Imunitas terhadap Penyakit

Infeksi

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 Natural IR to Extracellular Bacteria

1. Phagocytosis – Neutrophils, Monocytes, Tissues

Mo
>< Virulence : Resistance of Bacteria to
Phagocytosis & Digestion within Mo

2. Activation Complement System

Peptidoglycan (G+) > alternative pathway C3
convertase
LPS (G-) > alternative pathway C3

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C3b generation opsonize phagocytosis

membrane attack complex (MAC) Lysis

bacteria

Inflammatory Reponses
~ Recruiting & Activating Leukocytes

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SPECIFIC IR to Extraceller Bacteria
! Ab
 Ig G2 opsonize bacteria & Phagocytosis

 Ig M & Ig G Activate C C3b & i C3b (bind to

spec. type1 & 3 C R) Phagocytosis

 Ig M & Ig G Neutralize Bacteria Toxins :

Prevent Binding to target cells / Active site ;
Phagocytosis ;
Toxin Ab complex
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Ig A
Neutralize Toxin
secretary
prevent colonization ( inhibit binding microbe to
surface cells ) ( Ig A copro Ab )
external body fluids (tears, saliva, nasal
secretion)

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Immunity to Intracellular Bacteria ~ Fungi
Natural Immunity :
 Phagocytosis
Relatively Resistant to degradation Macrophage ,
inaccessible to circulating Ab
 Ineffective in controlling colonization & spread of
pathogenic Intracellular Bacteria

Tend to Chronic Infections / Recurrance / Difficult to

Eradicate

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 Specific Immune Response
Cellular Mediated Immunity ~ ! Protective – CD4 + T cells
CD8 +

Specificity ~ T cells
IFN γ
Effector ~ Activated M0
~ Delayed Type Hypersensitivity !
e g. miuramyl dipeptida adjuvant activate M0 Phagocytic
(cell wall)
The Pattern of IR to Intracellular Microbes ! Important Determinant
of Disease Progression & Clinical Outcome
(e g : leprosy ~ 2 polar forms : lepromatous ; tuberculoid)
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 Immunity to Viruses

Pathogenesis : an infectious Disease

 Port of Entry
 Life Cycle
- Local / Systemic
- Lytic , Cytophatic Effect / non CPE
- Intracellular
- Integrated DNA / non integrated

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 VIRUS

Entry :
Physiologic important – normal Cell
surface molecules
HIV → CD4 T cells
EBV → type 2 complement
receptor B cells
Rhino Virus → ICAM -1 (>>
epithelium)

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NATURAL IMMUNE RESPONSE TO VIRUS

 INTERFERON → inhibit viral replication

 NK CELLS ( Natural killer ) →
litic target infected cells

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SPECIFIC IMMUNE RESPONSE TO VIRUS

 Antibody → inhibit virus entry

 Tc cells ( T cytotoxic ) →
Lytic target infected cells

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 Evasion of Immune Mechanism by
Extracellular Bacteria
 Virulence ~ Tissue invasion. Toxin → kill the
Phagocytes
~ Colonization. Capsule → inhibit
Phagocytosis
~ Enzymes – menghalangi acute inflam.
Response
 Adhesive properties of Bacterial Surcface
Proteins
 Anti – Pahgocytic Mechanism ~ Encapsulated
Bacteria
 Inhibition of C / Inactivation of C Products

(e g. Sialic Acid Residues of G+ / G- Capsules)

 Genetic Variation of Surface Ag (e g. Pili) 14
 Evasion of Immune Mechanism by Intracellular
Bacteria
• Resist Phagocytosis
M. tuberculosis inhibit phagolysosome fusion ( cell
wall)
M. leprae menghambat – reactive oxygen (~ legionella)
(phenolic glycolipid) (outer coat)
Listeria monocytogenes forming pores in the
phagosome
(hemolysin)
(~Rickettsia) membrane releasing bacteria
Cytoplasma

persist – long periods chronic antigenic simulation

local collection of activated M0 (Granulomas)
Prevent – spreading microbes.
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