Dr.

MRR

Dr.MRR

INTRODUCTION

“Immunis” --- Exempt from taxes / charges
Mythridatism -- Greek king Pontis, Mythridate –VI

Variolisation: -- Practised in Ancient China & India--- Inhalation of Powdered crusts of Smallpox to protect from Smallpox.

Lady Mary Wortley Montague -- took it to England. Edward Jenner – 1796 --- Pioneered to identify “cross immunity” – Prepared vaccine for Smallpox from fluid from Cowpox lesions Sir Louis Pasteur – 1880 – Prepared Rabies vaccine --- “Vacca” – cow.
Dr.MRR

MRR .IMMUNITY Dr.

MRR .Dr.

MRR .INBORN OR INHERENT ABILITY TO RESIST ACQUIRED IMMUNITY – AFTER EXPOSURE TO THE OFFENDER Dr.IMMUNITY DEFINITION: Resistance offered by a host to an invader INNATE IMMUNITY -.

MRR .A) Cellular – Phagocytosis B) Humoral – Complement mediated bacterial lysis Neutralising substances in Blood Betalysins Lysosomes etc C) Microbial agglutination in Blood stream Dr.Surfaces & Secretions play a role Systemic --.INNATE IMMUNITY Constitutional / Natural Immunity Local --.

MRR .Dr.

Involves the participation of Immune System.Active Passive Artificial Acquired immunity --.Active Passive Dr.ACQUIRED IMMUNITY Acquired after birth due to exposure to offending agents. Natural Acquired Immunity --.MRR .

INNATE vs ADOPTIVE IMMUNITY Dr.MRR .

INNATE IMMUNE MECHANISMS INTERFERON PHAGOCYTIC CELLS INFLAMMATORY REACTION COMPLEMENT MICROBE ADOPTIVE IMMUNE MECHANISM T-CELLS B-CELLS .

MRR .IMMUNE RESPONSE Dr.

MRR . they provide distinctly different avenues for dealing with pathogenic organisms or altered host cells. Dr. the Immune Response (IR) can be divided into two major classes: humoral and cell-mediated. Overall. While these responses are not mutually exclusive.IMMUNE RESPONSE Response of a host to an antigenic stimulus Recognise React Respond Remember Host defense is present in many forms.

The immune response has memory.MRR . Primary response Secondary response Dr.IMMUNE RESPONSE The immune response is specific.

MRR .Permanent.EFFECTS OF IMMUNE RESPONSE IN VIVO : -- Inactivation of Ag Killing of the offender Immunity to repeat exposure ( Immune memory) --Temporary -.Diagnostic tests Dr. IN VITRO --Serological reactions ---.

Dr.Ag-Ab REACTIONS AFFINITY : Ability to attract Ag / Ab AVIDITY: Strengh of the bond between the Ag & Ab SENSITIVITY: Ability to detect even small quantity SPECIFICITY: Ability to detect specific Ab / Ag CROSS-REACTIVITY : Antigenic similarities or Sharing of Ag determinants leading to false positivity.MRR .

MRR .LYMPHOID TISSUES Primary (Responsible for maturation reactive cells) Thymus Bone marrow Secondary (Sites for Ag contact Lymph nodes and response) Spleen of Ag- (T-cell maturation) (B-cell maturation) (Expansion of lymphatic (Similar to lymph nodes Collects blood-borne Ags) system. separate from blood circulation. superficial cortex harbors mostly B-cells) Dr. Deep cortex harbors mostly T-cells.

Follicle (B-Cell Zone Germinal Centre Antigen Afferent Lymphatics Paracortex (T-CellZone) Medulla Efferent Lymphatics Artery Vein Capsule Trabaculae Dr.MRR Lymphocytes .

MRR .CELLULAR BASIS OF IMMUNE RESPONSE Dr.

CELLS OF THE IMMUNE RESPONSE Immune responsive cells can be divided into five groups based on i) the presence of specific surface components and ii) function: B-cells (B lymphocytes). Accessory cells (Macrophages and other antigenpresenting cells).MRR Killer cells (NK and K cells). . Dr. and Mast cells. T-cells (T lymphocytes).

Cell group Surface components Function Blymphocytes Surface immunoglobulin (Ag recognition) Fc Direct antigen recognition Differentiation Immunoglobulin receptor Class into antibody-producing plasma cells Antigen II Major Histocompatability Complex (MHC) molecule (Ag presentation) presentation within Class II MHC Dr.MRR .

