1. Lymphatic/Immune
System

2. Lymphatic/Immune System:
Major Role:
The main role of the immune
system is to destroy and remove
invading microbes and viruses
from the body. The lymphatic
system also removes fat and
excess fluids from the blood.
Major Organs:
Lymph, lymph nodes and vessels,
white blood cells, T- and B- cells.

3. SIRKULASI LIMFATIK
• cairan & protein yg berlebihan yg disaring
melalui kapiler sistemikyang berada di
ruang interstitial akan di angkut oleh
pembuluh limfe dalam bentuk cairan
limfe(cairan limfe)
• Untuk kemudian dikembalikan ke sirkulasi
sistemik melalui pembuluh2 pengumpul yg
letaknya dekat dengan vena yg
bersangkutan

4. Pembuluh limfe
• Membawa cairan limfe melalui ductus
thoracicus dan ductus lymphaticus dexter
ke dalam sistem vena subclavia (sirkulasi
limfe)
• Limfe : cairan jaringan yang mengandung
faktor pembekuan darah, protein, lemak
dan limfosit.

5. SISTEM LIMFOID
Limfosit terdapat di seluruh tubuh, dan
cenderung terpusat dalam jaringan limfoid
Yang termasuk Jaringan limfoid : kelenjar
limfe, limpa, timus, jaringan limfoid yg
berhubungan dengan permukaan mukosa,
& sumsum tulang

6. Kelenjar limfe
Paling banyak
Merupakan nodul nodul jaringan limfoid yg
diselubungi kapsul dan terdapat pada tiap
bagian tubuh

7. Limpa
Massa besar yg tdd limfosit & makrofag yg
dirangkai dalam aliran darah
Sinusoidnya dipenuhi oleh darah dan
diantaranya terdapat nodulus jaringan
limfoid

8. Timus
• Jaringan limfoid yg
terletak dalam
rongga dada
anterior & bagian
atas jantung dan
pembuluh2 darah
besar

9. Edema
• Akumulasi cairan di bagian interstisial,
yang menyebabkan pembengkakan
jaringan
• Penyebabnya adalah:
• hal hal yang menyebabkan keluarnya
cairan dari pembuluh darah:
1. Peningkatan tekanan darah, permeabilitas
kapiler
2. Katup vena yang inkompeten, penyumbatan
pembuluh darah
3. hypoproteinemia, protein plasma berkurang shg

10. Edema
• Kegagalan cairan
interstitital diangkut
oleh pembuluh limfe,
akibat
• Penyumbatan
(pengangkatan)
pembuluh limfe e.g
elephantiasis, post
mastektomi ec Ca
mammae

11. Defence Mechanisms
 non-specific ; inflamasi
 specific

12. Inflammation
The body’s response to
injury

13. Inflammation
Signs and Symptoms
Anatomical:
Redness, swelling, heat, pain, poor
function.
Histological:
Leukocytes accumulate in inflamed
tissues.

14. Inflammation
Degrees of severity
Acute:
Short duration (hours, days)
Possible neutrophil influx
Chronic:
Long duration (weeks, months)
Immune system recruited
(lymphocytes)

15. Inflammation
Underlying Mechanisms
Blood vessels: changes in diameter
and permeability.
Leukocytes: chemotactic emigration.
Both regulated by the production and
release of inflammatory mediators.

16. Inflammation
Inflammatory Mediators
 Derived from plasma proteins:
• e.g. products released during
clotting.
 Derived from cells:
• e.g. histamine, cytokines.
Only released/act locally.
(hormonal-like specificity)

17. Inflammatory
Response Tissue Pathogen
damage
Chemical
mediators
Increased released Chemotaxis
vascular
permeability
Increased numbers of
Fibrin mesh white blood cells
isolates injury site at injury site
Pathogens contained
& destroyed

18. Chemical defences
1. Complement
• group of about 20 serum proteins
• when combined with foreign substances a
“complement cascade” is activated
• complement proteins rupture bacterial membranes
2. Interferon
• stimulate body cells to resist viral infection
• inhibits viral replication

19. The Immune System
•Specific: via receptor ligand interactions
• Acquired: via “education” of
lymphocytes Memory: via survival of
lymphocytes
•Systemic: via emigration of
lymphocytes.

