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Immunology: Basic Principles of Adaptive Immunity and Immunizations

Immunology: Basic Principles of Adaptive Immunity and Immunizations. 2007. Adaptive Immunity. Recognize non self Respond to a foreign invader Distinguish between invaders( potential pathogen). Antigen.

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Immunology: Basic Principles of Adaptive Immunity and Immunizations

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  1. Immunology: Basic Principles of Adaptive Immunity and Immunizations 2007

  2. Adaptive Immunity • Recognize non self • Respond to a foreign invader • Distinguish between invaders( potential pathogen)

  3. Antigen • Is a substance( molecule) that the body identifies as foreign and it mounts an immune response. • It is also known as an immunogen • Most antigens are proteins • Some are glycoproteins, nucleoproteins, or polysaccharides

  4. Proteins as antigens • Proteins are generally more immunogenic • Their structure is more complex • Large proteins may have several epitopes or antigenic determinants

  5. Hepatitis antigens • Hepatitis surface antigen is a molecule attached to the exterior or the virus • Evokes an immune response • First antigen detectable

  6. Haptens • Haptens are smaller molecules that can be antigenic if they bind to a larger molecule • The antigen is the result of the combination. Neither is antigenic by itself

  7. Antibody • Antibodies are molecules that are produced as a response to foreign invaders • It is specific for an antigen • It has the capacity to bind to the antigen

  8. Titer • Titers are the quantitiy of an antigen required to evoke an immune response • It is quantifiable • Measured in clinical situations to determine immunity,the presence of disease,the course of an infection

  9. Antibody titer( definition and importance) • Quantity to bind to and neutralize a particular quantity of an antigen • Rubella is a virus that produces teratogenic effects in a fetus • Rubella titers are diagnostically significant in young women planning on pregnancy

  10. Effector Response • Recognition of a non self presence causes a series of response reactions • Divided into a. Humoral response – Based upon the presence to antibodies b.Cellular response – based upon the activity of special cells such as T lymphocytes

  11. Differentiation of stem cells into lymphocytes is influenced by other tissues B cells are differentiated in the bone marrow Found in the lymph nodes, spleen, gut associated lymphoid tissues( GALT) B CELLS T cells are are differentiated in the thymus They are located in lymph nodes They are the majority of circulating lymphocytes T CELLS Development of the immune system( Immune cells)

  12. T lymphocytes and cellular immunity • Attack and destroy • Produce cytokines that enhance specific immunity and non specific mechanisms of defense

  13. T lymphocytes

  14. T lymphocytes • Cytotoxic T cells – destroy virally infected cells and tumor cells • Helper T cells – they divide rapidly and secrete cytokines • Memory T cells – They are antigen specific cells • Regulatory T cells( suppressor T cells) – Cell mediated immunity • Natural Killer Cells – Connects the innate and the adaptive immune system • Other subsets of cells

  15. Natural Killer Cells( Doc Kaiser Microbiology)

  16. Apoptosis( Doc Kaiser Microbology)

  17. MHC - 1 • Endogenous antigens, such as viral proteins, pass through proteasomes where they are degraded into a series of peptides.2. The peptides are transported into the rough endoplasmic reticulum (ER) by a transporter protein called TAP.3. The peptides then bind to the grooves of newly synthesized MHC-I molecules.4. The endoplasmic reticulum transports the MHC-I molecules with bound peptides to the Golgi complex.5. The Golgi complex, in turn, transports the MHC-I/peptide complexes by way of an exocytic vesicle to the cytoplasmic membrane where they become anchored. Here, the peptide and MHC-I/peptide complexes can be recognized by CTLs by way of TCRs and CD8 molecules having a complementary shape.

  18. MHC I and viruses

  19. The result of circulating immunities When stimulated by an antigenm the B lymphocytes initate a process that leads to the release of antibodies Most effective at defending the body against viruses and bacteria Works on the basis of Specificity Diversity Memory Self vs. Non self Humoral immunity

  20. Humoral immunity • Dependent upon the ability of white blood cells to recognize specific antigens • Antigens are generally exposed on the outer surface of a pathogen or are toxins

  21. Each B cell carries an antibody on its outer membrane It has the ability to bind to a specific antigen The binding of an antigen sensitizes or activates the B cells This causes the cells to divide may times The B cell divides to produce Plasma cells that actively produce antibodies at a rapid rate They also produce a memory cell that retains the information necessary to produce the antibody Antibody Response

  22. B cells • After the binding of the antigen to the antibody, the B cells processes the antigen, by breaking it into tiny fragments • The fragments bind to molecules on the surface of the B cell MHCII

  23. APC( Antigen Presenting Cell)

  24. Antigen Presentation and MHC II • The antigen is presented on the surface of the B cell by MHC II • The T cells are activated to produce interleukin 2 • The activation further stimulates the production of more B cells - memory cells

