immunity Flashcards
what are is innate immunity?
innate - non-specific and no memory
what are the 2 types of acquired/activated immunity?
- specific and memory
- b and t lymphocyte
active
passive
what is active immunity?
natural - infection/ exposure
artificial - immunisation/ vaccines
antigen stimulates immune response
long term immunity
immunological memory
no immediate effect, faster and better response to the next antigenic encounter
what is passive immunity? give advantages and disadvantages
Natural → Placental transfer of IgG & Colostral transfer of IgA
Artificial → Immunoglobulin therapy or Immune cells
Advantages
- immediate protection
- quick fix
Disadvantages
Short-term effect – no immunological memory
Serum sickness – incoming antibody is recognised as a foreign antigen by the recipient
->anaphylaxis
Graft Versus Host Disease (cell grafts only) – incoming immune cells reject the recipient
e.g. donated bone marrow or peripheral blood stem cells attack the recipient
give an example of natural passive immunity
Maternal immunoglobulins (IgG)
transferred to the foetus/ neonate naturally using a specialised mechanism involving the neonatal Fc receptor
Transfer of antibodies from maternal blood into the fetal circulation
give an example of artificial passive immunity
Snake or spider bites, scorpion or fish stings
- Passive infusion of antibody specific to the toxin
Hypogammaglobulinaemia – primary or secondary
- Infusion of g-globulins to reduce infection
Specific Rabies Immunoglobulin
- given “Post-exposure prophylaxis” together with vaccination
what is a vaccination?
administration of antigenic material to develop adaptive immunity to a pathogen
what are the 4 types of vaccines?
1 - inactivated killed whole organism
2- live attenuated whole organism
3- subunit
4- toxoid
describe the functions of killed whole vaccines, give an example:
target organism e.g. polio
effective and easily manufacture
booster shots
describe live attenuated vaccines, and give examples:
mainly viruses
→ An avirulent strain of the target organism is isolated
more powerful and better than killing the whole organism
simulate natural infection
problems → may revert back to a virulent form
refrigeration required
e.g. TB, measles, rotavirus, oral polio, yellow fever
what are subunit vaccines? give advantages and disadvantages
Recombinant proteins
Advantages:
safe & easy to standardise
Disadvantages:
Not very immunogenic without an effective adjuvant
Need to understand how to generate immunity
Examples:
Hepatitis B surface antigen (HBsAg)
Human papillomavirus (HPV) proteins
what is an adjuvant?
pharmacological/ immunological agent that improves the immune response of a vaccine
what is a toxoid vaccine (modified)?
A toxin is treated with formalin → Toxoid (inactivated toxin)
retains antigenicity
no toxic activity
induces immunity against the toxin, not the organism that produces it.
e.g. tetanus, diphtheria
What vaccines are needed to give to travellers?
hepatitis a
typhoid
neisseria meningitidis
cholera
yellow fever
Japanese and tick-borne encephalitis
rabies
describe the immunisation schedule for children
non-routine at birth:
TB
Hepatitis B - children with positive mum
2,3,4,12 months, 3 years, 13-18 years
- polio, strep.pneumonia, rotavirus, tetanus, diphtheria, pertussis, Haemophilus influenza b, Neisseria meningitidis c
12/13 months + >3years - measles, mumps, rubella
2/3/4 - influenza
12 years - human papillomavirus (females)
what are some temporary contraindications?
febrile illness
pregnancy (temporarily immunocompromised)
what are some permanent contraindications?
allergy
immunocompromised - can’t be given live attenuated vaccines, may develop disease
what is herd immunity?
resistance to the spread of an infectious disease within a population that’s based on the pre-existing immunity of a high proportion of individuals (90-95% coverage as a result of previous infection or vaccination.
The primary aim of vaccination - protect the individual who receives the vaccination
→ Vaccinated individuals are less likely to be a source of infection to others
→ Reduces the risk of unvaccinated individuals being exposed to infection
what makes a good vaccine?
