INNATE (NON-SPECIFIC)

IMMUNITY

Agus Supriyadi
Dr. Wiryawan Permadi, SpOG (K)
 INTRODUCTION

Immune : Combination of cell, molecul, tissue

system Resistancy/ immunity againts infection
Maintain it’s solidity

Immunity  Natural (non specific)

consist of:  acquired (specific)
3.5% of population  autoimmun disease

Grave disease/hypethyroidsm

94% Type I DM

Anemia perniosa

Rheumatoid arthritis

Thyroiditis vitiligo

Multiple schelrotic
 Non Specific immunity system

Non specific to foreign

First defence system substance

Always ready and quick

response
Cellular barriers : Physical/mechanical barriers
-Phagocyt
-Macrophage
-NK cell Biochemical barriers
-Mast cell
Humoral barriers :
complemen, interferon, acute
phase protein collectin
 Humoral Barriers

Consist of some protein

Complement There are 9 basic complement

(C1-C9)

Function:
- Protect against infection
- Inflamation response (anaphylatocyn,
hematoxin, immune adherence, opsonin)

Complement system activated by:

- Classic route  by immune complex
- Alternatrive route + lechitin route  NO
 Classic route

Activation begin from C1

Protein is activated step by step

Result product 
C1 C2+C4 catalyze next reaction
glycoprotein  C3b  active C5, C6,
immune C7, C8, C9
C3a as
complex/C3 anaphylatocyn :
convertase
- Non scriate muscle contraction
- increasing capilary permeability
- Hystamin release
 Lipid A endotoxin

Active 1
classic
route protease
2

Uric crystal
3
4
5
Polynucleotide
CRP
 Alternative route

Begin from C3 (Without using C1, C2

and C4)

Started by bacteria’s cell wall

- Bacteria (endotoxin)
- Fungi, viruses, parasite
Clinic:
- IgA, IgG4
• C5-C9 deficiency  meningococcus
- Nepthritis factor
infection, gonorrhea
• C2 deficiency  lupus, glomerulonephritis
• C1-C4 deficiency  immune complex
disease
Overview of the main components and effector actions of complement
The Janeway CA, Traver P, Halport M, Jhlomchit MJ. The specific Immunns respons. 5th edition
 Interferon

Cytocin like Could activate NK

glycoprotein cell
Antiviral character
produced by
macrophage
 ACUTE PHASE PROTEIN
C-Reactive protein / CRP

Increasing concentration in
blood acute infection
Measurement 
inflammation activity
Activate classic route

CRP still increasing 

persistence infection
 Mannan Binding Lectin (MBL)

Acute phase
reaction Act as
opsonin

Collectin

Protein functioning  opsonin  carbon binding  complex

Binded by phagocyt receptor

 CELLULAR BARRIERS
Mononuclear phagocyt
Monocyt
functioned as: Cytocin production

Remodelling and fixing

tissue Complement’s
component production

Macrophage
Monocyte cell produced by bone
Differentiation Macrophage
marrow
MONONUCLEAR PHAGOCYT STAGE
Karmen B. Immunologi dasar.. Jakarta: Fakultas Kedokteran Universitas Indonesia
 Phagocytosis started

Catch, eat
Destruct and digest

Phagocytosis

Chemotocsic
Polymorphonuclear phagocyt / granulocyt
- Produced by bone marrow
- 60-70% amount of normal leucocyt
- Devided by hystological dye:
- Netrophil
- Eosinophil
- Basophil
Basophil and Mast cell

Only at vascular related tissues

• increasing vascular
permeability
Function as:
• Inflamatory reponse
• Bronchial muscle contraction
 K cell and NK cell

37% lymphocyte in bone

marrow

Cytotoxic lymphocyte

Cytotoxic product : perforin,

serin protease, nuclease, TNF,
ligan fas
 DETERMINAN
Specific part of
antigen’s
macromolecul
which bind with Influenced
antibody factors

Species Genetic and hormon temperature Nutrition Normal flora

age factor bacteria
 REPRODUCTION IMMUNITY

Fetus carry paternal MHC

1

Maternal respons
2

Maternal blood antibody

3
4
5
Immunocompetent lymphocyt

Fetal throphoblast
 Autoimmune Reproduction Disorder

Autoimmune endometriosis
- Peritoneal milleu (PG, cytocin)
 Ovulation failure, luteolysis, adhetion, implantation disturbance, tube
function disturbance

Autoimmune orchytis

- Inflamation testicular infiltration  spermatogenic function   azoosperm

Autoimmune premature ovarian failure

- Etiology : genetic, chemotherapy, injury, ovarian surgery, enzyme

defficiency, idioplatic

- Effect :  gonadotropin, amenorrhea, lipoestrogenism before

40 years old
 Man Infertiity

Aglutinin antibody 
nonmotile sperm
Vasectomy  immune
responce

10%  isoimmune
reaction
 Complement deficiency

Recurrent bacterial infection

 Sensitivy  autoimmune disclose

• Congenital >>
• Physiologic
• Acquired
• C1 defisiency hereditary angioedema
• C2 + C4 deficiency  LES
• C3 deficiency  pyogenic microbal infection
• C5 deficiency  chemotacys disturbance
• C6, C7, C8 deficiency  gonococcus, meningococcus
infection
Lisozym and interferons deficiency

 Cause by protein / calory malnutrition

 Imunonukleosis infection

NK cells deficiency

 Congenital  osteoclast defect

 Aquired  radiation and immunosuppretion
 Phagocyt system deficiency

 neutrophyl production  chemotherapy,

leukemia, reticular dysgenesis

 Detruction  oxacilin ;quinidin

Chediok-Higashi syndrome
Glucose-6-phosphate dehydrogenase
deficiency Job syndrome

Mieloperoksidase defisiency Adhetion leucosit defisiency

 CONCLUSION

NON SPECIFIC IMMUNE MECHANISM

- Not antigen-specific
- Immediately response
- Fast response
- Not exposure
- Response is antigen independent

Disadvantage
- Over reaction
- Exposure results in no. Immunologic memory
 - Complement system
- Interferons
Humoral - Acute phase protein
barriers - Lysozyme
- Interleukin

- Phagocyt cells
Cellular - Mast cells
bariers - NK cells
Determinant  immune system
- Species
- Hereditary and age factors Reproduvtive autoimune disease
- Hormon - Autoimmune endometriosis
- Nutrients factors - Autoimmune orchitis
- Temperature - Autoimmune ovarian premature
- Normal microorganism failure
- Infertility

Immune defisiency
- Complement defisiency
- Interferons defisiency
- Phagocyt system defisiency
THANK YOU