Imunologi Infeksi Tropis

8/11/2019 Imunologi Infeksi Tropis

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Imunologi Infeksi Tropis

dr. Godeliva Maria Silvia M., MSc

FK UKDW Jogjakarta

2014

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Sejarah Imunologi Infeksi

Sejak 132 SM sudah menjadi pemikiran orang-orang untukmemahami fenomena yang terjadi dalam tubuhnya

Sampai th 1700 an, percobaan para ahli mengarah pada

pembuatan vaksin

Pada 1845, Ellie Metchnikoff mencoba mengungkapkan

bagaimana mekanisme sel imun bekerja melawan benda asing,dengan menusukkan sebatang duri bunga mawar ke dalam

larva bintang laut, dan tampaklah kerumunan sel di dekat duri

bunga. Metchnikoff berkesimpulan bahwa sel yang dapat

bergerak (mobile) itu terlibat dalam respon imun, dengan kata

lain, respon imun bersifat SELULER. Hal serupa juga diamati oleh Koch dan Neiser

FAGOSITOSIS


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Sejarah Imunologi Infeksi

Penelitian dilanjutkan Fodor, 1886 yang menentang teori

seluler karena ia mengamati pengaruh serum imun terhadap

mikroba tanpa campur tangan komponen seluler.

Behring dan Kitasato (1890) juga mengukuhkan pendapat

tersebut dengan percobaan yang menunjukkan bahwa serumimun dapat menetralkan aktivitas tetanus dan difteri

Jules Bordet (1870-1961) ilmuwan muda mengemukakan

teori bahwa untuk melumpuhkan bakteri diperlukan 2

komponen yang masing-masing punya karateristik sendiri.

Dia juga menemukan komponen termostabil (antibodi) dan

termolabil (komplemen) HUMORAL


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immunology

is the future of medi ine


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Konsep Dasar Imunologi Infeksi

Infeksi dapat terjadi karena interaksi unik

antara host dan agen infeksi:

Faktor virulensi agen

(antigenisitas/imunogenisitas)

Sistem imunitas host

Escape/evade mechanism agen

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ASPECT OF HOST PARASITE RELATIONSHIP

1. Entry of the parasite

2. Multiplication and spread

3. Pathology4. Natural immunity

5. Adaptive immunity

6. Immunopathology

7. Parasite survival mechanism

8. Host-parasite balance

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1. Faktor Virulensi AgenFaktor yang membuat suatu agen menjadi patogenik

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IMMUNOGENICITY / ANTIGENICITY

SURFACE STRUCTURES OF PATHOGENS

BACTERIA

Gram-positive

Gram-negative

Mycobacteria Spirochaete


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VIRUSES

Viral proteins

(virion, infected cell membrane)

PARASIT

Surface membrane

Excretory - Secretory (ES Ag) ,Granules (Gra)


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1.1 Route of Microbial entrySite of entry Method of entry Examples

Skin

Wound, burns

Insect bites

Dog bites

Direct penetration

Staphylococcus, Streptococcus

Tetanus

Malaria, Trypanosome, Filaria

Rabies

Schistosome, Hookworm larvae

Nose and throat Attach to cellsAttach to teethAdenovirusesStrep. mutans

Respiratory tract Receptor on epitheliumMucus/ciliary defect

Influenza

B. pertusis

Gut

Attach & penetrate

Attach without penetration

Salmonella, Entamoeba, Polio

Cholera, Giardia, hookworms

Genito-urinary Attach to epithelium gonococcus

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1.2 Multiplication & spread

After entry microorganisms multiply in different

ways:

Virus, fungi, protozoarapidly multiply

Staphylococcus : 3 division/hour Mycobacterium : once in a week

Worms do not replicate

Worms: they may spread locally or

general via blood/lymph They may produce pathology

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2. Sistem Imunitas Host

Bagaimana tubuh menanggapi invasi agen infeksi

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Sistem Imun Host

brief reviewNatural/alami/innate/nave/native:

ada pada tubuh semua orang sehat, dipersiapkan untuk

mengeblok mikroba yang masuk (rapid response/first

line defense)

