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GOOD

R DAY

HOPING ALL OF YOU


IN
GOOD CONDITION
AND
SORRY CAN
I D’NT USE
UNDERWEAR
ENJOY THIS LECTURE
3/17/2019 1
HOST DEFENCE
Randanan Bandaso
Dept of Pathology
Faculty of Medicine
Hasanuddin University

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CURRICULUM VITAE

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3/17/2019 4
EDUCATION
 Faculty of Medicine Unhas 1969
 MSc Mahidol University Bangkok 1975
 Surgical Patology FK Unhas 1978
 Forensic Patology FK Unhas 1988
 Andrology Monash
University Melbourne Australia 1989
 DFM Netherland 2001
POSITION
 Retired Professor Faculty of
3/17/2019
Medicine Hasanuddin University 5
MOU
1. I WILL USE ALL MY ABILITY TO TEACH
YOU.
2. YOU HAVE TO PAY FULL ATTENTION TO
THIS LECTURE, OPEN YOUR EYES AND
EARS SO YOU CAN CATCH AS MUCH AS
POSSIBLE THIS LECTURE
3. FOR THOSE WHO ARE NOT INTERESTED
THIS LECTURE, D’NT BOTHER YOUR
FRIENDS AND I D’NT MIND IF GO OUT

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COMMENTS ON
MY LECTURE

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BAD COMMENTS

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SOME COMMENTS OF THE STUDENTS
IN THE SECOND SEMESTER Block 1 (Immunology)

 Lack of communication with students


 Improve communication skills
 Not so good explanation an elaboration.
Give some more examples.
 Make it more interesting, speak clearly
 Need to give the student understanding on
what he teaches.Don’t teach to fast
because we us a student need apropriate
time to understanding the topic
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COMMENT OF THE STUDENT
IN THE SECOND SEMESTER Block 1 (Immunology)

 Don’t to fast if talking and English bad.


The most important things is change the
illustration of the slide and put more
information about the subject in the slide
 Use english and Indonesian it can help
 No suggestion for the lecture except
please increase the quality of the
presentation and speaks English more
clear
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GOOD COMMENTS

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COMMENT OF THE STUDENT
IN THE SECOND SEMESTER Block 1 (Immunology)

 Good Lecture, explanation complete.


 Thank for teaching, like Dr.Randanan as
well, keep up a good work doctor
 Good explanation in lecture
 I like the way he teaches us

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THE PURPOSE OF THIS LECTURE

AT THE END OF THIS LECTURE YOU


SHOULD UNDERSTAND:
THE MECHANISM OF HOST DEFENCE:
PHYSICAL, CHEMICAL,
REFLEX, IMMUNORESPONSE
HOMEOSTASIS.
DEFECT IN IMMUNO RESPONSE
ACTIVE AND PASSIVE
ACQUIRED IMMUNITY
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MAN

OBSERVED

RECOVERY FROM INFECTION


 IMMUN

JENNER : VACCINATION OF SMALL FOX


SUCCESFULL APLICATION OF OBSERVATION
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H0W ANIMAL

BECOMES IMMUNE
NATURAL AND ARTIFICIAL

IMMUNOLOGY
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THE PIONEER
OF
IMMUNOLOGY

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3/17/2019 LOUIS PASTEUR (1822-1895= 73 THN) 17
(ATTENUATED VACCINE 1880)
3/17/2019 ELIE METCHNIKOFF (1845-1916 = 71 ) 18
(PHAGOCYTOSIS, CELLULAR DEFENSE THEORY)
3/17/2019 ROBERT KOCH (1843-1910 = 67) 19
(THE FOUNDER OF THE CAUSES TUBERCULOSIS)
3/17/2019 EDWARD JENNER BOOK (1798) 20
(THE FOUNDER OF THE VARIOLE VACCINE)
KIKI
KINTAN SANGKALA

