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Modul Infeksi dan Imunologi 2013

Prinsip Dasar dan Imuno-Patogenesis


Infeksi Bakteri, Jamur, dan Virus

Yeva Rosana, Anis Karuniawati


Departemen Mikrobiologi
Fakultas Kedokteran Universitas Indonesia

Patogenisitas

Kemampuan mikroorganisme menyebabkan


penyakit
Virulensi

Derajat patogenisitas
Faktor virulensi

Berbagai faktor yang terdapat pada mikroorganisme


patogen yang dapat berinteraksi dengan sel host
dan memungkinkannya untuk memasuki sel host,
menempel, mendapatkan nutrisi, dan menghindari
deteksi atau penghilangan oleh sistem kekebalan
tubuh

Mikroorganisme

Mikroorganisme
Flora normal

melayani fungsi penting bagi sel host


membantu dalam pencernaan makanan, memproduksi
vitamin, melindungi host dari kolonisasi dengan mikroba
patogen
Patogen

kemampuan menyebabkan penyakit


Oportunistik

kemampuan menyebabkan penyakit hanya jika sistem


kekebalan sel host terganggu

Flora Normal

Patogen
Menyebabkan kerusakan sel host sebagai bagian

dari strateginya untuk memperbanyak diri dalam


sel host atau untuk penyebaran ke atau dari sel
host.

Dikodekan oleh gen yang terkelompok bersama

pada genom patogen: pathogenicity island

Transmisi horizontal -terkait gen antara mikroba,

yang dimediasi oleh: bakteriofaga, plasmid,


transposon

Postulat Kochs (1890) oleh Robert Koch


Mikroba harus ada dalam setiap kasus penyakit
Mikroba harus dapat diisolasi dari hospes yang sakit

dan dapat tumbuh dalam kultur murni

Penyakit ini harus dihasilkan kembali jika kultur

murni dipaparkan ke host yang rentan tetapi tidak


sakit

Mikroba harus diperoleh kembali dari host yang

diinfeksi secara eksperimental

Pengecualian untuk Postulat Koch


Mikroba tidak selalu dapat ditumbuhkan di

laboratorium

Kofaktor atau faktor genetik dan imunologik pada

host mempunyai peran yang penting

Pertimbangan etik mencegah penerapan postulat

Koch terhadap penyakit dan patogen yang terjadi


hanya manusia

Penyakit tidak muncul sampai bertahun-tahun

setelah infeksi tertentu

Gradien Respon Biologik


Gambaran klinis tergantung

pada banyak variabel: dosis


dan rute infeksi, umur, jenis
kelamin, adanya mikroba
lain, status gizi dan latar
belakang genetik

Banyak variasi dalam tingkat

keparahan penyakit secara


klinis

Proses Infeksi
Masuk

kolonisasi, adhesi, dan invasi

Aksi patogenik

Jalan masuk
Kulit

Membran mukosa

Pernapasan, pencernaan, saluran


kencing, saluran
reproduksi, konjungtiva (membran
tipis yang
menutupi permukaan bola mata dan
kelopak mata )

Plasenta
(Rute parenteral)

Masuk
Jalan masuk
o Masuk tanpa harus melewati penghalang (inhalasi, makan)
o Untuk menyebabkan penyakit, mikroba tidak perlu masuk
jauh ke dalam jaringan, hanya permukaan mukosa
Penetrasi
o Masuk ke dalam jaringan setelah melintasi penghalang
epitel
o Gigitan serangga, rusaknya permukaan kulit
o Banyak mikroba memerlukan interaksi dengan reseptor
spesifik pada sel host

Beberapa patogen yang melalui plasenta


Pathogen

Condition in Adults

Effect on Embryo or Fetus

Toxoplasma gondii

Toxoplasmosis

Abortion, epilepsy, encephalitis,


microcephaly, mental retardation, blidness,
anemia, jaundice, rash, pneumonia, diarrhea,
hyporthermia, deafness

Treponema pallidum

Syphillis

Abortion, multiorgan birth defects, syphillis

Listeria
monocytogenes

Listeriosis

Granulomatosis infantiseptica, death

Cytomegalovirus

Usually
asymptomatic

Deafness, microcephaly, mental retardation

Parvovirus B19

Erythema infectiosum Abortion

Lentivirus (HIV)

AIDS

Immunosuppresion (AIDS)

