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immune Flashcards

1
Q

non-living vaccines

A

– Whole dead organisms
– Many bacterial examples, known as KILLED
vaccines; some viral examples known as
INACTIVATED vaccines
– or TOXOIDS,
– or antigenic fragments: SUB-UNIT vaccines,
– or CONJUGATES - an antigen covalently carrier-linked
for increased immunogenicity

Is protection needed to kill the organism
itself, or against a toxin it secretes?

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2
Q

toxoid vaccines

A

is a toxin after modification to render it harmless but still immunogenic

Eg.

  1. Diphteria
  2. Tetanus

pathology of both due to secreted toxins

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3
Q

adjuvant vaccines

A

Immunogenicity of some vaccines is
improved with an ADJUVANT - a non
specific stimulator of immune
recognition

Probably important in engaging Toll-Like Receptors on APC
• Two types currently used:
– pertussis organisms
– Aluminium compounds eg Al(OH)3 gel

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4
Q

attenuated vaccine

A

means non-pathogenic, but still capable of limited multiplication and colonization
– Attenuation - these days, may be
genetically engineered by knocking out genes

– eg Aro mutants of Salmonella (typhoid, etc.)
– May occur after repeated growth in culture; historically an important approach
– eg BCG (for TB); Mycobacteria,
stands for bacille Calmette-Guerin

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5
Q

important examples of live vaccines

A

Important bacterial example:
– BCG for tuberculosis
• Important viral examples:
– OPV Oral Polio Vaccine
– MMR Measles, Mumps and Rubella

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6
Q

How vaccines are seen by the immune system:

NON-LIVING

A

A non-living vaccine will be processed by APCs
and antigen epitopes will be

presented in class II MHC molecules

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7
Q

how vaccines are seen by immune system

Live attenuated

A

A live attenuated virus vaccine or live attenuated
intracellular bacterial vaccine will ALSO result in
cass I MHC presentation - on the INFECTED
HOST CELLSURFACE of cells which are
colonised

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8
Q

risks from live attenuated vaccines

A

risk for:

  • a patient with an impaired immune system
  • includes treatment for malignancy as well as those on immunosuppressives or with known immunodeficiency disease
  • – or a foetus

• may be dangerously pathogenic in them causing
virulent infection.

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9
Q

routinely used vaccines

A
  • Dip and Tet are toxoids, with alum
  • • aP: acellular Pertussis. Pert is currently whole dead cells, and also adjuvates Dip and Tet
  • • IPV inactivated polio virus*
  • • Hib and MenC are conjugates of coat carbohydrate on carriers
  • • MMR - all attenuated virus
  • • BCG - attenuated mycobacteria
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10
Q

CD4

A

A cell surface molecule:
• characteristic of one of the major subsets of T
cells, also known as Helper T cells (TH)
• also expressed on dendritic cells (DC) and
macrophages – DC probably usual portal of
entry for HIV infection
• CD4 stabilises a TH cell’s interaction withMHC
• specific for MHC Class II
• internally it recruits signalling molecules

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11
Q

in HIV, The numbers of CD4+ cells are depleted by:

A
  • direct cytopathicity of virus
  • killing by specific cytotoxic CD8+ cells
  • Memory pool particularly depleted
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12
Q

common non-pathogen causes of acquired
(i.e. secondary) immunodeficiency

A

_Nutrition: malnutrition (w_orld wide this is a very
common cause of immunodeficiency) or
malabsorption / protein loss

• Physiological “gap”: Bottle fed babies x60 more
pneumonia in 1st quarter than breast fed

• Malignancies
– eg: chronic lymphocytic leukemia, myeloma.
such patients suffer 5-10 times number of infections in agematched controls
• Aging
– T cell production falls away
• Drugs - iatrogenic
– Deliberately immunosuppressive – eg for transplant, or treating autoimmune disease
– corticosteroids
– Others – eg anti-convulsants for epilepsy
• Stress
– eg bereavement, or excessive “training”, as in Infectious mononucleosis (“glandular fever” EBV infection) in athletes
• Splenectomy
– eg post RTA trauma - Pneumococcal disease !