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THE FOUNDER OF IMMUNOLOGY
Holy Bible
Genesis 1: 26-27
26. Then God said, let us make man in
our image, according to Our
likeness,……
27. So God created man in His own
Image; in the image of God. He
created him male and female. He
created them.
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GOD
GOD
GOD MUST
CREATED THE
MAN SAME
IN HIS WITH
IMAGE MAN

HAS TWO
ETES AND EARS
ONE NOSE

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WHAT DOES IT MEANS
THE MAN IS
VERY PERFECT
COMPLETE AND
SOPHISTICATED

MORE SOPHISTICATED
THEN THE MOST SOPHISTICATED COMPUTER
IN THE WORLD
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THE WORLD
FULL OF MICROORGASME Because
God created
Created
human-being
Very perfect
And
Sophisticated
More sophisticated
Than the most
BACTERIA,VIRUS, PARASITES Sophisticated
Computer
In the world

INFECTION UNCOMMON
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God gives
NATURAL RESISTENCE
ANATOMIC BARRIER
PHAGOCYTOSIS
COMPLEMENT

HOST DEFENCE

LOCAL
BACTERIA,VIRUS, PARASITES SYSTEMIC

NONSPECIFIC
SPECIFIC

HUMORAL
CELLULAR
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HOST DEFENCE

LOCAL
SYSTEMIC

NONSPECIFIC
SPECIFIC
BACTERIA,VIRUS, PARASITES

HUMORAL
CELLULAR

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AGE

NUTRITIONAL

PSYCHOLOGICAL
HORMONAL

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HOST DEFENCE

SENSATION/REFLEX PHYSICAL DEFENCE

HOMEOSTASIS CHEMICAL DEFENSE

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IMMUNORESPONSE 29
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REFLEX AND SENSATION
MOSQUITO
FLY

FEELING

THE HAND
WILL FLAP
IT
PULL

HOT OR COLD
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TOUCH
HOMEOSTASIS

STABILIZATION
OF PHYSIOLOGICAL FAIL OR EXCEED
CONDITION
IN
THE BODY DISEASES

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HOMEOSTASIS

STABILIZATION OF INTERNAL ENVIROMENT IN THE BODY

ANY CHANGES  STABILIZATION 


THE BODY MAINTAIN PHYSIOLOGICAL CONDITION

FAIL OR EXCESSIVE  DISEASES


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MECHANISM OF HOMEOSTASIS
AUTOREGULATION EXTRINSIC REGULATION

HYPOXIA
NERVE SYSTEM
OR ENDOCRIN SISTEM

SUBSTANCES THE BODY NEED OXIGEN

HEART BEAT INCREASE


THE BLOOD MORE LIQUID
BLOOD SUGAR
INCREASED
O2 MORE EASY COMES
THE CELL INREASE INSULIN
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HOMEOSTASIS FAILED

BLOOD PRESSURE
EAT TO MUCH DROPS

BLOOD SUGAR INCREASED ADRENALIN


INCREASED

INSULIN FAILED FAILED BLOOD P DROPS


TO MUCH  HYPERTE
TO INCREASE  DM
NSION
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BLOOD PRESSURE ADRENALIN

BLOOD FLOW

KIDNEY
TUMOR

BLOOD FLOW

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NON SPECIFIC IMMUNITY

LOCAL
BODY SURFACE PRODUCTION OF CHEMICAL
ANTI MICROBES

DISCHARGE BACTERIAL
MICROORGANISME INTERFERENCE
FROM THE BODY (Lactobacillius)

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HOW HUMAN BODY PROTECT ITSELF

RESP/DIGES
SKIN
TRACT

BATHED A PROTECTIVE LACTIC ACID


FLOWING LAYER OF OTHER SUBSTANCE
MUCUS IN SWEAT

TRAP,DISSOLVE AND MAINTAIN ACIDIC pH


SWEEP AWAY PREVENT COLONIZATION
FOREIGN SUBSTANCES OF BACTERIA

RELATIVELY STATIC  IN TIME OF NEEDS  CAN BE ENHANCED


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NON SPECIFIC IMMUNITY

FIRST LINE SCOND LINE

SKIN,
SKIN FAT, MONOCYT
NORMAL MACROPHAGE
FLORA OF THE SKIN, GRANULOCYTE
HIGH TEMPERATURE, NEUTROPHYL
MUCOUS, GASTRIC ACID EOSINOPHYL
SALIVA, PERISTALTIC, BASOPHYL
COUGH, TISSUE UNDER SKIN
NORMAL FLORA OF TISSUE UNDER MUCOUS
SKIN,COLON, VAGINA
AND MOUTH
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EPITHELIAL CELLS
AS CENSOR TO INFECTION
OF BACTERIA