Rubivirus

German measels

Severe birth defects or death

Baumann, RW. Microbiology. Pearson International Ed. 2009

Kolonisasi atau Infeksi


Kolonisasi
Berada di dalam atau permukaan badan;

Tidaka ada tanda dan gejala sakit atau infeksi


Kadang-kadanng sebagai carrier

Infeksi
Berada dalam bagain tubuh
Diikuti tanda dan gejala infeksi (seperti: demam, lesi, sekret

luka) atau meningkatnya hitung sel darah putih


Dibutuhkan pengobatan

Receptor molecule on Host Cells


typically glycoprotein containing sugar molecule such as

mannose and galactose

Not present for the benefit of the infectious agents; they

have specific functions in the life of the cells

Present only in certain cells, which are then uniquely

susceptible to infection (specificity of pathogens for


particular hosts):

N.gonorrhoeae has adhesin on its fimbrae that adhere to cells lining

the urethra and vagina of human

Lost the ability to make ligands:


Genetic change or mutation
Exposure to certain physical or chemical agent

harmless or avirulent
Some bacterial pathogens do not attach to host cells

directly, but instead interact with each other to form a


sticky web of bacteria and polysaccharides called a
biofilm, which adheres to a surface within a host
(example: dental plaque)

Pathogenesis of
Bacterial Infection

Virulence Factor: Adhesion/ Attachment


The process by which microorganisms attach
themselves to cells
Adhesion factors:
Specialized structures
Adhesion disk (protozoa), suckers, hooks (helminthes)
Ligands: Surface lipoprotein and glycoprotein

(bacteria, viruses)

Adhesin (bacteria): found on fimbrae, flagella,

glycocalyses
Attachment protein (viruses)

Bacterial Adhesin
Gram-negative bacteria
Pili (fimbriae)
Surface protein: invasin
Capsules

Gram-positive bacteria
Surface proteins: fibronectin
Capsules

Virulence Factors: Enzymes


Extracellular Enzymes
Hyaluronidase and collagenase degrade
specific molecules to enable bacteria to
invade deeper tissue
Coagulase blood protein, providing a
hiding place for bacteria within a clot
Kinase such as staphylokinase and
streptokinase digest blood clots

Virulence Factors
Toxins
Exotoxin
Cytotoxins: kills host cells in general or affect

their function
Neurotoxins: specifically interfere with nerve
cell function
Enterotoxins: affects cell lining the
gastrointestinal tract

Endotoxin
Lipid A, lipid portion of the membranes
lypopolysaccharide

Activities of lipopolysaccharide

Virulence Factors
Antiphagocytic factors
Capsules

Composed of chemicals that are normally found in the


body (including polysaccharides) do not stimulate a
hosts immune response
Antiphagocytic chemicals
Prevent the fusion of lysosomes with phagocytic

vesicles, which allows the bacteria to survive inside of


phagocytes
S.pyogenes produces a protein on its cells wall and
fimbrae (M protein), that resist phagocytosis and thus
increases virulence

Virulence Factors
Invasion factors
Mechanisms that enable a bacterium to invade eukaryotic

cells facilitate entry at mucosal surfaces

Some are obligate intracellular, most are facultative

intracellular pathogens

The specific bacterial surface factors that mediate

invasion are not known in most instance

Virulence Factors
Siderophores
Organisms require iron for metabolism and growth
In blood : iron is bound either to Hb or transferrin

In milk or other solution (tears, saliva, etc.) iron is bound to


lactoferrin
Siderophores : substances produced by many bacteria to

capture iron from the host

The binding constants of the siderophores for iron are so

high that even iron bound to transferrin or lacctoferrin is


confiscated and taken up by the bacterial cells

Competition between host cells and bacterial pathogens for iron

Immunopathogenesis
The symptoms of a bacterial infection can be produced by excessive
immune and inflammatory responses triggered by the infection
e.g.
Endotoxin : acute phase protein can cause the life-threatening symptoms associated with
sepsis and meningitis
Tissue damage induced by neutrophils, macrophage and complement induced by CD4 T
cells and macrophages for Mycobacterium tuberculosis
The bacterial M protein of S, pyogens antigenically mimics heart tissues such that anti-M
protein antibodies cross react with initiate damage to the heart (rheumatic fever)
Immune complexes deposited in the glomeruli of the kidney, cause post-streptococcal
glomerulonephritis

