IMMUNITY presentation for education.pptx

Immunity

1. IMMUNITY Presented by :- Dr. Rohan Shrivastava MDS – JR1

2. CONTENTS Immunity Introduction Components of immune system Classification Innate immunity & mechanism Adaptive immunity & mechanism Antigen Antigen Classification Antibody Immunoglobulin Structure Classification Functions of each antibody Auto-Immune diseases Conclusion References

3. Introduction – Our environment contains infectious microbes- viruses, fungi , protozoa, multicellular parasites- can cause diseases in host. Body is protected against invading microorganisms by physical barriers- skin, bile, mucus, epithelial linings- first line of defence. If these fail- second line of defence – immune system is activated.

4. Immunity Resistance exhibited by the host against injury caused by microorganisms and their products. This resistance plays a major role in prevention of infectious diseases Immune system- Biological structures & processes within an organism that protect against diseases by identifying & killing pathogens & tumour cells.

5. Classification

6. Line of Defense

7. Innate Immunity Also known as NATIVE IMMUNITY. Resistance possessed by birth. By virtue of his genetic and constitutional make-up. Does not depend on prior contact with foreign antigen. SPECIFIC – Resistance to a particular pathogen is concerned. NON SPECIFIC- Indicate a degree of resistance to infections in general.

8. Again classified as SPECIES IMMUNITY - Entire human species is resistant to plant pathogen. RACIAL IMMUNITY- Particular races of that species are resistant. E.g.- American negroes are more susceptible to TB than the white race. INDIVIDUAL IMMUNITY- Resistance to infection varies with different individuals of same race and species. E.g - Homozygous twins show similar resistance/ susceptibility to Leprosy/ TB , not seen in heterozygous twins.

9. FACTORS INFLUENCING INNATE IMMUNITY AGE- Two extremes of life- fetus and old persons – higher susceptibility to various infections. Foetus- immature immune system , Old age- gradual waning of immune response. 2 . HORMONES- Hormonal disorders – Diabetes mellitus , Hypothyroidism enhance susceptibility to infections. 3 . NUTRITION- Immune response is reduced in malnutrition patients.

10. Mechanism of Innate Immunity EPITHELIAL SURFACES – First line of defence (Mechanical barrier) Skin – Bactericidal property. High concentration of salts in drying sweat . Sebaceous secretions Respiratory tract - Inhaled particles arrested in nasal passages. Mucous secretion act as trapping mechanisms . Cough reflex- important defence mechanism.

11. Intestinal Tract- Saliva – inhibitory effect on micro-organisms. Digestive juices. Conjunctiva- Lysozymes present in tears- bactericidal action. Genitourinary tract - Urine’s flushing action eliminate bacteria from urethra. Semen- contains some antibacterial substances. Acidity of adult vagina- inhospitable to many pathogens.

12. ANTIBACTERIAL SUBSTANCE- Present naturally in blood and tissues. Beta lysin- thermostable substance active against anthrax and related bacilli. Lactic acid- muscle tissues and inflammatory zones. Lysozymes - present in tears Interferons - activated against viral infection. Complement system- destruction of pathogenic micro-organisms invading blood and tissues.

13. 3. CELLULAR FACTORS Phagocytic cells are – Microphages- Polymorphonuclear leucocytes( neutrophills ) Macrophages- Mononuclear phagocytic cells Natural killer cells (NK)- A class of lymphocytes- non specific defence against viral infection and tumours.

14. 4. INFLAMMATION Occurs as a result of tissue injury/ irritation. Important nonspecific defence mechanism. Inflammation Vasodilation Inc. vascular permeability & cellular infiltration Microorganisms phagocytosed & destroyed, fibrin barrier laid at infection site.

15. 5. FEVER Rise in body’s temperature - natural defence mechanism . Accelerates physiological process. Destroys infecting pathogens. Stimulates production of interferons .

16. 6. ACUTE PHASE PROTEINS Sudden increase in plasma concentration of certain proteins following injury/ infection- acute phase proteins. This include- - C reactive proteins Mannose binding proteins Alpha- 1 - acid glycoprotein Enhance host resistance, prevent tissue injury, repair of inflammatory lesions.

17. Acquired Immunity Resistance acquired by individual during his life . Adaptive immunity .

18. ACTIVE IMMUNITY Resistance developed by individual – antigenic stimulus . Involves active functioning of host’s immune apparatus to produce antibodies & immunologically active cells. Once developed , it is long lasting. When actively immunised individual encounters subsequent attack of same antigen , immune response occurs more quickly.

19. A. Natural active immunity Results from clinical / inapparent infection by microbe . E.g - Person recovered from attack of measles develop natural active immunity. Life long immunity following many viral diseases Immunity following bacterial infection is generally less permanent.

20. B. Artificial active immunity Resistance induced by vaccine Examples of vaccines- Bacterial vaccine – Live (BCG for tuberculosis ) Killed (Cholera vaccine) Killed whooping cough (pertussis) vaccine Bacterial products(Tetanus toxoid) Viral vaccines- Live (Oral polio vaccine- Sabin) Killed Covid19 vaccine

21. Mechanism of Active Immunity – Stimulates both humoral immune response & cell mediated immune response Humoral/ antibody mediated immunity (HMI/AMI ) Primary defence against viruses that infect respiratory / intestinal tract. pathogenesis of hypersensitivity (Type I, II,III) & autoimmune diseases. Synthesis of antibodies by plasma cells.