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13
Q

M. tuberculosis – the “life cycle”

A

• Bacilli are expectorated by patients with active TB
– Inhaled by susceptible persons
– Bacillary replication in lung macrophages
• Induction of a pathogen‐specific immune response
– Contains bacillary replication (dormancy)
• Results in latent infection
• Fails to eradicate the bacilli
• Reactivation of latent infection
– Bacillary replication
– Cavitory lung disease
– Expectoration of bacilli

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14
Q

TB primary infection

A

– Phagocytosis of M. tuberculosis
• Failure of innate immunity to control MTB replication
– Generation of cell mediated immunity
• Control of MTB replication within granulomas (95%)

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15
Q

TB clinical latency

A

– Control of MTB within granulomas
• Immunological evidence of MTB infection (skin test)

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16
Q

reactivation

A

– Loss of control of the infection
• MTB replication, tissue destruction, cavitation
– Expectoration of bacilli

17
Q

Primary TB stages

A

HOST

  • Phagocytosis of bacilli by lung macrophages
  • Transformation of phagocytes into antigen‐presenting cells
  • Migration of antigen‐presenting cells to the regional lymph nodes
  • Generation of MTB‐specific T‐lymphocytes
  • Recruitment of MTB‐specific T‐cells to the site of infection
  • Activation of MTB‐infected phagocytes by these T‐cells
  • Formation of granulomas
18
Q

TB innate immune response

A

Phagocytosis by macrophages

• Recognition by Toll‐like receptors (TLR‐2, TLR‐4)

19
Q

TB adaptive immune response

A

Generation of MTB‐specific T lymphocytes
Dendritic Cells (DC)
– Transformation from immature DC (phagocytes) to mature DC (antigen‐presenting cells)

– Production of Immune Regulatory Cytokines
• Immune stimulatory (TH1): Tumor necrosis factor‐alpha (TNF‐α), Interleukin‐12 (IL‐12)
• Immune inhibitory: IL‐10

20
Q

Generation of MTB‐specific T‐Lymphocytes

A

Immunological synaps:

• A_ntigen‐presenting cell (DC):_
– Antigen presenting molecules (MHC,CD1)
– Co‐stimulatory molecules (CD40, CD80, CD86, ICAM‐1)
– TH1 Cytokines (IL‐12, TNF‐α)

• Naïve T‐Lymphocytes:
– Receptors for:
• Antigen recognition (T‐cell receptor)
• Co‐stimulatory molecules (CD40L, CD28,
CTLA‐4, LFA‐1)
• Cytokines (IL‐12 receptor)

21
Q

M. Tuberculosis specific T‐cells

A 
_**Different lymphocyte subsets**:_
 • **CD4+ T**‐cells (**MHC class II‐restricted**)
 – _Most important mediators of host resistance to MTB_
*• **CD8+ T‐cells** (MHC class I / CD1‐restricted)*
 • **CD4‐CD8‐ T‐cells** (“double negative” T‐cells)
**• gamma delta T‐cel**l receptor‐expressing lymphocytes

Actions:
• Macrophage activation (MTB inhibition)
– Production of TNF-alpha and IFN‐gamma

• Destruction of MTB infected macrophages
– Apoptosis (FAS mediated)
– Necrosis (perforin, granzymes, granulysin)

22
Q

Activation of macrophages in TB

A

Activation of macrophages by IFN‐gamma and TNF-alpha

– Induction of inducible nitric oxide synthase (iNOS)
• Generation of reactive nitrogen intermediates (RNI) such as nitric oxide
(NO), NO2 ‐, and HNO2

23
Q

latent TB

A

• Persistent cytokine activation of infected macrophages and T‐cell mediated immunity are important in the control of latent/chronic MTB infection

