Imunologi Infeksi Tropis
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Transcript of 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!