22. Cell- mediated immunity (CMI) mediated by T lymphocyte cells. Protects against fungi, viruses, intracellular bacteria allograft rejection , graft vs host reactions mediates pathogenesis of delayed hypersensitivity(type IV) immunity against cancer

23. PASSIVE IMMUNITY Resistance transmitted passively to recipient in a readymade form Recipient immune system plays no active role No antigenic stimulus, preformed antibodies administered Immunity lasts for days to weeks Less effective , employed when instant immunity is desired.

24. A. Natural passive immunity Resistance passively transferred from mother to baby. Human infants- maternal antibodies transmitted through placenta. Human foetus acquires ability to produce antibodies – 20 th week of life. Till then, maternal antibodies give passive protection against diseases.

25. B. Artificial passive immunity Resistance passively transferred to recipient by administration of antibodies . Agents used- HYPERIMMUNE SERA OF ANIMAL/HUMAN ORIGIN Antitetanus serum prepared from hyperimmune horses. Temporary protection Disadvantage- hypersensitivity & immune elimination

26. DIFFERENCE-

27. IMMUNE SYSTEM LYMPHOID ORGANS Central lymphoid organs – Thymus Bursa of Fabricius in birds. Bone marrow in mammals Peripheral lymphoid organs- Spleen Lymph nodes Mucosa associated lymphoid tissues(MALT) Lymphoid tissues in gut, lungs, liver, bone marrow.

28. CELLS- Lymphocytes In circulating blood- 70% are T Lymphocytes {T for thymus dependent} , 20% B Lymphocytes {B for Bursa/ Bone marrow 10% Null cells} 2. Plasma cells

29. Difference between B cells & T cells

30. ANTIGEN Antigen is a molecule which introduced into a body evokes immune response.

31. CLASSIFICATION OF ANTIGEN

32. They may also be classified as- Complete antigen- Substances which induce antibody formation by themselves & react specifically with these antibodies. Haptens- Substances incapable of inducing antibody formation by themselves but can react specifically with antibodies. Haptens are of 2 types- COMPLEX HAPTENS SIMPLE HAPTENS

33. ANTIBODIES- IMMUNOGLOBULINS Substances which are formed in serum & tissue fluids in response to antigen and react with that antigen specifically and in some observable manner. CHEMICAL NATURE- GLOBULIN – named as IMMUNOGLOBULIN. Immunoglobulin 20 -25% total serum protein. Synthesised by plasma cells. NOTE: All antibodies are immunoglobulins , but all immunoglobulins may not be antibodies.

34. STRUCTURE OF IMMUNOGLOBULINS

35. CLASSES OF IMMUNOGLOBULIN

36. FUNCTIONS OF IMMUNOGLOBULINS

37. ROLE OF ANTIBODIES IN IMMUNITY NEUTRALIZATION- Pathogen can no longer infect host because it is bound to an Ab OPSONIZATION - Ab bound to Ag increases phagocytosis Antibodies together with proteins of complement system- cell lysis

38. ANTIGEN- ANTIBODY REACTION Morphologically, PRECIPITATION REACTION AGGLUTINATION REACTION Functionally, NEUTRALIZATION COMPLEMENT FIXATION RADIOIMMUNOASSAY IMMUNOFLUORESENCE ENZYME LINKED IMMUNOSORBENT ASSAY(ELISA)

39. USES IN VIVO- Basis of immunity against infectious diseases. Lead to tissue injury in some hypersensitivity reaction/ autoimmune diseases. IN VITRO- Diagnosis of infections. Detection of antigen/ antibody.

40. IMMUNITY BOOSTER Healthy ways to strengthen our immune system Diet rich in fruits & vegetables Regular exercise Maintain a healthy weight Adequate sleep Avoid smoking & drinking Measures to avoid infection- washing our hands frequently Minimizing stress

41. FOOD THAT ENHANCE IMMUNITY CITRUS FRUITS RED BELL PEPPER BROCCOLI SPINACH GINGER YOGURT TURMERIC

42. ALMONDS SUNFLOWER SEEDS GREEN TEA PAPAYA HONEY

43. PROBIOTICS Include Good Bacteria Live micro organisms that can be consumed through fermented foods & supplements. Helps to boost our immunity Inhibit growth of harmful gut bacteria Promote production of natural antibodies Boost immune cells – T lymphocytes, IgA producing cells, NK cells Lactobacillus acidophillus - common probiotic strain – boost immunity

44. CLINICAL CONSIDERATIONS

45. IMMUNODEFICIENCY SYNDROMES A state in which immune system ability to fight infectious disease is compromised / entirely absent. 2 Types Primary - Congenital- resulting from genetic defects in some components of immune system. Secondary - Acquired- As a result of other disease / condition – HIV infection, malnutrition, immunosuppression.

