Immunity against Infectious Agents:

unique interaction between host and parasites

Marsetyawan HNE Soesatyo

Department of Histology & Cell Biology
Faculty of Medicine UGM
General Scope of Immunology
Figure 1-
1-32
Bone marrow-derived cells of the immune system

Figure 1-
1-3
 Immune responses
I Natural--/innate
Natural /innate--/nonspecific immunity
– Humoral
Humoral:: type I IFN (IFN-
(IFN-α/β), lysozyme,
Complement proteins
– Cellular: phagocytes (neutrophils,
macrophages), NK cells
I Adaptive--/acquired-
Adaptive /acquired-/specific immunity
– Humoral cells
Antibodies
Humoral:: B cells
Antibodies:: IgM, IgG,
IgA, IgE, IgD
– Cellular: T cells:
I CD4+ Th, CD8+CTL (cytolytic T lymphocytes)
PROTECTIVE FUNCTIONS OF THE IMMUNE
SYSTEM

 NON PATHOGENS - INERT ANTIGEN /

IMMUNOGEN
 PATHOGENS - VIRUS
- BACTERIA
- PARASIT
- FUNGI
IMMUNOGENICITY / ANTIGENICITY

SURFACE STRUCTURES OF PATHOGENS

antigenic
 BACTERIA

☺ Gram-positive
☺ Gram-negative
☺ Mycobacteria
☺ Spirochaete
 VIRUSES

☺ Viral proteins
(virion: nucleocapsid/envelope,
infected cells: viral antigens)
 PARASIT

☺ Surface membrane
☺ Excretory-Secretory (ES) antigens,
Granule (Gra) proteins
 MECHANISMS OF IMMUNITY
 The first line of defence :
Independent on antigen recognition
- barriers (physical, chemicals, mechanical)
- complement, cytokines (TNF, IL-1, IFN)
- cells :phagocytes (mononuclear, polymorphonuclear)
NK cells
 The second line of defence :
Dependent on antigen recognition
- humoral : antibodies
- cell-mediated : T cells, Mφ
- combination : ADCC
BACTERIAL INFECTIONS : A model for studies

 Immunopathogenicity
 Natural responses
☺ Against LPS
☺ Complement activation
☺ Phagocytic activity
 Adaptive responses
☺ Antibody response
☺ T-cell response
MECHANISMS OF IMMUNOPATHOGENICITY

 Toxicity without invasiveness

→ Ab response
 Invasiveness without toxicity
→ cell-mediated response
 Both activities
→ Ab & cell responses
MECHANISM OF ACTION OF LPS
MICROBICIDAL EFFECTS OF PHAGOCYTIC CELLS

 Oxygen - dependent
ִ ROI
ִ RNI

 Oxygen - independent
ִ Cathionic protein
ִ Acidification of pH
ִ Lactoferrin, lysozyme
 Ab responses

 bacterial toxin → neutralization IgG, IgM

 against attachment
Ab to fimbriae, lipoteichoic acid, some
capsules : IgG, IgM, SIgA
 trigger C-mediated lysis
 opsonization via Fc and C3 receptors
 neutralize spreading factors, enzymes
(e.g. hyaluronidase)
 T cell responses
 Tc (CTL) - intracellular pathogens
e.g. γδ T cells / CD8+
 Against superantigens (staphylococcus, streptococcus,
mycoplasmas)
ִ binds directly to Vβ of Ag receptors
Ag
ִ no processing and presentation

Massive cytokine / lymphokine release

Toxic shock syndrome

 EVADE MECHANISMS AGAINST PHAGOCYTE-
MEDIATED KILLING

 secret repellents / toxins → inhibit chemotaxis

 bear capsules / outer coats → inhibit attachment
 releases molecules (M. tuberculosis) → interfere
phagolysosome fusion
 secret catalase → break down hydrogen peroxide
 possess a phenolic glycolipid (M.leprae) → scavenges
free radicals
 release lipoarabinomannan (Mycobacteria) → block
the ability of Mφ in respond to IFN-γ stimulus
 others : anatomic sequestration, antigenic mimicry,
antigenic variation (parasites)
EXCESSIVE RELEASE OF CYTOKINES
 CONCLUSION
 The immune responses to pathogenic agents /
immunity of infectious diseases are primarily
conducted by natural immune responses, and
working in concert with adaptive responses
 The successful of pathogens to invade into, and
persist in the body is pretty much depending on the
status of immunity, the virulence factors of the
agents and their ‘smart’ evade mechanisms against
effector function of the immune system