Ag responses recognition) CD4 Helper Tcells (TH) molecule Recognizes antigen presented within Class II MHC Promotes differentiation of B-cells and cytotoxic T-cells Activates macrophages Downregulates Suppressor CD8 molecule T-cells (TS) Cytotoxic the activities of other cells Recognizes T- CD8 molecule cells (CTL) Dr.Tlymphocytes CD3 molecule Involved in both humoral T-cell receptor and cell-mediated (TCR.MRR antigen presented within Class I MHC Kills cells expressing appropriate antigen .

Dr.MRR .

MRR (enhances phagocytosis) .Accessory cells Macrophages Variable Phagocytosis and cell killing Immunoglobulin Fc receptor Complement component C3b receptor Class II MHC molecule Bind Fc portion of immunoglobulin (enhances phagocytosis) Bind complement component C3b (enhances phagocytosis) Antigen presentation within Class II MHC Secrete IL-1 (macrokine) promoting T-cell differentiation and proliferation Can be "activated" by T-cell lymphokines Dendritic cells Class II MHC molecule Immunoglobulin Antigen presentation within Class II MHC Bind Polymorphonu clear cells (PMNs) Fc portion of immunoglobulin Fc receptor (enhances phagocytosis) Complement Bind complement component C3b component C3b Dr.

tumor cells. ADCC) Mast cells High affinity IgE Fc receptors Bind IgE and initiate allergic responses by release of histamine Dr.MRR .g.Killer cells NK Variable Unknown Direct Kills cell killing cells K Immunoglobulin variety of target cells (e. transplanted cells) Bind cells Fc receptor Fc portion of immunoglobulin Kills antibody-coated target cells (antibodydependent cell-mediated cytotoxicity. virus-infected cells.

CYTOKINE STEM CELL APC T-CELL Differentiation of CTLs B-CELL CYTOKINE Ag SPECIFIC INTERACTION Ab CELLULAR INTERACTIONS OF IMMUNE RESPONSE PLASMACELL .T-CELL T-CELL CYTOKINE THYMUS T-CELL T-CELL Macrophag e activation CYTOKINE T-CELL Ag SPECIFIC INTERACTION CYTOKINE Inflammation via PMN etc.

ANTIGEN Dr.MRR .

– Accessible (the immune system must be able to contact the molecule). More specifically. and – Foreign (not recognizable as "self").CHARACTERS OF AN ANTIGEN Antigen (Ag): -.COMPLETE // HAPTEIN A molecule which elicits a specific immune response when introduced into an animal. antigenic (immunogenic) substances are: – Generally large molecules (>10. – Structurally complex (proteins are usually antigenic).MRR .000 daltons in molecular weight). Dr.

Dr.MRR .

MRR .Epitope Dr.

Immunoglobulins (Igs) come in different forms (IgA. We will use the term "immunoglobulin" to describe any antibody. IgG. The term "immunoglobulin" is often used interchangeably with "antibody".MRR . IgD. IgM) that reflect their structure. and the term "antibody" to describe an antigen-specific "immunoglobulin". regardless of specificity.Antibody (Ab): A glycoprotein produced in response to an antigen that is specific for the antigen and binds to it via non-covalent interactions. Dr. IgE.

MRR . The immunoglobulins derive their name from the finding that they migrate with globular proteins when antibody-containing serum is placed in an electrical field Dr.Immunoglobulins (Ig) Glycoprotein molecules that are produced by plasma cells in response to an immunogen and which function as antibodies.

ANTIBODY--Ig
BASIC IMMUNOGLOBULIN STRUCTURE

Kappa lambda

Dr.MRR

FUNCTIONS OF IMMUNOGLOBULINS
Immunoglobulins generally assume one of two roles: act as i) plasma membrane bound antigen receptors on the surface of a B-cell or ii) as antibodies free in cellular fluids functioning to intercept and eliminate antigenic determinants.

In either role, antibody function is intimately related to its structure
Dr.MRR

Dr.MRR

ISOTYPE / ALLOTYPE / IDIOTYPE
ISOTYPE-Specificity -Antigenic features of a class of Ig. determines the type of IR

ALLOTYPE— Antigenic variation in one Ig Specificity among individuals – due to genetic diversity. IDIOTYPE – Specificity Unique antigenic determinant on the Hypervariable region of Ig.– takes part in immune regulation. Dr.MRR

Ig M

Ig E Ig G

ISOTYPES OF Ig

Ig A

Ig D

Dr.MRR

Four subclasses. IgG4. IgG + - + + IgE - + - - IgA - - - - Two subclasses. Involved in opsonization and ADCC.Isotype Placental transfer Binds mast cell surfaces Binds phagocytic cell surfaces Activates complement Additional features IgM - - - + First Ab in development and response.MRR . IgG1. IgG2. Involved in allergic responses. Also found as dimer (sIgA) in secretions. IgG3. IgA2. Dr. IgA1. IgD - - - - B-cell receptor.