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TO PRODUCE INFECTION
 MICROORGANISME TO PRODUCE
INFECTION  SLIP TO THE BARRIER
OF SURFACE DEFENCES
 THIKNESS OF EPITHELIAL IS
DIFFERENT
 NONSPECIFIC

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HOST DEFENCE AGAINST ATTACHEMENT TO EPITHELIAL CELL

NORMAL MICROBIAL
FLORA,
ANTIBODY ON MUCOUS
LOCAL FACTOR:
SURFACE  Ig A
FIBRONECTIN,
LACTOFERIN
GLYCOPROTEIN
pH

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bacteria

stimulate

epithel
cytokin

lymphocyte
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macrophage
CELLULAR SYSTEM OF
SYSTEMIC IMMUNITY

PROFESIONAL PHAGOCYTIC NONPROFESIONAL


PMN PHAGOCYTIC
MACROPHAGE ENDOTHELIAL, EPITHELIAL,
FIBROBLAST

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SIGNIFICANCE OF EPITHELIAL
CELL PROLIFERATION
 MICROBIAL ATTACHEMENT IS NOT NECESSARY
FOLLOWED BY CELL PENETRATION
 M.PNEUMONIAE, C.DIPHTERIAE,
B.PERTUSSIS,V.CHOLERA  SURFACE
 SHIGELLA PENETRATE EPITHELIAL CELL
 SALLMONELA  PROCEED TO SYSTEMIC
INFECTION
 INTRAEPITHELIAL PATHOGENS  PROTECTECTED
FROM ANTIBODY, ANTIBIOTIC, AND INGESTION
AND KILLING BY PMN
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SUPERFICIAL

INTRACELLULAR

PENETRATE EPITHELIAL

ENTER BLOOD VESSEL


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SYSTEMIC INFECTION
DISCHARGE MICROORGANISME FROM THE BODY

10 TRILIUN

DEFECATION
MUCOCILIARY ELIMINATE
10.000.000.000.000/DAY
ESCALATOR
URINATION ELIMINATE
OF RESPIRATORY BACTERIAL
TRACT COLONIZING IN URETHRAL
OROPHARYNX EPITHELIUM.
COUGH OR RETENTION OF URINE
SWALLOWED ENHANCE
DESQUAMATION THE RISK OF INFECTION
OF EPITHELIAL SALIVATION,LACRIMATION,
CELL REMOVE LARGE SNEEZING
DISPLACE POTENTIALLY
AMOUNT OF
INFECTIVE
BACTERIAL
3/17/2019 MICROORGANISME 48
NORMAL MICROBIAL FLORA
(COMMENSALS)

