Immune response to
infections
Factors influencing
the severity of infection
• Pathogen factors
– Dose
– Virulence of organism
– Route of entry
• Host factors
– Integrity of non-specific defence barriers
– Competence of the immune system
– Genetic influences
– Previous exposure to antigen
– Existence of co-infection
Immune response to viral
infections
– Non-speciphic immunity
• Interferons ( a and b)
• Natural killer cells (NK cells)
• Receptor-like molecules in various secretions
– Speciphic immunity
• Antibodies – neutralization of extracellular viruses
• Tc lymphocytes – elimination of virus-infected cells
Mechanisms of antiviral immunity
The action of interferon (IFN)
Natural killers (NK cells)
• Originate in non-T non-B lymphocyte lineage.
• Morphologically: large granulated lymphocytes
(LGL).
• Recognition of target cells in antigen non-
speciphic.
• Virus infected and tumor cells are killed.
• Target cells are recognisd mainly by decreased
HLA-I expression.
• Cytotoxic mechanisms are similar to Tc cells:
perforin and induction of apoptosis.
Viral strategies to evade the
immune response
• Antigenic variations
– antigenic drift - minor changes
– antigenic shift - major changes
• Long-term survival in a host
– Viral persistence – virus van be detected in
periphery (e.g. chronic hepatitis B)
– Viral latency – virus is „hidden“ e.g.
herpesviruses
– Oncogenic transformation
• Immunosuppressive effect of viruses
Immunosuppressive effects
of viruses
• Suppression of T-cells : HIV, morbilli, CMV,
• Inhibition of MHC antigens expression:
CVM (binds b-2 microglobulin),
Adenoviruses, RSV - decreased expression
of HLA antigens
• Production of inhibitory cytokies: EBV (IL-10
- like factor)
Damage of a host caused by
anti-viral immune response
• Autoimmune diseases: hemolytic anemia after
EBV infection (polyclonal stimulation),
autoimmune hepatitis induced by hepatitis-B
virus (aberrant HLA-II expression and other
mechanisms).
• Immune complex diseases: arthritis in hepatitis
B, vasculitis.
• Tc - mediated diseases: rash in exanthematic
viral diseases, myocarditis caused by coxackie
virus.
Immune responses to
bacterial infections
• Non-specific immunity
– Mechanical barriers
– Phagocytosis
– Complement system
• Specific immunity
– Antibodies - opsonisation, complementactivation,
neutralisation of toxins,
binding to receptors
– T-lymphocytes - against intracellular
parasites
Bacterial evasions of immune
defences
• Antiphagocytic machanisms: toxins,
capsular polysaccharides
• Inhibition of the complement system: Str.
pyogenes, E. coli, N. meningitidis
• Antigenic variations: Borrelia recurrentis
• Proteases lysing IgA - Neisseria,
Haemophilus
• Sequestration in avascular regionsSalmonella
typhi in the gall bladder and
urinary tract
• Intracellular parasitism
Macroorganism damage caused by the
immune response to bacterial infection
• Autoimmune diseases
– Cross-reactivity of bacterial and body
antigens - rheumatic fever
– Type-II hypersensitivity - autoimmune
hemolytic anemia caused by Mycoplasma
infection
– Heat shock proteins
– Superantigens (streptococcal,
staphylococcal)
• Immunocomplex diseases
• Type IV hypersensitivity- cavitation in
pulmonary tuberculosis
Activation of TCR by antigen and
superantigen
MHC class
II
Signal
transduction
Superantigen
T cell
APC
TRC
Signal
transduction
αβ
α β
αβ
α β
Antigen
Mechanisms of anti-fungal
resistance
• Normal bacterial flora
• Phagocytic cells
• T-lymphocytes -probably most
important
• Antibodies - usually present, but
have no protective effect
Imunity against parasites
• Different mechanisms involved against different
parasites.
• Immune response frequently leads to premunity –
the situation when the parazite perzists, however
it does not lead to dissemination and new
infections.
• IgE and esinophils play a crucial role.
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© 2005 Elsevier
Role of IgE and mastocytes in protection against
parasites