46. Primary Immunodeficiency syndromes & classification A) HUMORAL IMMUNODEFICIENCIES (B Cell defect) X linked agammaglobulinemia Transient Hypogammaglobulinemia of infancy Failure of pre - B cells to differentiate into mature B cells. Pt suffers from recurrent infections. Abnormal delay in initiation of IgG synthesis in some infants. Ig concentration in majority patients normalise by 2-4 yrs of age.

47. Selective Immunoglobulin deficiencies Selective IgA deficiency selective deficiency of one / more immunoglobulin classes other immunoglobulin classes remain normal / elevated. Absence/ near absence of serum & secretory IgA. Increased susceptibility to respiratory & GIT infections.

48. B) CELLULAR IMMUNODEFICIENCIES (T CELL DEFECT) Thymic Hypoplasia (DiGeorge’s Syndrome) Development defect – affects 3 rd & 4 th pharyngeal pouches aplasia / hyperplasia of thymus & parathyroid glands. T cells absent/ deficient.

49. C) COMBINED IMMUNODEFICIENCIES (BOTH T & B CELL DEFECTS ) Ataxia Telangiectasia Majority pt lack IgA & IgE , some posses antibody to IgA . Cell mediated immunity also defective results in delayed hypersensitivity & graft rejection.

50. Wiskott - Aldrich syndrome X linked recessive disease Thrombocytopenia eczema, bleeding recurrent infections Cellular immunodeficiency with abnormal Ig synthesis Depressed cell mediated immunity . Pt susceptible to recurrent diseases. Haemolytic anaemia common.

51. Secondary Immunodeficiency Depression of Humoral Immune responses Depression of Cell- Mediated Immunity Results when B cells are depleted – Lymphoid malignancy – Chronic lymphatic leukaemia Excessive loss of serum proteins – Exfoliative skin diseases Multiple myeloma – Excessive production of abnormal Ig. Occurs in AIDS , Hodgkin’s lymphoma , Lepromatous leprosy

52. AUTOIMMUNE DISEASE Autoimmune disorders affecting orofacial region predominantly- Systemic Autoimmune diseases with oral manifestations Sjogrens syndrome Benign lymphoepithelial lesion( mikulicz’s disease) Aphthous stomatitis Periodontal disease Pemphigus Bullous pemphigoid Epidermolysis bullosa SLE Myasthenia gravis

53. SJOGRENS SYNDROME Autoimmune disorder Diminished lacrimal & salivary gland secretion (sicca complex) Results in Keratoconjuctivitis sicca & Xerostomia Primary- Xerostomia & Xerophthalmia Secondary- Triad – Xerophthalmia, Xerostomia & Connective tissue disorders(Rheumatoid arthritis, SLE)

54. BENIGN LYMPHOEPITHELIAL LESION (Mikulicz’s Disease) Systemic/bilateral chronic, enlargement of lacrimal, parotid, submandibular salivary gland , attributed to chronic infection Related to Sjogrens syndrome Mild pain, local discomfort & xerostomia. Associated with fever, respiratory disorders, oral infections

55. APHTHOUS STOMATITIS(Aphthous ulcers, canker sores, recurrent aphthous stomatitis) oral ulceration Hereditary, trauma, dietary deficiency, psychological , allergic, infections, drugs, Immunological Elevated levels- IgA & IgG in patient sera Females(10-30 yrs ) Burning sensation Initially localised area – erythema, small white papule forms, Ulcerates & enlarges. Yellowish grey Pseudo membrane

56. PERIODONTITIS Inflammatory disease – destruction of both soft & hard tissues in periodontal region . Over activation of host immune response activates osteoclastic activity & alveolar bone loss.

57. PEMPHIGUS VULGARIS Rapid appearance of vesicles/ bullae NIKOLSKY SIGN- loss of epithelium by rubbing apparently unaffected skin. ASBOE HANSEN SIGN - bulla spread phenomenon

58. BULLOUS PEMPHIGOID Rashes – remains for several week- vesicles & bullae Rarely painful Buccal mucosa, gingiva commonly involved Edema & gingival inflammation

59. SYSTEMIC LUPUS ERYTHEMATOSIS Autoantibodies , immune complex formation & immune dysregulation Damage to kidney, skin, blood cells & CNS Oral lesions- Multiple white plaques with dark reddish purple margins Hyperaemia & oedema Bleeding & superficial ulceration Xerostomia, Glossitis, dental caries, periodontitis

60. MYASTHENIA GRAVIS Life threatening condition Drooping of one/more eyelids Double vision Difficulty in speech/ swallowing Limited facial expression Weakness in muscles

61. CONCLUSION The immune system is like an army- With the task of protecting the host against infection by potential pathogens There is always a synergy between adaptive immune system & its innate counterpart Defects in either system can lead to autoimmune diseases, immunodeficiencies & hypersensitivity reactions. Thus a thorough knowledge of immune reactions is of prime concern in our day to day clinical treatment procedures.

62. REFERENCES Textbook of microbiology for dental students – C P Baveja Essential Pathology for Dental students- Harsh mohan Oral health & disease- Nisengard & Newman Shafer’s Textbook of oral pathology General medicine for dental students- Harmanjit singh hira