– In mice
• Treatment directed against TNF‐alpha, IFN‐gamma, NOS2 or CD4 T‐cells results in worsening of chronic stable TB

– In man
• MTB‐specific CD4+/CD8+/CD4‐CD8‐ T‐cells are present in peripheral blood of PPD‐positive persons and household contacts of TB patients
• Immune suppression with glucocorticosteroids or TNF‐alpha neutralizing mAbs, solid organ transplantation and HIV‐induced CD4+T‐cell depletion are associated with increased rates of reactivation of latent MTB infection

24
Q

reactivation (post-primary) TB

A

Host Susceptibility to TB
• Genetic polymorphisms (may be population specific)
– Defects in the IL‐12/IFN‐γ pathway confer susceptibility to atypical mycobacterial (and salmonella) infections

– NRAMP1 (SLC11A1; encoding a phago‐lysosome membrane protein), Vitamin D receptor, HLA class II, IFN‐γ, IL‐12RB1, IL‐8 associated with susceptibility to TB

• Non‐genetic (“environmental”) factors
– Nutritional status, age‐related immune impairment, immune suppressants, diabetes mellitus
Virulence of the M. tuberculosis strain

25
Q

generally, CD8 cells

A

cytotoxic lymphocytes

Kill target cells with proteins in lytic granules (perforin, granzymes, granulysin)

important in viral, intra-cellular pathogens, tumour respons

produce IL-2 =>it stimulates CD8 Tcell proliferation, differentiation

CD4 Th1 cells help CTLs, by IL-2, INFgamma

26
Q

what is necessary to activate naive T cells?

A

interaction of MHC with TCR is insufficient ot activate naive cells

signal 2 (co-stimualtory melecules) are required to activate T cells +> stimulate T cell rpoliferation

slignal 3 (different cytokynes) regulate T cell differentiation

27
Q

generally CD4 Th1

A
  1. help other immune factors
  2. activate, regualte macrophages, CTL
  3. produce INFgamma, IL-2, CCL2
  4. target INTRACELLULAR pathogens mainly
  5. induces macrophage differentiation in bone marrow
  6. activates endothelium to bind macrophages
28
Q

generally CD Th2

A

stimulate B cells to produce antibody

DO NOT activate macrophages

produce IL-2, IL-4 (important for B cells), IL-5, IL-13

Target: extracellular pathogens, toxins

29
Q

IgG

A

main antibody

good at osponisation for NK cells

4 subclasses

30
Q

IgA

A

mucosal, breast milK

forms dimers in gut to protect from enzyme degradation

monomeric in plasma

2 subtypes

31
Q

IgE

A

parasitic infections

binds mast cell via Fc region (without antigen) =>causes degranualtion => release of histamine

Increased in allergies

32
Q

IgM

A

pentamer

10 binding sites

high AVIDITY

default Ig that B cells start with in developmenet

pentamers too large to diffuse through placenta or into tissues

present during active response first

v. efficient at activating somplement through CLASSICAL pathway

33
Q

killing mechanism in neutrophils

A

reactive oxygen intermediates

Respiratory burst after phagocytosis => Increased O2 uptake

O2 reduced by NADPHoxidase to form HYDROXYL radicals, hypochlorite

Causes DNA damage, alterations in bacterial membrane

34
Q

killing mechanisms in macrophages

A

L-arginine + O2 => L-citrulline + NO radicals (catalysed by inducible NO synthase <= induced by cytokines, bacterial componenets)

Causes DNA damage, membrane damage

35
Q

major components of the cell walls of Gram-positive bacteria and are recognized by

A

peptidoglycans

TLR2

36
Q

major constituent of the outer cell membrane of Gram-negative bacteria and recognised by

A

lipopolysaccharide LPS

TLR4 < molecules on monocytes,
macrophages, dendritic cells, mast cells, and intestinal epithelial cells bear toll-like receptor 4

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