BACTERIA, VIRUSES,FUNGI,PROTOZOA
LIVE ON OR WITHIN THE HUMAN HOST
BUT RARELY CAUSE DISEASE

OROPHARYNX: streptococci, neisseria,


Hemophylus, Bacteroides, spirochetes

SKIN: Staphylococci, Diphteroid

LARGE INTESTINE: Streptococci,


Enterococci, Clostridia,Lactobacili,
Enteric bacilli, Bacteroides

VAGINA; Streptocci, Lactobacilli,


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Normal Flora Pathogens

Difficult
To differentiate

SYMPHTOM AND SIGNS


OF INFECTION
NO SYMPHTOMS
AND
COUGH AND FEVER
SIGNS
INFLAMMATORY CELL

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ISOLATION IS A DIAGNOSTIC
OBLIGATE PATHOGEN OF INFECTION

INFECTION OCCUR
OPPURTUNISTIC INFECTION IN IMMUNOCOMPROMISED HOST

THE SYMBIOSIS BETWEEN


THE COMMENSAL
COLONIZATION DISTURBED 
OVERGOWTH OF
EXOGENOUS BACTERIA

REPLACEMENT
NOSOCOMIALLY
OF NORMAL FLORA
ACQUIRED
IN THE HOSPITAL
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 RESISTENT TO MULTIPLE AB
INFLAMMATION
 BLOOD SUPPLY INCREASED
GLUCOSA
OKSIGEN
 INCREASED IN CAPILLARY
PERMIABILITY
 MIGRATION OF NEUTROPHYL,
MACROPHAGES, LYMPHOCYTE

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INFLAMMATION
BLOOD SUPPLY INCREASED
GLUKOSA MICROORGANISM
OKSIGEN

INCREASED
PERMIABILITY

MACROPHAGE

NEUTROPHYL

LYMPHOCYTE

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TUMOR
CALOR
RUBOR
DOLOR
FUNCTIO
LAESA

MUCUS IN CERVIX

LACTOBACILLUS

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CONTROL OF INFLAMMATION
 PRODUCTS OF PLASMA ENZYMES
 CYTOKINES
 VASOACTIVE
MEDIATOR
MAST CELLS
BASOPHILS
PLATELETS

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MEDIATOR OF INFLAMATION(1)
 HISTAMINE MAST CELLS +
BASOPPHYL  VASCULAR
PERMIABILITY, SMOOTH MUSCLE
CONTRACTION
 SEROTONIN  PLATLETS  VASC
PERMIABILITY, SMOOTH MUSCLE
CONTRACTION

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MEDIATOR OF INFLAMATION (2)
 IL8  LYMPHOCYTES  MONOCYTE
LOCALIZATION
 C3A  COMPLEMENT C3  MAST
CELL DEGRANULATION + SMOOTH
MUSCLE CONTRACTION.
 BRADYKININ  KININ SYSTEM 
VASODILATATION

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KERATIN

MELANIN

COLOUR OF THE SKIN


PROTECT FROM SUN RAYS
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PHYSICAL DEFENCE BY HAIR
HAIR
PROTECT BODY FROM HOT

EYEBROW
NOSE HAIR

SWEAT AND
INSECT AND DUST
FOREIGN BODY

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PHYSICAL DEFENCE IN RESPIRATORY TRACT

A LOT OF CAPILLER IN NOSE

COVER BY TIGHT EPITHEL

GOBLET CELL PRODUCE MUCOUS

THE CILIA ESCALATES THE MICROBES


AND PARTICLES
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REFLEX DEFENCE IN RESPIRATORY TRACT

COUGH  IRRIATATION
LARYNX, TRACHEA AND BRONCHI

SNEEZING
STIMULATION OF NOSE MUCOSA

LARYNGEAL SPASM 
CHEMICAL, FOREING BODY, WATER
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IMMUNE RESPONSE IN RESPIRATORY TRACT

MUCOUS  Ig A, PMN, SPESIFIC


ANTIBODY

ALVEOLAR MACROPHAGE 
CLEAN THE ALVEOLI
FROM MICROBES
AND FOREIGN BODY

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THE MICROBES ENTER THE BODY THROUGH
THE SKIN

Acid pH and normal flora of the skin,


non saturated fatty acid

Intact skin

Tissue fluid  Lyzosome

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Phagocytosis and inflammations 67
THE MICROBES ENTER THE BODY THROUGH
THE RESPIRATORY TRACT

HAIR OF THE NOSE,HOT TEMPERATURE


IN THE NOSE, SNEEZING,epiglottis

MUCUS AND CILIA, COUGH

Tissue fluid  Lyzosome

Phagocytosis and inflammations

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THE MICROBES ENTER THE BODY THROUGH
THE DiGISTIVE TRACT

SALIVA

MUCUS AND GASRIC JUICE

DEFECATION

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URINATION

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MUCUS IN CERVIX

LACTOBACILLUS

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TAKE A REST
ASK QUESTION
AND TALK TO YOUR
NEIGHBORS

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SUMMARY
OF
NONSPECIFIC RESISTENCE