Potent antibody IgG response – high antibody titer
Potent CD8+ cytotoxic T-cell response
CD4+ T helper response
Memory
Why do we need T-cell responses against infections?
CD4+ T cells drive B cells to produce more antibodies → to generate a potent antibody response
Diseases e.g.
Tuberculosis (BCG) vaccine generates a CD4+ T helper cell response to destroy Mycobacterium tuberculosis
what are 5 challenges when facing vaccines?
Cannot elicit immunity against all infectious disease
Persistence
* Generation of memory cells → antibodies against specific pathogen
Protection of vulnerable groups (young & old & immunocompromised)
Antigenic shift and drift, and strain diversity.
The cold chain network
what is type l hypersensitivity? what are the effects?
antibody-mediated
immediate phase (minutes)
- allergen introduction stimulates TH2 reactions and IgE production
IgE binds to Fc-epsilon-RI on mast cells
mast cell activation and mediator release
effects: Vasodilation, oedema and vascular congestion …etc.
late phase (hours)
Eosinophil, neutrophil and T cell infiltration
what is the role of mast cells?
Mast cells release granules that contain Histamine and lipid mediators
usually released against helminth parasites.
what is atopy?
genetic tendency to develop allergic diseases
e.g.
allergic rhinitis, asthma and atopic dermatitis (eczema).
associated with heightened immune responses to common inhaled or food allergens
Predisposition to allergy - the tendency to overproduce IgE to harmless environmental substances.
what is type ll hypersensitivity?
Injury caused by anti-tissue antibody
Antibody (IgG) in extracellular matrix interacts with leukocytes (neutrophils & macrophages)
cause tissue injury and proinflammatory immune response.
Depends on specificity → Antibodies recognise antigens in tissue.
what are some examples of diseases caused by type ll hypersensitivity?
acute rheumatic fever
graves disease - hyperthyroidism
insulin-resistant diabetes
what is type lll hypersensitivity?
Immune complex-mediated tissue injury
Immune complexes of antibodies and antigens formed in circulation and deposited in blood vessels and other sites.
These immune complexes induce vascular inflammation and subsequent ischemic damage to the tissues.
what are examples of diseases caused by type lll hypersensitivity?
systemic lupus erythematosus
polyarteritis nodosa
post-streptococcal glomerulonephritis
what is type lV hypersensitivity?
delayed
cytokine-mediated inflammation
Cytokines → inflammation → tissue injury
OR
T cell-mediated cytotoxicity
T cells → direct cell killing and tissue injury
give examples of autoimmune diseases associated with type IV hypersensitivity
type 1 diabetes
rheumatoid arthritis
multiple sclerosis
what is systemic autoimmune disease?
The autoimmune process is diffused throughout the body
Affects more than one organ - not necessarily the same ones in different individuals
e.g.
- Systemic lupus erythematosus
what is organ-specific autoimmune disease?
Autoimmune process directed against one organ
e.g.
- Type 1 Diabetes - pancreas
- Autoimmune Thyroiditis
what is immune tolerance?
state of unresponsiveness to specific antigens
that would normally be expected to excite an immunological response.
Immune cells normally target pathogens and not self-tissues.
e.g. some B cells are specific for pathogens and others are for autoantigens.
- Antigens can be self or foreign
Prevents adaptive responses that are damaging (immune pathology)
B cells and T cells
Can be exploited by microbes and tumours
→ Pregnancy, transplantation, autoimmune disease and cancer
what is a hypersensitivity response?
damaging responses produced during normal immune responses
Chronic activation can lead to autoimmune disease – different effector mechanisms influence the disease phenotype
what is autoimmune disease?
a failure or breakdown of the immune system that maintains tolerance to self-tissues.
Loss of tolerance is probably due to abnormal selection or lack of control of self-reactive lymphocytes
(B and T-cells)
describe how type 1 diabetes works:
The Islet of Langerhans damage in type 1 diabetes is mediated by CD4+ Th1 T-cells that are reactive with islet autoantigens.
They drive the influx of CD8+ T cells to destroy
insulin-producing b-cells
