BASIC IMMUNOLOGY

PRESENTED BY:
AARYA.H.NAIR
FIRST YEAR MDS
DEPARTMENT OF ORAL MEDICINE & RADIOLOGY
CONTENTS
• Introduction
• Cells & tissues of the immune system
• Classification
• Antigens
• Antibodies
• Antigen-antibody reactions
• Normal immune response
• Hypersensitivity
• Immunodeficiency diseases
• Autoimmunity
• Immunology of transplantation & malignancy
• Immunohematology
 INTRODUCTION

Immunology

Response to antigen &

recognition of self/non-self

Immune
Immunity
system
Protection against Cells & molecules
infections responsible for
protection
3
 IMMUNE SYSTEM

LYMPHORETICULAR SYSTEM

LYMPHOID CELLS
RETICULOENDOTHELIA
•Lymphocytes & plasma cells
L SYSTEM
•Responsible for specific
•PMNLS & macrophages
immunity
•Scavenger
LYMPHOID ORGANS
functions,elimination of
microorganisms & other
PRIMARY SECONDARY foreign particles from blood
Spleen,Lymphnodes,
& tissue
Thymus MALT,Lymphoid
Bone marrow tissues in
lungs,liver,gut
 LYMPHOCYTES
• T cellsRegulatory T cells: T helper cells
Suppressor T cells
Effector T cells: Cytotoxic T-cells
Delayed type
hypersensitivity cells
• NULL CELLS: neither T-cells nor B-cells
– Eg: Natural killer cells(NK cells),Lymphokine activator
cells(LAK cells)

• B cells: undergo blast transformation plasma cells

Synthesizes specific antibodies
 PHAGOCYTIC CELLS
• Macrophages: Blood macrophages: Monocytes
Tissue macrophages: Alveolar
macrophages in the
lungs, Kuppfer cells in the liver
• Polymorphonuclear microphages:
Neutrophils
Eosinophils
Basophils
 DENDRITIC CELLS
• Antigen presenting cells
• Langerhans cells suprabasilar portion
of squamous epithelium
 IMMUNITY

INNATE ACQUIRED

SPECIES ACTIVE PASSIVE

RACIAL
NATURAL ARTIFICIAL
INDIVIDUAL
 INNATE IMMUNITY
• Species immunity:
– Eg: B.anthracis infects human beings but not chickens
• Racial immunity:
– Eg: In humans, Afro-americans are more susceptible to
TB than American race
• Individual immunity:
– Eg: Homozygous twins –similar susceptibility /
resistance to infections compared to heterozygous
twins
DIFFERENTIATING FEATURES

• ACTIVE  PASSIVE
– Produced actively by  Received passively
the immune system  Ready-made antibodies
– Infection/contact  Effective immediately
– Effective only after lag  No memory
period  Applicable in
– Memory immunodeficient
– Not applicable in persons
Immunodeficient  Treatment of acute
persons infections
– Prophylaxis
11
 ACQUIRED IMMUNITY
• NATURAL ACTIVE • NATURAL PASSIVE
IMMUNITY: IMMUNITY:
– Acquired by natural – Transferred from the
clinical/subclinical infection mother to foetus/infant
– Eg: Chickenpox infection – Eg: IgG
• ARTIFICIAL ACTIVE
IMMUNITY: • ARTIFICAL PASSIVE
– Produced by vaccination IMMUNITY:
– Eg: Live vaccines: – Through parenteral
MMR,BCG administration of
Killed vaccines: Hepatitis antibodies
vaccine,Salk vaccine – Eg: ATS
V
Sl AGE DISEASE VACCINATION
A No:
C
1 AT BIRTH HEPATITIS B HEP B VACCINE-I
C
I 2 POLIO ORAL PV-0 DOSE
N 3 BIRTH-6 TB BCG
A WKS
T 4 4-6 WKS HEP B HEP B VACCINE-II
I 5 6 WKS DPT,POLIO DPT,OPV-I
O 6 10 WKS DPT,POLIO,HEP B DPT II,OPV II,HEP B VACCINE III
N 7 14 WKS DPT,POLIO,HEP B DPT III,OPV III,HEP B VACCINE IV
S
8 24 WKS HEP B HEP B
C
H 9 9-12 MNTHS POLIO,MEASLES OPV IV,MEASLES VACCINE
E 10 15-18 MNTHS MMR MMR VACCINE
D 11 18 MNTHS DPT,POLIO DPT BOOSTER-I,OPV-V
U 12 24 MONTHS TYPHOID TYPHOID VACCINE
L
13 4-5 YEARS DPT,POLIO DPT BOOSTER-II,OPV-VI
E
 IMMUNE RESPONSE
HUMORAL IMMUNITY
•Mediated by B cells
•Role:
(1)Defense against viruses that
infect through respiratory or
intestinal tracts
(2)Immediate hypersensitivity
(3)Certain autoimmune diseases
CELL MEDIATED IMMUNITY
•Mediated by sensitized T cells
•Can be transferred from donor to
recipient with intact lymphocytes,not
with antisera
•Role:
(1) Delayed hypersensitivity
(2) Infectious diseases
(3) Transplantation immunity
(4) Immunity against cancer
(5) Certain autoimmune diseases.Eg:
thyroiditis
INDUCTION OF CELL MEDIATED
IMMUNITY
Antigen presenting
Foreign antigen
cells