Adaptive/dapatan/acquired:distimulasioleh mikroba yang menginvasi jaringan, beradaptasi

dengan jenis mikroba yang masuk (second line defense)

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2.1 Natural Immune Response

Selular: fagosit, makrofag, NK sel

Humoral: komplemen, sitokin (TNF, IL-1, IFN)

Fisik:barier endotel, mukus, fili

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Figure 1-4 part 3 of 3


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Video I.21

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Recognitionpengenalan antigen oleh sel

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Video I.23

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2 2 A apt ve Immune Response


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2.2 A apt ve Immune Response

dependent on antigen

recognitionSelular/cell mediated: sel limfosit T,

makrofag

Humoral: limfosit B (antibodi)

Kombinasi:ADCC (Antibody Dependent

Celular Toxicity)

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Specific mmune Responses

Selective attack aimed at "target" following prior exposure

Two classes of responses:

Humoral immunity - antibodies produced by B lymphocytes

Cell-mediated immunity - activated T lymphocytes
http://health.howstuffworks.com/immune-system11.htmhttp://www.blink.uk.com/immunoanimations/index1.htmlhttp://www.blink.uk.com/immunoanimations/index1.htmlhttp://health.howstuffworks.com/immune-system11.htm


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Lymphocytes:

Originate as stem cells in the

bone marrow

Some migrate to the thymus &

develop into T-cellsOthers remain in the Bone

marrow & develop into B-

cells.

Both B- & T-cells then migrate

to lymphoid tissue.


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Function of B and T Cells

B lymphocytes (or B cells)

most effective against bacteria & their toxins

a few viruses

T lymphocytes (or T cells)

recognize & destroy

body cells gone awry (non-self),

including virus-infected cells &

cancer cells.


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How B T cells recognize

unwanted cells other material?

Antigen = foreign protein (e.g., an antigenic protein from the outer

surface of bacterium or parasites)

Each B & T cell has receptors on surface for binding with a particular

antigen.

B-cells: Antibody-mediated immunity

B-cells that bind with an antigen will subsequently differentiate into

Plasma cells & Memory cells

Plasma cells - begin to produce antibodies (up to 2,000 per

second) Memory cells - remain dormant until a person is again exposed

to the same antigen


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Mekanisme sel B memproduksi Antibodi

The B cell uses its receptor to bind a

matching antigen, which it proceeds toengulf and process.

Then it combines a fragment of antigen with

its special marker, the class II protein (on

surface of cell membrane)

This combination of antigen and marker is

recognizedand boundby a T cell carrying a

matching receptor.

The binding activates the T cell, which thenreleases lymphokinesinterleukinsB cell

transform to plasma cellproduce antibody


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Hummoral immunityAntibodies

Grouped into 5 subclasses:

1. IgM - B cell surface receptor for antigen attachment;

secreted early in an immune response

2. IgG - most abundant antibody; produced in large numbers

3. IgE - mediator for common allergic responses(hay fever,asthma, & hives)

4. IgA - found in secretions of digestive, respiratory, urinary,

& reproductive systems, as well as in breast milk and in

tears5. IgD - found on the surface of many B cells; function is

unknown
http://rex.nci.nih.gov/PATIENTS/INFO_TEACHER/bookshelf/NIH_immune/html/imm19.htmlhttp://www.maxanim.com/immunology/IgE%20Mediated%20(Type%20I)%20Hypersensitivity/IgE%20Mediated%20(Type%20I)%20Hypersensitivity.htmhttp://www.maxanim.com/immunology/IgE%20Mediated%20(Type%20I)%20Hypersensitivity/IgE%20Mediated%20(Type%20I)%20Hypersensitivity.htmhttp://www.maxanim.com/immunology/IgE%20Mediated%20(Type%20I)%20Hypersensitivity/IgE%20Mediated%20(Type%20I)%20Hypersensitivity.htmhttp://www.maxanim.com/immunology/IgE%20Mediated%20(Type%20I)%20Hypersensitivity/IgE%20Mediated%20(Type%20I)%20Hypersensitivity.htmhttp://rex.nci.nih.gov/PATIENTS/INFO_TEACHER/bookshelf/NIH_immune/html/imm19.htmlhttp://rex.nci.nih.gov/PATIENTS/INFO_TEACHER/bookshelf/NIH_immune/html/imm19.htmlhttp://rex.nci.nih.gov/PATIENTS/INFO_TEACHER/bookshelf/NIH_immune/html/imm19.htmlhttp://rex.nci.nih.gov/PATIENTS/INFO_TEACHER/bookshelf/NIH_immune/html/imm19.html