IMMUNOGLOBULIN GENES Dr.MRR .

MRR . Ig produced as a result will have the same specificity as original Ig M Dr.ISOTYPE SWITCHING Class Switching – Ig M Ig G Results from sequential association of VH gene with different CH gene.

MRR .ANTIBODY MEDIATED IMMUNITY Dr.

Dr.MRR .

MRR .ANTIGENIC SPECIFICITY OF B-CELLS Dr.

MRR .Dr.

Dr.MRR .

MRR .IMMUNE RESPONSE CURVE Dr.

MRR .IMMUNOLOGICAL MEMORY Dr.

POLYCLONAL AND MONOCLONAL ANTIBODIES Dr.MRR .

COMPLEMENT SYSTEM COMPLEMENT CASCADE CLASSICAL PATHWAY ALTERNATE PATHWAY BIOLOGICAL EFFECTS OF COMPLEMENT Dr.MRR .

MRR .Dr.

MRR .Dr.

MRR .Dr.

MRR .PHAGOCYTOSIS Dr.

MRR .PHAGOCYTOSIS Dr.

MRR . Dr.PHAGOCYTOSIS OF EXTRACELLULAR MICROORGANISMS Nonencapsulated organisms.

PHAGOCYTOSIS OF CAPSULATED MICROORGANISMS (EXTRACELLULAR) Dr.MRR .

Macrophage activity on Intracellular microorganisms Dr.MRR .

MRR . they survive within the phagocyte and eventually kill iT Dr.Once engulfed. however.

CELLMEDIATED IMMUNITY T-CELL MATURATION T-CELL ACTIVATION CLUSTER DIFFERENTIATION.MRR .CD4 & CD8 FUNCTIONS OF T-CELLS – EFFECTOR /REGULATOR NK CELLS K CELLS Dr.

MRR . the functional "effectors" of this response are various immune cells. These functions include: Phagocytosis and killing of intracellular pathogen Direct cell killing by cytotoxic T cells Direct cell killing by NK and K cells Dr. As the name implies.Cell Mediated Immunity The second arm of the immune response is refered to as Cell Mediated Immunity (CMIR).

T-CELL SUBSETS & CYTOLYTIC & CYTOTOXIC REACTIONS CTL NK CELL K CELL K CTL CTL TCR NK NK-R FCR Ag MHC-I NK.MRR ADCC .DET Ab Ag TARGET CELL TARGET CELL TARGET CELL CYTOTOXICITY CYTOLYSIS Dr.

MRR .TH 1 & TH 2 SUBSET ACTIVATION Dr.

MRR .Ag PRESENTATION THROUGH MHC-I Dr.

MRR .Ag PRESENTATION THROUGH MHC-II Dr.

Ag PRESENTATION THROUGH MHC-II Dr.MRR .

B. that act as antigens and are important in determining the acceptance or rejection by the body of a tissue or organ transplant These antigens are one histocompatibility proteins group of the so-called Two individuals with identical HLA types are said to be histocompatible. and D) in humans that code for a group of glycoproteins. present on the surface of plasma membranes.MRR tissues. Successful transplantation requires a minimum number of HLA differences between the donor's and recipient's Dr. .MAJOR HISTOCOMPATIBILITY COMPLEX – HLA SYSTEM HLA system (human leucocyte antigen system) A series of four gene loci (A. C.

MRR .178 HLA C 439 Minor Antigens HLA E 9 HLA F 21 HLA G 43 MHC class II HLA -A1 -B1 -B3 to -B51 Dr.MAJOR HISTOCOMPATIBILITY COMPLEX – HLA SYSTEM MHC class I locus Major Antigens HLA A 767 HLA B 1.

.

MRR .MAJOR HISTOCOMPATIBILITY COMPLEX Dr.

Dr.MRR .

Heart Disease etc Encepalopathy following Neural vaccines. Cross reacting Antigens -. Rh.Fraussman Ag – Ag determinants shared between individuals.g.SPECIFICITY AND CROSS REACTIONS SPECIFICITY: Antigen – Antibody reactions are usually specific. Dr.MRR . genera and Species as well Antibodies against cross reacting antigens may cause disease e.: AGN .

g.Antibodies produced against the antigens shared between different species or serotypes may give rise to diagnostic dilemmas.g. Previous exposure to different serotype of Influenza virus Nonspecific activation of immune mechanism e. BCG immunisation for leprosy & also in malignancies Dr.” They may also give rise to Cross protection due to Neutralisation of some of the Antigenic determinants by the Abs e. “ANAMNASTIC REACTIONS.MRR .

The role of cross-immunity in invasion of new strain The likelihood of coexistence Phenotypic diversity Invasion under sub-threshold condition Dr.MRR .