  25. MHC I and II

  26. There are five classes of Immunoglobulins - The basic form of antibodies • IgG • IgA • IgM • IgD • IgE

  27. Basic structure • Basic unit is a Y shaped structure • They are composed of four polypeptide chains • The chains are held together by disulfide bonds • They possess both variable and constant regions

  28. IgG • IgG-The main class of antibodies • Produced as a secondary response • Attach to antigens on microorganisms and their receptors attach to phagocytic cells • They work effectively with phagocytic cells • The tails section also activates complement • Crosses the placenta

  29. IgM • Pentameric structure( secreted by Plasma cells) • Monmeric on the surface of B cells • It is the first antibody made in response to an infection • It has ten antigen binding regions • Activates complement and causes clumping of microbes

  30. IgA • Occurs in bodily secretions • Found in breast milk • Attaches to the lining of the digestive, respiratory, and gastrointestinal tract • Transported through epithelial cells • Attaches to microbes before they invade tissues • Activates complement • Exists as a dimer

  31. IgD • Found primarily on the membranes of B cells • It may help in immune responses • It also may be active in allergic responses

  32. IgE • Has specially affinity for receptors on the basophils • In the blood or mast cells in the tissues • When IgE binds to antigens, the associated B cells secrete specific molecules that are related to allergic responses • Histamine is one of these molecules • IgE is found primarily in tissues and bodily fluids

  33. Immune Disorders- SCIDS

  34. SCIDS • Most cases of SCID are due to mutations in the gene encoding the common gamma chain (γc), • A protein that is shared by the receptors for InterleukinsIL-2, IL-4, IL-7, IL-9 and IL-15. • These interleukins and their receptors are involved in the development and differentiation of T and B • Another well-known form of SCID is caused by a defective enzyme, adenosine deaminase (ADA), • Necessary for the breakdown of purines. Lack of ADA causes accumulation of dATP. • This metabolite will inhibit the activity of ribonucleotide diphosphate reductase, the enzyme that reduces ribonucleotides to generate deoxyribonucleotides

  35. Genetic Diseases of the Immune System • Severe combined immunodeficiency • Multiple types • X linked and autosomal • Affect both cellular and humoral aspects of the immune system T cell-negative (T-), B cell-negative (B-), natural killer cell-positive (NK+) Gene map locus 11p13, 11p13 SCIDS

  36. Immune Disorders

  37. Immune disorders • #301000,WISKOTT-ALDRICH SYNDROME; WAS • The manifestations of Wiskott-Aldrich syndrome are eczema, thrombocytopenia, proneness to infection, and bloody diarrhea. • Death usually occurs before age 10 years. • Bone Marrow transplants are a treatmentpossibility

  38. Genetics of Immunoglobulins

  39. Generation of Immunoglobulins

  40. Genetics of Immunoglobulins • Genes for the constant region • Genes for the variable region • Light and heavy chained molecules are synthesized separately • The diversity of antibody-binding sites comes from the random combinations of variable gene segments that join with constant gene segments

  41. Naturally Acquired Active immunity • The immune system responds to an invader by producing antibodies and activated lymphocytes • This can produce a life long immunity

  42. Naturally Acquired Passive Immunity • Antibodies transferred across the placenta to the fetus • Transfer of antibodies through the colostrum in the breast milk • Both of these provide temporary immunity to an infant

  43. Artificially Acquired Passive Immunity • When antibodies made by other hosts are introduced into a new host • An example of this is rattlesnake antivenin injection • Antivenins are antibodies produced by other animals such as horses or cows • The host does not make new antibodies - the antibodies supplied circulate for as long as a month and are eventually destroyed in the host

  44. Venom • Rattlesnake venom is a mixture of enzymes that possess the ability to destroy cells • Can be a neurotoxin as well • Injected like a hypodermic

  45. Antivenin • Antivenin is a polyvalent preparation of globulins prepared by the fractionation of horse’s serum • It is a mixture of globulins from different types of rattlesnakes One of antigens in rattlesnake venom

  46. Artificially Acquired Active Immunity • When an individual is exposed to a vaccine • The vaccine might include attenuated ( weakened) organism, portions of the organism, toxins, subunits of antigenic portions of the organism

  47. Chicken Pox – Varicella Zoster • Chickenpox begins as a cold • Sneezing, coughing, and a runny nose • Two days later a rash begins • Usually begins on the chest and face • It may spread all over the body

  48. Chicken Pox • Infection spread by aerosolized droplets • It is contagious 1-2 days prior to the onset of symptoms • It takes 20 days to develop symptoms • It takes 5-10 days for the immune system to defeat the virus

  49. All children between 12 and 18 months of age should have one dose of chickenpox vaccine. • Children who have had chickenpox do not need the vaccine. • No tests need to be administered to determine immune status - a parent's recollection of the disease is considered a reliable measure of previous infection and therefore immunity.･ • Children between 19 months and their 13th birthday who have not had chickenpox should be vaccinated with a single dose.･People 13 and older who have not had chickenpox should get two doses of the vaccine 4 to 8 weeks apart.

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