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MECHANICAL FACTOR OF
NON SPECIFIC RESISTENCE 1

Form a physical barries to the entrance


INTACT SKIN
of microbes

MUCOUS MEMBRANE Inhibit the entrance of many microbes, but not


as effective as intact skin

MUCOUS Traps microbes in respiratory and digestive tract

Together with mucous traps and remove microbe


CILIA
And dust from upper respiratory tract
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ANTIMICROBIAL SUBSTANCE OF
NON SPECIFIC RESISTENCE

INTERFERRON (IFN) Protect uninfected host cell from viral infections

Caused lysis of microbes,promotes phagocytosis


COMPLEMENT Contributes to inflamations, serve us chemotactic
agent

Work with complement to bring about


PROPERDIN same responses as complement.

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OTHERS
NON SPECIFIC RESISTENCE

Ingestion and destruction of foreign particulate


PHAGOCYTOSIS
matter by macrophage and microphage

INFLAMMATIONS Confine and destroy microbes and repair tissue

Inhibit microbial growth and speed up body


FEVER reactions and repair.

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CHEMICAL FACTOR OF
NON SPECIFIC RESISTENCE 1

Destroy bacteria and


GASTRIC JUICE
most toxins in stomach

ACID pH OF SKIN Discourage growth of many microbes

LYZOZYMES Antimicrobial substance in perpiration, tears,


Saliva, nasal secretions and tissue fluid

URINE Wash microbes from urethra


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MECHANICAL FACTOR OF
NON SPECIFIC RESISTENCE 2

LACRIMAL Tear dilute and wash away irritating substances


APPARATUS And microbes

Washes microbes from surface of teeth and


SALIVA Mucous membrane of mouth

EPIGLOTTIS Prevent microbes and dust


from entering trachea

FAECES DISCARD MICROORGANISME


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SPECIFIC IMMUNITY TO
INFECTION

HUMORAL CELL MEDIATED


IMMUNORESPONSE IMMUNERESPONSE

KEY AND HOLE


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ACQUIRED IMMUNITY

ACTIVE PASSIVE

TRANSPLACEN/ ADMINISTRATION
INFECTION VACCINATION OF IMMUNE SERUM
COLOSTRUM

CLINICAL SUBCLINICAL

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IMMUN MOTHER
IMMUN MOTHER

FOETUS IMMUN
FOETUS

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PASSIVE IMMUNIZATION

HORSE
TAKE THE SERUM MAN

IMMUN

TETANUS

3/17/2019 SUFFER TETANUS


82
Cow  Cowpox Human  Small Pox

MILKER

DONOT SUFFER SMALLPOX


EPIDEMIOLOGI OF SMALL POX
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INFECTION IMMUNITY

INSEPERABLE
3/17/2019 84
DEFECT IN IMMUNE RESPONSE

CONGENITAL ACQUIRED

AIDS
DEFICIENT
AGING
T CELL
MALNUTRITION
B CELL
KIDNEY DISEASE
B&T CELL
IMMUNO-
COMPLEMET
SUPRESSIVE
PHAGOCYTOSIS
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RADIATION 85
SUMMARY
 THE BODY IS VERY COMPLEX AND
SOPHISTICATED.
 HOST DEFENCE IS VERY IMPORTANT
TO SURVIVE
 HOST DEFENCE CAN BE PHYSICAL,
CHEMICAL, REFLECS,
BACTERIOLOCIGAL
 NON SPECIFIC OR SPECIFIC
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SUMMARY
 SOME FACTORS INFLUENCES THE
HOST DEFENCE
 IMMUNE RESPONSE CAN BE
DEFICENT CONGENITALLY OR
ACQUIRED
 ACQUIRED IMMUNITY CAN BE ACTIVE
OR PASSIVE.

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