Goering, RV., et.al. Mims Medical Microbiology.4th Ed.Mosby Elsevier.2008

Goering, RV., et.al. Mims Medical Microbiology.4th Ed.Mosby Elsevier.2008

Types of Infection and Their Role in Transmission


Type of Infection
Respiratory Tract

Host Defenses

Microbial Evasion Mechanism

Examples

Mucociliary clearence

Adhere to epithelial cells, interfere


with ciliary action

Influeza virus, pertusis

Alveolar macrophage

Replicate in alveolar macrophage

Legionella, M.tbc

Intestinal tract

Mucus, peristaltis, acid,


bile

Adhere to epithelial cells, resist


acid, bile

Rotavirus, Salmonella,
Poliovirus

Liver

Kuppfer cells and


endothelial cells

Localize in sinusoid, bypass


Kupffer cells and endothelial cells

Hepatitis virus

Reproductive tract

Flushing action of urine


and sexual secretions,
mucosal defenses

Adhere to urethral/vaginal epithelial


cells

Gonococus, Chlamydia

Urinary tract

Flushing action of urine

Adhere to urethral/epithelial cells

E.Coli

Reach urine from tubular


epithelium

Polyomavirus

Reach CNS via nerves or blood


vessels that enter skull or vertebral
column

Bacterial meningitis,
viral encephalitis

Central Nervous
System

Enclosed in bony box


of skull and vertebral
column

Goering, RV., et.al. Mims Medical Microbiology.4th Ed.Mosby Elsevier.2008

Types of Infection and Their Role in Transmission


Type of Infection
Skin, mucosa

Vascular system

Host Defenses

Microbial Evasion Mechanism

Examples

Layers of constantly
shed cells (mucosa)

Invade skin/mucosa from below

Varicella, measles

Dead keratinized cell


layers (skin)

Infect basal epidermal layer

Papillomaviruses

Infect via minor abrasion

Staphylococci,
streptococci

Penetrate intact cells

Schistosomiasis,
ancyclostomiases.
Leptospirosis

Infection of microbe by biting


vector, replication in blood cells
or in vascular endothelial cell

Malaria, yellow fever

Skin

Goering, RV., et.al. Mims Medical Microbiology.4th Ed.Mosby Elsevier.2008

Pathogenesis of
Fungal Infection or Mycosis

Classification
Endemic Mycosis
Infections caused by pathogens that are restricted geographically and
are true pathogens because they have the ability to cause serious
systemic infection in healthy individual

Opportunistic Mycosis
Infections caused by fungi that not true pathogens because they
cause life-threatening systemic disease only in immunosuppressed patients

Classification
Subcutaneous Mycosis

A group of fungal diseases that involved the skin, subcutaneous


tissue, and lymphatic
Superficial and Cutaneous Mycosis

Common fungal infections limited to the skin and skin structures


Systemic/Invasive

Risk Factors
Patients with immunological impairment
HIV infection
Leucopenia (hematological malignancy patients),
After surgery, organ transplantation
Cancer therapy
Widespread use of broad-spectrum antimicrobial agents
Immunosuppressive agents and corticosteroid therapy

Encounter
2 main mechanisms:
Exogenous
Most fungi live freely in the environment, and people encounter
them incidentally in the course of everyday living
Endogenous

The source is the normal human flora

Entry
Level of innate immunity to pathogenic fungi is high in most humans

most of fungal infection are mild and self-limiting


Increasing the likelihood of entry and subsequent infection:
Alteration in the balance of the normal flora

Violation of the natural barriers by trauma or foreign bodies allows entry of

fungi into sterile areas of the body

Host Responses
Innate immunity
Neutrophil phagocytosis and killing
For fungi that are too large to be ingested: phagocytic cells line

up along the surface of the hyphal structure and secrete


lysosomal enzymes that damage the organisms

Host Responses
Adaptive Immunity
Antibodies: the role is minor
T cell-mediated immunity

Some pathogens persist within macrophages without being killed

Damage and Severity


Determined by:
size of inoculums
virulence
ability to multiply
the adequacy of the host defense

Virulence Factors (VF)


Phenotypic switching
a very important part of fungal adaptability to the changing of

environment during invasion of the human organism


change their morphology, cell surface properties, colony

appearance, biochemical properties and metabolism to become


more virulent and more effective during infection

VF: Phenotypic switching


Candida albicans:
the white-opaque switching: a white, oval and smooth colony a

grey, rough colony


the opaque cells produce aspartyl proteinases 1 and 3 less

virulent, white cells secrete aspartyl proteinase 2 more virulent


during systemic infection

How? Probably chromosomal rearrangements and a SIR2-like

regulation take part in this process

VF: Phenotypic switching


Cryptococcus neoformans
Aspergillus fumigatus
produce melanin a grayish, brown or black pigment, in the cell wall

may be a result of fungal adaptation to environmental changes


It provides protection against ultraviolet radiation, extreme

temperatures and other adverse environmental conditions.