T cells

Memory cells Blast transformation

Effector cells
Cell lysis
Secrete cytokines
HUMORAL IMMUNITY

ANTIGEN

• Introduction evokes  Formed in the serum

immune response & tissue fluids in
• TYPES: response to an
– Complete antigen antigen
– Incomplete
antigen(haptens)

16
• The 2 attributes of antigenicity are:
– Induction of an immune response
– Specific reaction with antibodies or sensitized cells
• The smallest unit of antigenicity

Antigenic Antibody:
determinant/epitope Paratope

Determine the specificity of

immunological reactions
 DETERMINANTS OF ANTIGENICITY
• Size
• Chemical nature
• Susceptibility to tissue enzymes
• Foreignness
• Species specificity
• Isospecicficity
• Autospecificity
• Organ specificity
• Heterogenetic (heterophile specificity)
ANTIBODIES
IgG IgD

IgE

IgM IgA
PRODUCTION OF ANTIBODIES
Follows a characteristic pattern:
Lag phase
Log phase
Plateau
Phase of decline
• Regulated by T cells
• Helper T cells stimulate & suppressor T cells
inhibit antibody production
• The only immunoglobulin that is transported through
placenta IgG
• The earliest synthesized Ig by foetus IgM
• Ig referred to as “Millionnare Molecule” IgM
• Ig responsible for hypersensitivity reactions IgE
• Ig present in Oral Mucous membrane IgA
• Igs present in saliva IgG,IgM,IgA
• Predominant Ig in GCF IgG
 ORAL MUCOSAL IMMUNOLOGY
• Continuous shedding – prevents the bacterial
colonization
• Presence of Langerhans cells
• Production & upregulation of cytokines
• Saliva:
– Igs
– Lactoferrin,myeloperoxidase,salivary peroxidase:
bacteriostatic
– Lysosomes
– Complement
– Orogranulocytes: living PMNs in saliva
• GCF
ANTIGEN-ANTIBODY REACTIONS

USES

In the body/ In Vivo In the laboratory / In

•Immunity Vitro
•Hypersensitivity •Diagnosis
reactions & •Detection &
autoimmune quantification of
diseases either antigens /
antibodies
 CHARACTERISTICS
• Specific
• Entire molecules react
• Surface antigens
• Firm,reversible
• Combination in varying proportions
 PRECIPITATION
REACTIONS
Eg:VDRL test for
syphilis

AGGLUTINATION
Eg:
Paul Bunnel test
Coombs test
DIAGNOSTIC IMMUNOFLUORESCENCE
TESTS
Eg:
For diagnosis of
autoimmune diseases
COMPLEMENT
FIXATION TEST
Eg: Wassermann
reaction NEUTRALISATION
TEST Eg:
Schick test
Antistreptolysin O test
 HYPERSENSITIVITY
• IMMEDIATE TYPE
• Appears & recedes
rapidly
• Antibody mediated
• Passive transfer possible
with serum
• Desensitisation easy but
short lived
• Antigens or haptens,by
any route
• DELAYED TYPE
• Appears slowly in 24-72
hours & lasts longer
• Cell mediated
• Cannot be transferred
with serum
• Difficult but long lasting
• Induction by antigen
injected intradermally or
by skin contact
• COOMB & GEL CLASSIFICATION
– TYPE I: ANAPHYLACTIC
– TYPE II: CYTOTOXIC
– TYPE III: IMMUNE COMPLEX
– TYPE IV: DELAYED OR CELL MEDIATED
ALLERGIC MUCOSAL REACTIONS TO
SYSTEMIC DRUG ADMINISTRATIONS
• “Stomatitis medicamentosa”

