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Host defense
The document discusses host defense mechanisms against pathogens. It describes three lines of defense: 1) physical barriers like skin and mucous membranes, 2) inflammatory response and defensive cells, and 3) the immune system. The immune system has both innate and acquired branches. Innate immunity provides non-specific protection using physical and chemical barriers while acquired immunity involves adaptive, antigen-specific responses. Key cells of the immune system that provide defense include macrophages, neutrophils, lymphocytes and natural killer cells. Antibodies and the complement system are important components that help eliminate pathogens.
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Host defense
- 1. HOST DEFENSE Dr. AneetinderKaur PG 1st year Department of Conservative Dentistry & Endodontics
- 2. Defense Lines 01 Inflammation 02 Immunity 03 Structure and Functionsof Immunity 05 Immune Response 06 Hypersensitivity 07 CONTENTS Components of Immunity 04 08 References
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- 4. FIRST LINE (PHYSICAL) BARRIERS Body Systems & Factors Involved Active Components Skin Squamous Cells, Sweat & Sebaceous Glands Mouth Saliva GIT Wall, Gastric Secretions Respiratory Tract Tracheal Cilia, Coughing Reflex Nasopharynx Nasal Hair & Mucus Eye Tears CVS Phagocytic Cells, NK Cells Serum Lactoferrin, Transferrin, Interferons, TNF α, Lysozyme, Fibronectin, Complement Proteins Acute Phase Proteins Alpha 1 Acid Glycoprotein Urinary System Acidic pH & Flow Breast Milk Antibodies, Lactoferrin, Transferrin, Interferons, Mucin, Lysozyme, Fibronectin Fever High Temperature Paniker’s 9th Edition
- 5. SECOND LINE (DEFENSIVE MECHANISM)BARRIERS ◦ Inflammation ◦ Defensive cells ◦ Complement System THIRD LINE BARRIER ◦ Immune system Paniker’s 9th Edition
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- 7. INFLAMMATION ◦ Inflammation isa protective response involving host cells, blood vessels, and proteins and other mediators that is intended to eliminate the initial cause of cell injury, as well as the necrotic cells and tissues resulting from the original insult, and to initiate the process of repair. Pathologic Basis of Disease – Robbins & Cotran
- 8. Pathologic Basis ofDisease – Robbins & Cotran
- 9. SEQUENCE OF EVENTS IN INFLAMMATION RECOGNISE RECRUIT ACTIVATE CONTROLAND TERMINATE DAMAGE REPAIR Pathologic Basis of Disease – Robbins & Cotran
- 10. ACUTE INFLAMMATION Pathologic Basisof Disease – Robbins & Cotran
- 11. Pathologic Basis ofDisease – Robbins & Cotran
- 12. Pathologic Basis ofDisease – Robbins & Cotran
- 13. Pathologic Basis ofDisease – Robbins & Cotran
- 14. Pathologic Basis ofDisease – Robbins & Cotran
- 15. CHRONIC INFLAMMATION INFILTRATION TISSUE DESTRUCTION ATTEMPTS AT HEALING CELLSAND MEDIATORS ➢Macrophages ➢Lymphocytes ➢Eosinophils ➢Mast Cells ➢Neutrophils Pathologic Basis of Disease – Robbins & Cotran
- 16. TISSUE REPAIR Pathologic Basisof Disease – Robbins & Cotran
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- 18. TYPES OF IMMUNITY IMMUNITY INNATE/ NATIVE NON- SPECIFIC SPECIFIC ACQUIRED/ ADAPTIVE ACTIVEPASSIVE Paniker’s 9th Edition
- 19. MECHANISMOFINNATE IMMUNITY EPITHELIAL SURFACES ANTIBACTERIAL SUBSTANCESIN BLOOD AND TISSUES MICROBIAL ANTAGONISMS CELLULAR FACTORS INFLAMMATION ACUTE PHASE PROTIENS TOLL-LIKE RECEPTORS INNATE IMMUNITY FACTORSAFFECTING INNATEIMMUNITY AGE HORMONES NUTRITION Paniker’s 9th Edition
- 20. TYPES OF ACQUIRED IMMUNITY •NATURAL ACTIVE • ARTIFICIAL ACTIVE (Vaccines) ACTIVE • NATURAL PASSIVE • ARTIFICIAL PASSIVE (Sera of animal / human origin , Gamma Globulin , Convalescent sera) PASSIVE COMBINED IMMUNISATION Paniker’s 9th Edition
- 21. ACTIVE IMMUNITY PASSIVEIMMUNITY Produced Actively by Hosts Immune System Received Passively No Active Host Participation Induced by Infection or Immunogens Readymade Antibody Transfer Durable Effective Protection Transient, Less Effective Effective only after Lag Period Immediate Immunity Booster Effect on Subsequent Dose Less Effective Subsequent Dose Negative Phase May Occur No Negative Phase Not Applicable in Immunodeficient Applicable in Immunodeficient Paniker’s 9th Edition
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- 23. ANTIGENS ◦ An antigenis a substance which when introduced into a body evokes immune response to produce a specific antibody with which it reacts in an observable manner. ◦ Attributes: ◦ Immunogenicity ◦ Immunological Reactivity Types Complete Antigen Haptens (Simple/Complex) Epitope Paniker’s 9th Edition