VF: Morphological dimorphism


The ability to switch between unicellular yeast cells and

filamentous forms called hyphae and pseudo-hyphae


Response to changes of physiology environmental

conditions:
physiological temperature of 37C,
pH equal to or higher than 7.0,
CO2 concentration of 5.5%
the presence of serum or carbon sources which stimulate hyphal-

growth

VF: Adhesion and adhesion molecules


adherence to the host cells/tissues/a set of diverse host

proteins, followed by dissemination within the human


organism
C. albicans:
On the cell wall surface, presents receptors which are responsible
for adhesion to epithelial and endothelial cells, serum proteins and
extracellular matrix proteins
Adhesion to different artificial substrates and formation of biofilm
on medical devices

VF: Secreted hydrolytic enzymes


Proteases, lipases and phospholipases
These enzymes play a role in nutrition and also in:
Tissue damage
dissemination within the human organism
iron acquisition and overcoming the host immune system

strongly contribute to fungal pathogenicity.

VF: Secreted hydrolytic enzymes


Candida albicans produces :
Phospholipases: responsible for hydrolysis of one or more ester
linkages of glycero-phospholipids
lipases which can hydrolyze ester bonds of mono-, di- and tri-

acylglycerols
SAPs (secreted aspartyl proteinases). The family of SAP genes

includes at least ten different genes SAP1SAP10 which encode


enzymes with similar functions and character, but different
molecular properties

VF: Secreted hydrolytic enzymes


Cryptococcus neoformans
proteases and phospholipases, which play a role in nutrition and

tissue damage
phospholipase enhances the adhesion to the lung epithelium

Aspergillus fumigatus
serine and aspartic protease, metallo-proteinase,

dipeptydylpeptidases and phospholipases facilitating lung and


other tissue colonization

VF: Capsule formation


C. neoformans:
A thick polysaccharide capsule can be obtained during lung

infection, in contrast to the natural environment where it is weakly


encapsulated
After the invasion, C. neoformans can be rehydrated and acquires the

capsule composed of glucuronoxylomannan (GXM) and connected


with the fungal cell wall through glucan bridges

VF: Mannitol Production


Cryptococcus neoformans
produces a large amount of the hexitol d-mannitol

development of meningo-encephalitis. Mannitol increases the


osmolality of the surrounding fluid, brain edema and prevents
oxidative damage to the fungus
mannitol can protect the fungi from oxidative killing by PMN or

by cell-free oxidants

VF: Toxin
Aspergillus fumigatus
Aflatoxin: hepatotoxic and carcinogenic, its expression is regulated by

many genes under influence of environmental conditions


Gliotoxin: inhibit macrophage phagocytosis, T-cell activation and

proliferation, and can induce macrophage apoptosis, slowing ciliary


beating in the respiratory tract and for epithelial layer damage, so the
fungal cells cannot be efficiently removed from the host organism

VF: Toxin
Aspergillus fumigatus
Resticotocin: cleaves a phosphodiester bond in 28S rRNA of
eukaryotic ribosomes
immunosuppressive toxins: the 14-kDa conidial inhibitory factor

and AfD, A. fumigatus diffusible product


fumitremorgins, fumagilin, fumagatin and helvolic acid: pyrogenic,

cytotoxic and shock-evoking activities

Pathogenesis of Viral Diseases


Maintain a reservoir
Enter a host
Contact and enter susceptible cells
Replicate within the cells
Release from the host cells
Virus-host interactions engender host immune response
Be either cleared from the body of the host, establish a
persistent infection, or kill the host
Be shed back into the environment

Nature of the Disease


Target Tissue
Portal of entry of virus
Access of virus to target tissue
Tissue tropism of virus
Permissiveness of cells for viral replication

Viral Pathogen (strain)