Dr.Cross-immunity? Infection with an influenza subtype A strain may provide cross protection against other antigenically similar circulating strains Influenza type A H2N2 H1N1 H1N1 H3N2  Little evidence support the existence of cross-immunity between influenza A subtypes  Houston and Seattle studies show that cross-immunity exists between strains within the same subtype.MRR .

Ag-Ab REACTIONS --SEROLOGICAL TESTS -DIAGNOSTIC IN INFECTIVE AS WELL AS IMMUNOLOGICAL DISEASES Dr.EFFECTS OF IMMUNE RESPONSE IN VIVO ---IMMUNE PROTECTION DISEASE CAUSATION ( HS & AI ) IN VITRO -.MRR .

MRR .IMMUNE ABNORMALITIES HYPERSENSITIVITY AUTOIMMUNITY IMMUNODEFICIENCY DISEASES Dr.

MRR .HYPERSENSITIVITY Dr.

Immunological Defects Primary Defects Bone Marrow & Stem Cells Acquired Defects SCID Immunosuppressives Lymphoid Stem Cells HypoGG Syndrome Pre B-cells B-cells Thymus T-cells DiGeorge PNP Deficiency Selective Deficiency Myeloma Hypercatabolism Plasma cells TH-cells TS-CELLS AIDS Immunoglobulins Dr.MRR CTLs .

TUMOUR AND TRANSPLANTATION IMMUNITY MAINLY CMI AMI ALSO PLAYS A ROLE --through ADCC & afferent inhibition Dr.MRR .

VACCINES LIVE VACCINES KILLED VACCINE WHOLE CELL VACCINES MICROBIAL PRODUCTS SUBUNIT VACCINES SYNTHETIC VACCINES RECOMBINANT VACCINES. Dr.MRR .

MRR . Dr.IMMUNITY IN INFECTIONS BACTERIAL – EXTRACELLULAR– AMI INTRACELLULAR – CMI VIRAL INFECTIONS – CMI – PROTECTIVE AMI.DIAGNOSTIC PARASITIC INFECTIONS.

MRR . INFLAMMATORY PERIODONTAL DISEASES -GINGIVITIS & PERIODONTITIS -JUVENILE PERIODONTITIS -GINGIVAL HYPERPLASIA -ACUTE NECROTISING ULCERATIVE GINGIVITIS Dr.IMMUNOLOGICAL BASIS OF DENTAL DISEASES.

Infiltration of leucocytes.Major Immunological features: Dental Plaque induces inflammation of surrounding tissue. Complement Activation .MRR . Dr. Local defence is not sufficient and Bacteria tend to furthur adhere to tooth surface– AMI & CMI both play role. Release of Enzymes and cytokenes and production of serous crevicular exudate Bacterial virulance products and host immunological defences result in gingivitis and periodontitis.

MRR . Evidence of CMI to the same antigens. Lymphocytic infiltration present at the earliest stage of the disease. Dr.APHTHOUS STOMATITIS. Association with HLA –B 12 Favourable response to topical or systemic corticosteroids. Presence of circulating antibodies to oral mucosa in some persons which may crossreact with oral organisms. Presence of circulating immune complexes in some patients.

AIDS PEMPHIGUS BENIGN PEMPHIGOID CH.E. ERYTHEMA MULTIFORME LICHEN PLANUS INFLAMMATORY BOWEL DISEASES SARCOIDOSIS SJOGREN’S SYNDROME SLE RH.SYSTEMIC DISEASES WITH ORAL MANIFESTATIONS.DISCOID L.MRR . ARTHRITIS PROGRESSIVE SYSTEMIC SCLEROSIS Dr.

Dr.INFECTIONS HERPES SIMPLEX MEASLES CHICKENPOX TREPONEMAL INFECTIONS ORALCANDIDIASIS.MRR .

Which is associated with impaired CMI. Dr. Trt.DENTURE STOMATITIS Inflammation of mucous membrane under the denture. Associated with Candida inf. For candidiasis cures the problem.MRR .

Tobacco. CMI deficiency . Impaired CMI & Fall in Tcell counts is found in metastatic cancers. and Viral infections (HSV&HPV) are found to predispose to oral malignancy. Alcohol.MRR . Dr.ORAL TUMOURS Leading cause of death in 3% of men and 1% of women.

Patients with oral cancers have high HSV-I Ig-M suggesting a reactivation of infections Dr.– the viral genes probably induce transformation.CMI response is found in oral leucoplakia Fall in lymphocyte response to HSV is found to preceed the development of malignant change in preexisting benign hyperkeratosis.MRR . High levels of HSV-Ab in smokers suggests possibility of reactivation of HSV-I .

MRR .Dr.