- 24. Size Chemical Nature Susceptibility to Tissue Enzymes Foreigness Antigenic Specificity Heterogenic Specificity Determinantsof Antigenicity Biological Classification of Antigens T Cell Dependent T Cell Independent Super Antigens Paniker’s 9th Edition
- 25. ANTIBODIES - IMMUNOGLOBULINS Immunoglobulin –Proteins of animal origin endowed with known antibody activity and /for certain other protein related to them by chemical structure. ◦ Antibodies have unique structural features and motifs and bind to antigens to destroy them effectively. ◦ Synthesised by endoplasmic reticulum of plasma cells and to some extent by lymphocytes. ◦ Constitute 20~25% of total serum proteins. WHO (1964) Paniker’s 9th Edition
- 26. Textbook of Microbiology– CP Baveja 4th Edition
- 27. Criteria IgG IgMIgA IgD IgE Half Life (Days) 23 5 6-8 3 2 Percentage in Serum (%) 80 5-8 10-13 1 1 H chain gamma alpha mu delta epsilon Serum Concenratio n (mg/ml) 8-16 0.5-2 0.6-4.2 0.03 In nano grams Molecular Weight 150000(7S) 900000- 1000000(19S) 160000(7S) 400000 180000(7S) 190000(8S) Protective function mainly Body Fluids (GCF) Blood Stream Body Surfaces (Colostrum Saliva Tears) Recognition Molecule Reagenic Hypersenstivit y Main Serum Ig, only maternal Ig (across placenta), Late antibody Millionaires Molecule , oldest Ig class, synthesised by fetus (20 wks) 2ndmost abundant Resembles IgG Heat Labile (56Deg.C), Anaphylactic Ig Paniker’s 9th Edition
- 28. COMPLEMENT SYSTEM ◦ Refersto a system of factors that occurs in the normal serum and is activated characteristically by antigen – antibody interaction which subsequently mediates a number of biologically significantly consequences. • Classical Complement pathway • Alternative Complement pathway • Lectin Complement pathway TYPES Phagocytosis Inflammatory Response Hypersenstivity Rxns Autoimmune Disease Endotoxic Shock Immune Adherence Conglutination BIOLOGICALEFFECTS Paniker’s 9th Edition
- 29. Pathologic Basis ofDisease – Robbins & Cotran
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- 33. LYMPHORETICULAR SYSTEM Is acomplex organisation of cells of diverse morphology distributed widely in different organs and tissues of body responsible for immunity TYPES ◦ Humoral immunity (antibody mediated ) ◦ Cellular immunity Paniker’s 9th Edition
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- 36. CELLS of IMMUNESYSTEM ◦ Granulocytes ◦ (polymorphonuclear leukocytes, PMNs) neutrophils, eosinophils, and basophils; lymphocytes. ◦ Monocytes. ◦ Tissue macrophages ◦ Mast cells . ◦ LYMPHOCYTES – ◦ B Cells ◦ Plasma B-Cells ◦ Memory B-Cells: ◦ Types of T Cells ◦ Regulatory or Effector Cells ◦ CD4 + or CD8+ ◦ Helper/Inducer (TH Cells) ◦ TReg Cells ◦ Cytotoxic/Cytolytic (TC ) ◦ Memory cells (TM ) ◦ Antigen-presentingcells ◦ Dendriticcell ◦ Natural Killer Cells Paniker’s 9th Edition
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- 40. TYPES OF IMMUNERESPONSES Humoral/Antibody mediated Immunity Cell mediated Immunity Paniker’s 9th Edition
- 41. Humoral/Antibody mediated Immunity ANTIBODYRESPONSES ◦ Primary response ◦ Secondary response ANTIBODY PRODUCTION Paniker’s 9th Edition • Genetic Factors • Age • Nutritional Status • Route of Administration • Size and No. of Doses • Multiple Antigens • Adjuvants Factors Affecting Antibody Production (AMI)
- 42. Cell mediated Immunity AntigenPresentation by APC to T Lymphocytes Sensitised T Lymphocytes change into Memory and Effector Cells Activated Lymphocytes release Lymphokines T Cell recognises Antigens when presented with MHC Molecules CD4+ Cells recognise MHC2 and Antigen, change into Th and Td cells Tc attach to target cells and release cytolysins Paniker’s 9th Edition
- 43. Pathologic Basis ofDisease – Robbins & Cotran
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- 45. HYPERSENSITIVITY ◦ Immune responsesthat normally are protective are also capable of causing tissue injury. Injurious immune reactions are grouped under hypersensitivity, and the resulting diseases are called hypersensitivity diseases. Paniker’s 9th Edition
- 46. Pathologic Basis ofDisease – Robbins & Cotran
- 47. Pathologic Basis ofDisease – Robbins & Cotran
- 48. Pathologic Basis ofDisease – Robbins & Cotran
- 49. Pathologic Basis ofDisease – Robbins & Cotran
- 50. Pathologic Basis ofDisease – Robbins & Cotran
- 51. Pathologic Basis ofDisease – Robbins & Cotran Systemic Inflammation as a Consequence of Local Infection
- 52. References • Pathologic Basisof Disease – Robbins & Cotran (SAE) • Essential Pathology for Dental Students – Harshmohan, 4th Edition • Textbook of Microbiology – Ananthanarayan & Paniker’s, 9th Edition • Textbook of Microbiology – CP Baveja 4th Edition • Abbas & Lichman, Cellular & Molecular Immunology, 5th Edition
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- 55. 1 . Typeof T cells that predominate Pulpal tissue .