Viral receptors determines tropism
Virulence factors

Entry and Attachment


Entrance: one of the body surfaces; needle sticks, blood transfusions,

organ transplants, insect vectors


Adsorption or attachment: process of penetrates a host cells to

gain access to the cells replicative machinery


Adsorption occurs because of specific protein ligand:
Enveloped virus use spikes (viral protein that protrude from their membrane)
Naked virus: their ligands as part of their capsid protein

Virus Immune cells Interaction

Binding of a virus to its receptor on the host cell surface result


in penetration of the cell or the delivery of virus nucleic acid to
the cytoplasm of the cell

Nucleic acid enters the host cell by:


1. Direct entry of just the nucleic acid, as with poliovirus
2. Fusion of the viral envelope with the cell membrane and
subsequent uncoating, as with influenza virus
3. Endocytosis and the release of nucleic acid from the capsid
(uncoating), as with Poxviruses

Mechanisms
of entry of
virus

Replication:
at the site of entry and cause disease at the same site, or
spread to sites distant from the point of entry and replicate at
these site
2 release mechanisms from the host:
Very dramatic and results in relatively large numbers of virions leaving

the host cell at the same time and host cell death

Budding or blebbing: a newly formes nucleocapsid pushes against the

host cell membrane until the membrane evaginates and pinches off
behind the virus. The released virus is coated with host cell membrane,
called the viral envelope. The release is slower process than lysis

The process of Budding in Enveloped Viruses

Virus-host interaction
Cytopathic viruses
Ultimately kill the host cell, the result is often local necrosis

Can trigger apoptosis or programmed cell death

Non-cytopathic viruses
Do not immediately produce cell death and result in latent or persistent
infections
Productive: virus produce persistent infection with the release of only
a few new viral particles at a time
Non-productive: viruses do not actively make virus at detectable levels
for a period of time (latent infection)

Cytopathogenesis
Abortive infection
Viral mutants that cause abortive infections no multiplication
disappear
Permissive cell:
Provides biosynthetic machinery:
Transcription factors
Post-translational processing enzymes

Semi-permissive cell:
Very inefficient in supporting viral replication
May support some but not all the steps in viral replication

Cytopathogenesis
Replication of the virus can initiate changes in cells

Cytolisis or alterations of the cells:

Appearance
Functional properties
Antigenicity

Changes may be due to:

Viral takeover of macromolecular synthesis


Accumulation of viral proteins or particles
Modification or disruption of cellular structures

Cytopathogenesis

Lytic Infections

Syncythia formation

Expression of glycoproteins of some paramyxo-viruses, herpes


viruses and retroviruses triggers the fusion of neighboring
cells into multinucleated giant cells syncitia

Lytic Infections: Syncythia formation

Cell-to-cell fusion:
May occur in the absence of new protein synthesis
Senday virus
Other paramyxoviruses
May require new protein synthesis :
HSV= Herpes Simplex Virus

Allows the virus to spread from cell to cell and escape

antibody detection
Syncythia formatin of HIV causes cell death

Lytic Infections: Apoptosis


Apoptosis:
Preset cascade of events that leads to cellular suicide, when triggered
Viral infection or cytolytic immune responses may induce

apoptosis in the infected cell


Consequence of apoptosis towards viral replication:
may facilitate release of the virus from the cell
But, also limits the amount of virus that is produced due to
destruction of the viral factory (the infected cells)

Lytic Infections:Characteristic changes


Changes of the appearance and properties of the target cells:

Some viral infections cause characteristic changes in the


appearance and properties of the target cells

Example:

Chromosomal aberrations and degradation:

Virus-induced changes in the membrane or chromosomal structure


HSV-infected and Adenovirus-infected cells

Lytic Infections:Characteristic changes


Inclusion bodies
Found within nucleus and cytoplasm
Represent the sites of:
viral replication
accumulation of viral capsids

The nature and locations of inclusion bodies


are characteristic of particular viral infection
facilitates laboratory diagnosis

Inclusion bodies
Negri bodies (intracytoplasmic): Rabies
Owls eye (intranuclear): Cytomegalovirus
Cowdry type A (intranuclear):
Herpes simplex virus
Subacute sclerosing panencephalitis (measles) virus
Intranuclear basophilic: Adenoviruses
Intracytoplasmic acidophilic: Poxviruses
Perinuclear cytoplasmic acidophilic: Reoviruses

Lytic Infections

Syncythia
Inclusion Bodies

Nonlytic Infections: Persistent Infections


Occurs in an infected cell that is not killed by the
virus
A latent or immortilizing infection may result from
DNA virus infection of a cell that restricts or lacks
the machinery for transcribing all the viral genes
The specific transcription factors required by
viruses causing latent infection may be expressed:
In specific tissues
In growing but not resting cells
After hormone or cytokine induction