Lichenoid eruptions
•Amphotericin B
•Captopril
•Fenclofenac
•Ketoconazole
•Para-amino salicylic acid

Fixed drug eruptions

•Salicylates
•Tetracycline
•Barbiturates
•Sulfonamides
 ALLERGIC CONTACT STOMATITIS

• “Stomatitis venenata”
• Food,food additives,chewing
gums,dentrifices,etc.

PERIORAL DERMATITIS
• Bubble gum,tartar-control tooth
paste,moisturizers,night creams,etc
 MUCOSAL CONTACT REACTIONS TO
DENTAL AMALGAM
• Antigen: mercury/mercury
compound
• “Galvanic lesions”: electric current
that developed between restorative
metals
• Lichenoid reactions
ANGIOEDEMA
• Acute oral/facial swelling,may
compromise airway
• Provocation: histamine releasing
drugs,aspirin,pencillins,etc
 ALLERGIC REACTIONS TO LOCAL
ANESTHETICS

CONTACT DERMATITIS
& DELAYED SWELLING URTICARIA &
AT THE SITE OF ANAPHYLAXIS
ADMINISTRATION
ALLERGIC REACTIONS TO NICKEL
ALLERGIC REACTIONS TO LATEX
ALLERGIC REACTIONS TO
ACRYLIC
 PATCH TESTING
• Determines whether a specific substance
causes allergic inflammation of the patient’s
skin.
 MANAGEMENT
• MILD (DELAYED) ONSET ALLERGIC
REACTION:
– P OSITIONING: upright position
– A IRWAY: ensure that airway is open by talking to patient
– B REATHING: ensure that breathing is adequate
– C IRCULATION
– D ISPENSE / ADMINISTER:
• DIPHENHYDRAMINE( BENADRYL) 25-50mg oral/IM
• Repeat dose up to 50 mg every 6 hours orally for 2 days, if needed.
– E NSURE : vital signs, drug administration, and patient
responses are properly monitored and recorded
• SEVERE (IMMEDIATE) ONSET ALLERGIC
REACTION:
– P OSITIONING:
• With concious patient: upright position
• Unconcious patient: supine position & call EMS

– A IRWAY
– B REATHING
– C IRCULATION
– D ISPENSE:
• EPINEPHRINE 0.3-0.5mg 1:1000 SC/IM,or IV
• Oxygen maintained at low flow rate of 5-6L/min
• Repeat epinephrine, every 5-10 minutes as needed.

– E NSURE: vital signs & drug administration are

monitored
– F ACILITATE MEDICAL CARE:
• If transport to hospital is pending:
– Give repeat doses of epinephrine 0.3-0.5 mg 1 : 1000 SC
or IM, every 5-10 minutes as needed.
– Also administer 25 to 50 mg diphenhydramine (Benadryl),
once patient’s life is no longer in danger.
• If dentist has ACLS training and laryngeal edema is
involved:
» Provide steroids—hydrocortisone sodium succinate,
100 mg SC or IM or IV
» Perform CPR if patient stops breathing and has no
pulse
» Use cricothyrotomy if needed
 IMMUNE DEFICIENCY DISEASES
PRIMARY IMMUNE
DEFICIENCIES
•Genetically determined: gene
mutations
•Eg:
X-linked Agammaglobulinemia
Isolated IgA deficiency
Thymic hypoplasia
SECONDARY IMMUNE
DEFICIENCIES
•Secondary to other diseases or
therapies
•Patients with
malnutrition,infection,cancer,renal
disease
Eg: Depression of Humoral immune
responses: chronic lymphatic
leukemia
Depression of Cell-mediated
immunity: AIDS,Hodgkin’s
lymphoma, etc
 CLINICAL SIGNIFICANCE:
• Increased frequency of infections
• Unusually severe infection
• Prolonged duration of infection
• Unexpected complication/manifestation
• Infection with a minor pathogen
 AUTOIMMUNITY