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- 58. 3. Acquired ImmunologicTolerance ◦ Immunological tolerance is defined as a state in which contact with an antigen specifically abolishes the capacity to mount an immune response against that particular antigen when it is administered subsequently, the immune reactivity to other antigens being unaffected.
- 62. ◦ Management hingeson confirming the diagnosis. All individuals with confirmed asthma should receive self-management education, including a written action plan. Very mild intermittent asthma may be treated with a short-acting beta2-agonist (SABA) taken as needed. SABAs are recommended for relief of symptoms; individuals 12 years of age and over with moderate to severe asthma (particularly those who are exacerbation prone and have poor control) who are taking an ICS/LABA formulation approved also for use as a reliever may do so. Inhaled corticosteroids (ICS) should be introduced early as the initial maintenance treatment for asthma even in individuals who report asthma symptoms less than three times a week. LTRA are second- line monotherapy for mild asthma. If asthma is not adequately controlled by low doses of inhaled corticosteroids, additional therapy should be considered. In children 6 years of age and over, the ICS should be increased to a medium dose before adding an adjunct agent such as a long-acting beta2-agonist (LABA) or LTRA. In children 12 years of age and over and adults, a LABA should be considered first as adjunct therapy. A LABA should only be used in combination with an ICS. Increasing to a medium dose of ICS or the addition of an LTRA are third-line therapeutic options. Theophylline may be considered as a fourth-line agent in adults. Severely uncontrolled asthma may require additional treatment with prednisone. Omalizumab may be considered in individuals 12 years of age and over with atopic asthma poorly controlled despite high doses of ICS and appropriate add-on therapy, with or without prednisone. Asthma symptom control and lung function tests, inhaler technique, adherence to asthma treatment, exposure to asthma triggers in the environment, and the presence of co-morbidities should be reassessed at each visit and before altering the maintenance therapy. Consider also assessment of sputum eosinophils in adults with uncontrolled moderate to severe asthma managed in specialized centres. After achieving acceptable asthma control for at least a few weeks to months, the medication should be reduced to the minimum necessary dose to achieve adequate asthma control and prevent future risk of exacerbations. HFA: Hydrofluoroalkane; IgE: Immunoglobulin E; mcg: Micrograms; PEF: Peak expiratory flow; yrs: Years
- 63. 4. Role ofDPSCs in Inflammation
- 64. 5. Endogenous andExogenous Antigen ◦ Endogenous antigens are proteins found within the cytosol of human cells. Examples of endogenous antigens include: ◦ Viral proteins produced during viral replication; ◦ Proteins produced by intracellular bacteria ◦ Proteins that have escaped into the cytosol from the phagosome of phagocytes such as antigen- presenting cells; ◦ Tumor antigens produced by cancer cells; and ◦ Exogenous antigens are antigens that enter from outside the body, such as bacteria, fungi, protozoa, and free viruses. These exogenous antigens enter macrophages, dendritic cells, and B-lymphocytes through phagocytosis or pinocytosis.
- 65. 6. Epitope, Idiotope,Paratope ◦ The actual portions or fragments of an antigen that react with receptors on B-lymphocytes and T-lymphocytes, as well as with free antibody molecules, are called epitopes or antigenic determinants. The size of an epitope is generally thought to be equivalent to 5-15 amino acids or 3-4 sugar residues. ◦ An idiotope is the unique set of antigenic determinants (epitopes) of the variable portion of an antibody. In some cases it can be the actual antigen-binding site, and in some cases it may comprise variable region sequences outside of the antigen-binding site on the antibody itself ◦ A paratope, also called an antigen- binding site, is a part of an antibody which recognizes and binds to an antigen. It is a small region (of 5 to 10 amino acids) of the antibody
- 66. 7. Complementarity-Determining Regions ◦The variable domain is also referred to as the FV region and is the most important region for binding to antigens. To be specific, variable loops of β-strands, three each on the light (VL) and heavy (VH) chains are responsible for binding to the antigen. These loops are referred to as the complementarity-determining regions (CDRs). In the framework of the immune network theory, CDRs are also called idiotypes.