Oncogenic Viruses
Some DNA viruses and retroviruses establish
persistent infections that also stimulate
uncontrolled cell growth

Transformation or Immortalization :

Continued growth without senescence


Alterations in cell morphology and metabolism
Increased cell growth rate and sugar transport
Loss of cell-contact-inhibition of growth
Ability to grow in a suspension or a semisolid agar

Oncongenic virus
Transformation or Immortalization
of infected cell

Mechanisms:

Promotion or provision of
growth-stimulating genes
Removal of the inherent
braking mechanisms that
limit DNA synthesis and
cell growth
Prevention of apoptosis

Protooncogenes: genes that


play a role in cell division
Factors contribute to the
inhibition of oncogene
repressor and the activation
of oncogenes (UV, radiation,
carcinogens and viruses)

Viruses cause 20-25% of human cancers in several ways:


carry copies of oncogenes as part of their genome
Promote oncogenes already present in the host
Interfere with normal tumor repression when they insert (as

proviruses) into repressor genes

INFEKSI VIRUS

KEMAMPUAN DAN KECEPATAN RESPON IMUN INDIVIDU JENIS INFEKSI

The Stages of Infectious Diseases

Baumann, RW. Microbiology. Pearson International Ed. 2009

Portal Exit

Baumann, RW. Microbiology. Pearson International Ed. 2009

Transmission

Baumann, RW. Microbiology. Pearson International Ed. 2009

Transmission

Goering, RV., et.al. Mims Medical Microbiology.4th Ed.Mosby Elsevier.2008

Kekebalan non spesifik


Pencegahan terhadap masuknya mikroba

Kulit
Mukosa
Sekresi : kimia dan mekanik
Struktur anatomi
Antagonisma mikroba oleh flora normal

Pengaruh keadaan umum


Kesehatan, faktor predisposisi, genetik, hormonal, status
gizi, dll.

Kekebalan non spesifik

Mekanisme kekebalan setelah invasi


Reaksi radang
Fagositosis
Sel yang berperan :
Lekosit polimorfonuklear
Fagosit mononuklear : sel kupfer, sel Schwan, sel makrofag alveoli,
sel langerhans, bebas dalam darah

Interferon, sel NK

Kekebalan non spesifik

Sistem Komplemen
Aktivasi komplemen dapat terjadi melalui 2 jalur :
Alternatif : respon imun tidak spesifik
Klasik : respon imun spesifik
Kedua jalur ini mengaktifkan komplemen terpenting : C3,
sehingga :
C3b mengikat antigen
fagositosis
C3a teraktivasi menjadi zat kemotaksis
Jalur lisis (kekebalan spesifik)

Kekebalan non spesifik

Fagositosis

Reaksi Radang

Kekebalan non spesifik


terhadap virus

Interferon

Sel NK

Kekebalan spesifik
Antigen
Benda asing yang bila masuk kedalam tubuh manusia/hewan akan
merangsang terbentuknya antibodi terhadapnya dan dapat
bereaksi secara khas.
BM > 5000 (protein, polisakarida, lipida, asam nukleat)
Determinan antigen (epitop) :
Bagian tertentu pada permukaan molekul antigen yang dapat
bereaksi secara khas dengan antibodi

Imunitas Humoral
Sel limfosit B
Diproduksi oleh sumsum tulang
Prekursor sel plasma, penghasil antibodi
Sebagian sel limfosit B akan menjadi sel
memori yang berfungsi pada infeksi kedua
oleh antigen yang sama

Fungsi Antibodi
Netralisasi toksin
Sel fagosit mempunyai
reseptor Fc
opsonisasi

Terikat pada komplemen


jalur klasik
lisis sel

Jalur klasik

lisis sel

Imunitas selular
Melindungi tubuh dari infeksi bakteri intraseluler,
virus, jamur, parasit, tumor, penolakan organ
transplantasi
Sel limfosit T, diproduksi sumsum tulang
Maturasi dan diferensiasi didalam kelenjar timus
Produksi limfokin

Peran MHC

Peran MHC klas II

Peran MHC klas I

Peran makrofag

Respon antibakteri

Respon anti-virus

Interferon

Penyebab Kekebalan Nonspesifik dan Spesifik