toxoid.

54
Q

What are the four hypersensitivity reactions?

A

Type I: IgE-mediated mast cell response

Type 2: IgG mediated cell cytotoxicity (ADCC) of coated cell, and complement induction

Type 3: IgG immune complex formation resulting in complement

Type 4: delayed type hypersensitivity - activation of CD4 T cells -> macrophage activation

55
Q

Type I hypersensitivity?

A

Mast cells have Fc episolon receptors that bind IgE. When stimuilated they release granules containing chemoattractants, vasodilators, complement and platelet activation, smooth muscle contraction, mucus secretion

Rhinitis - house dust mite
pollens
animal dander

Insect stings

Food allergies

Drugs

56
Q

What are the common sites for allergies to occur?

A 
Respiratory tract:
Sinusitis
Conjunctivitis
Asthma
Rhinitis

Skin
Urticaria
Angioedema

Food allergy
Gut

Multiple organs

57
Q

Type II hypersensitivity?

A

An antibody binds to a cell surface antigen and activates K lymphocytes or complement. Frustrated phagocytosis

Haemolytic disease of the newborn

58
Q

Type III hypersensitivity?

A

Soluble antigens: dependent of ratio.

Localise in capillaries - complement mediated damage -> kidneys, skin

Immune complex-induced vasculitis and nephritis

59
Q

Type IV:

A

Delayed type hypersensitivity

CD4 T cell activation

Contact sensitivity.

Antigen uptake - CD4 activation - recruit more cells - macrophage activation

Nickle ions - bind to a hapten (carrier protein)

60
Q

What is the organ specific hypersensitivity and the systemic?

A

Type II and type III

61
Q

What is an example of a type III hypersensitivity disease?

A

Sytstemic lupus erythematosis

Rheumatoid arthritis

62
Q

What are the treatments of autoimmune diseases?

A

Replacement - insulin

Suppression -

BII (14 decks)

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