20. The Immune System
Specificity is driven by receptor-ligand type
interactions.
Two main pathways:
1. Humoral pathway (involves B lymphocytes).
2. Cell mediated pathway (uses T lymphocytes)

21. Humoral Pathway
ANTIBODIES: proteins secreted
by activated B lymphocytes, that
bind to antigens
(immunoglobulins).
ANTIGENS: any chemical which
elicits an immune response
(usually foreign).

22. B-lymphocytes
Produce antibodies against foreign proteins
5 main classes
1. IgG - most abundant
2. IgM - first circulating Ig released
3. IgE - involved in inflammatory responses
4. IgA - body secretions
5. IgD - surface receptor

23. Antigenic Determinants
Different
antigenic
determinants
Antigen

24. Humoral Response

25. Humoral Response
Consequences of immune complex
formation.
1. Neutralisation of toxic antigens.
2. Activation of leukocytes.
3. Formation of inflammatory mediators.
4. Destruction of bacteria.

26. Cell Mediated Response
Antigen-receptor interactions occur on the
cell surface.
Two types of interaction:
 Antigen presenting cells (APC) and Helper T
cells.
 Cytotoxic T cells and abnormal cells.

27. Cell Mediated Response
APC
Antigen Helper T cell
MHCII
MHCII-antigen T-cell
complex receptor
Cytokines
Released
MHC = Major-Histocompatibility-Complex molecule.

28. Cell Mediated Response
Infected Cell Cytotoxic
Virus T cell
MHCI
MHCI-antigen T-cell
complex receptor
Infected cell
Killed

29. Cytotoxic T-cell Response
Cell lysis
initiated
Virus infected cell
Time
Killer T cell

30. “Education” by Clonal Selection
ATTACK
Memory cells

31. Reaksi Alergi
= Hipersensitivitas merupakan
keadaan cedera tubuh akibat
interaksi antara antigen dan antibodi
Reaksi Alergi ada 4 tipe yaitu :
1. Reaksi tipe I (anafilaktik),
diperantarai oleh antibodi IgE yang
terikat pada permukaan sel mast.

32. 2. Reaksi tipe II (Sitotoksik),
diperantarai oleh antibodi IgG atau
IgM yg bereaksi dengan antigen
pada permukaan sel target
– ADCC (antibody dependent, cell-
mediated cytotoxic)

33. 3. Reaksi tipe III (Kompleks imun),
diperantarai melalui pembentukan
kompleks-kompleks antigen antibodi,
sebagian besar dengan antibodi Ig G
Reaksi tipe IV (diperantarai sel),
diperantarai oleh limfosit T yg
mengalami sensitisasi
 dematitis kontak alergi

34. SINDROM IMUNODEFISIENSI
Keadaan dimana jaringan limfoid
tidak dapat bereaksi secara normal
thd berbagai antigen
Primer (genetik), cth:
agammaglobulinemia terkait-X
(defisiensi sel B),
Sekunder, cth: keganasan, AIDS

35. AIDS
Bentuk spektrum imunologis & klinis yg
paling ekstrim dari infeksi HIV
HIV ditransmisikan melalui kontak
seksual, darah atau produk darah yg
terinfeksi, & cairan tubuh tertentu, serta
melalui perinatal
HIV menginfeksi sel molekul CD4 (limfosit
T4), monosit, makrofag, dendrit,
Langerhans dan mikroglia

36. Setelah virus memasuki sel RNA nya
ditranskripsi menjadi DNA. DNA yg baru
saling bergabung masuk sel target dan
membtk provirus. Provirus ini
menghasilkan protein virus baru yg
merupakan pabrik bagi virus yg baru.
Sel target normal akan membelah dan
memperbanyak diri, pd keadaan ini
provirus menyebarkan anak-anaknya

37. TERIMA KASIH