• Autoantibodies against its own tissues, which

leads to structural or functional damage of
tissues.
 MECHANISMS
• HIDDEN OR SEQUESTRATED ANTIGENS:
present in closed system & have no access to immune
apparatus
• ANTIGEN ALTERATION: alteration by
physical,chemical or biological factors
• CROSS REACTING FOREIGN ANTIGENS:sharing
of antigens
• T AND B CELL DEFECTS: enhanced function of T-
helper cells & decreased T suppressor cell function
 ORAL CAVITY LESIONS
• PEMPHIGUS:
• LICHEN PLANUS:
– Vesicles,bullae or irregular shallow ulcers of the
oral mucosa
– Associated with desquamative gingivitis

• SJOGREN’S SYNDROME:
– Chronic autoimmune disease
– Oral & ocular dryness,lymphocytic infiltration &
destruction of the exocrine glands
– Salivary & lacrimal glands affected primarily
• Rheumatic heart disease:
– Subacute bacterial endocarditis: potential to cause
autoimmune valvular damage
 IMMUNOLOGICAL TOLERANCE
• Non responsiveness to antigenic stimulus

• Natural: non-responsiveness to self antigens

• Acquired: potential antigen induces a state of
unresponsiveness to itself
 TRANSPLANT/GRAFT

DONOR RECIPIENT

RELATIONSHIP BETWEEN DONOR & RECIPIENT:

50
 ALLOGRAFT

ACCEPTED INITIALLY

VASCULARIZED

MORPHOLOGICALLY & FUNCTIONALLY HEALTHY-2-3

DAYS

4TH DAY: INFLAMMATION

BLOOD VESSELS OCCLUSION

NECROSIS GRAFT SLOUGHS OFF

BY 10TH DAY
 GRAFT FROM THE SAME DONOR

REJECTION IN AN ACCELERATED FASHION

SLOUGHS OFF BY 6TH DAY

•Antigens that participate in graft rejection:

MAJOR HISTOCOMPATIBILITY
Decides the fate of
ANTIGENS
allograft
•Humans: HUMAN LEUCOCYTE
ANTIGEN(HLA) 52
 ABO Blood group compatibility
 HLA compatibility
 Immunosuppression
 Immunologically privileged site
GRAFT-VERSUS-HOST REACTION:

•Graft mounts immune response against the antigens of the host

Retardation of growth
Diarrhea
Hepatosplenomegaly Runt disease
Lymphoid atrophy
Anemia

53
 SECONDARY BONE GRAFTING IN
CLEFT LIP SURGERY

54
 ALVEOLAR RIDGE AUGMENTATION
FOR IMPLANT PLACEMENT:

55
 BONE GRAFTING
IN COMBINED
ENDO-PERIO
LESIONS:

56
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58
 SUMMARY
IMMUNITY

INNATE ACQUIRED

HUMORAL CELL MEDIATED

ANTIGEN ANTIBODY
HYPERSENSITIVITY

IMMUNE DEFICIENCY ANTIGEN-ANTIBODY DIAGNOSTIC

CONDITION REACTION PURPOSES

AUTOIMMUNITY

IMMUNOLOGICAL
TOLERANCE
 CONCLUSION

• Understanding of the underlying mechanism is

required for proper care of our patients in various
conditions
• Our primary goal must be to boost the immune
mechanism of the patients, rather than the
administration of medications to treat them.
 References
• Ananthanarayanan & Paniker’s textbook of
microbiology:7th edition
• Combined endodontic - Periodontal lesion: A clinical
dilemma:Pushpendra Kumar Verma, Ruchi Srivastava1,
K. K. Gupta1, Amitabh Srivastava1
• Oral drug reactions:D.Alan Tak
• Alveolar ridge augmentation using chin bone graft,
bovine bone mineral, and titanium mesh: Clinical,
histological, and histomorphomtric study Jihad
Khamees, Mohammad Atef Darwiche1, Nabil Kochaji2
• Immunology in pediatric dentistry
• Carranza textbook of periodontology
THANK YOU