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Video 10.IV 1


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Respon Imun mengeradikasi agen infeksi


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M ll


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Memory cells:

remain dormant but respond quickly if exposed to the antigen a

second time

responsible for SECONDARY RESPONSE, a response so fast &

effective that infection is typically prevented. form the basis for long-term immunity

Primary and Secondary antibody responses


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Active immunity vs.

Passive immunity

Active('natural') = production of antibodies as a

result of exposure to an antigen (immunization)

Passive = direct transfer of antibodies formed by

another person (or animal), e.g., transfer of IgGantibodies from mother to fetus across placenta

or in colostrum ('first milk') OR treatment for

rabies or poisonous snake venom
http://www.cat.cc.md.us/courses/bio141/lecguide/unit3/u3fg26.htmlhttp://www.cat.cc.md.us/courses/bio141/lecguide/unit3/u3fg26.html


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Vaccine

As long ago as the 5th century B.C., Greek physicians notedthat people who had recovered from the plague would neverget it again - they had acquired immunity.

This is because, whenever T cells and B cells are activated,

some of the cells become "memory" cells. The next time that

an individual encounters that same antigen, the immunesystem is primed to destroy it quickly.

The degree and duration of immunity depend on the kind of

antigen, its amount, and how it enters the body.

An immune response is also dictated by heredity; some

individuals respond strongly to a given antigen, others weakly,and some not at all.


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Development of memory B cells and effector B cells (plasma cells) occurs in two

phases.

Short-lived plasma cells that make mostly IgM (but some IgG) are generated

during the primary response and occupy sites, such as lymph nodes. The second phase involves the formation of the memory B-cell pool and

seeding of long-lived plasma cells to the bone marrow.


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Pasive immunity

Infants are born with relatively weak immune responses. They

have, a natural "passive" immunity; which protect them during thefirst months of life by antibodies they receive from their mothers.

The IgG which travels across the placenta, makes them immune to

the same microbes to which their mothers are immune.

Children who are nursed also receive IgA from breast milk; it

protects the digestive tract. Passive immunity can also be conveyed by antibody-containing

serum obtained from individuals who are immune to a specific

infectious agent. Immune serum globulin or "gamma globulin" is

sometimes given to protect travelers to countries where hepatitis is

widespread. Passive immunity typically lasts only a few weeks


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Active immunity

Active" immunity can be triggered by both infection andvaccination.

Vaccines contain altered microorganisms will produce an

immune responses.

Some vaccines are made of killed microbes.

microbes that have been changed slightly so they can no

longer produce infection or unable to multiply.

Some vaccines are made from a live virus that has been

weakened, or attenuated, by growing it for many cycles in

animals or cell cultures.


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2.3 Imunopatologi

Adaptive immunity are potentially dangerous

to the host for 2 reasons:

1. effector mechanism may pasively damage

uninfected host tissue (hypersensitivity)

2. antigenic similarity between host and

parasites (mimicry)response originally

directed to parasite may also targetted to hosttissue (autoimmunity)

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3. Ecsape/evade Mechanism

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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

Min respond to IFN-stimulus

others: anatomic sequestration, antigenic mimicry,

antigenic variation (parasites)


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PARASITE ESCAPE MECHANISM

Type Effector mechanismconcealment Intracellular

Capsule

Cysts

Mimicry of host

Host antigen coating

variation Mutation, recombination,

Gene switching

supression Non-specific

Specific tolerance bymacrophages

T suppressor cells

Parasite products


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Immunology is

fun fun fun!

Imunologi Infeksi Tropis

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