PowerPoint ® Lecture Slide Presentation by Patty Bostwick-Taylor, Florence-Darlington Technical College Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings PART B 12 The Lymphatic System and Body Defenses

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Immunology  Immune response — is the immune system’s response to a threat  Antibodies are proteins that protect from specific antigens

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Antigens (nonself substance)  Any substance capable of activating immune system and causing an immune response  Examples of common antigens  Foreign proteins (strongest)  Large carbohydrates  Some lipids  Pollen grains  Microorganisms

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Three aspects of adaptive defense 1.Antigen specific—recognizes and acts against particular foreign substances 2.Systemic— works throughout body 3.Memory—recognizes and mounts a stronger attack on previously encountered pathogens

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Self-antigens  Human cells have many surface proteins  Your immune cells do not attack our own proteins  recognize your proteins  In another person, your proteins can trigger an immune response  Restricts donors for transplants

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Comparisons  Red vs White Blood Cells  Leukocytes vs. Lymphocytes

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings If I asked you to organize these words…  Use the terms below to construct a tree or graphic organizer based on your understanding of them (feel free to color code if it’s helpful): - White blood cell- Macrophage - Lymphocyte- Phagocyte - Neutrophil- Natural killer cell - B cell- T cell - Monocyte- Innate immune system - Adaptive immune system

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Types of Immunity in Immune Response  Humoral immunity “antibody-mediated immunity”  Defense by antibodies  found in body fluids  Lymphocytes don’t kill directly  Cellular immunity “cell-mediated immunity”  Lymphocytes directly destroy virus- infected cells, cancer cells, and foreign cells

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Cells of the Adaptive Defense System  Lymphocytes  respond to specific antigens  B lymphocytes (B cells)  T lymphocytes (T cells)  Macrophages help lymphocytes BUT MACROGPHAGES DO NOT respond to specific antigens

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Lymphocyte Differentiation and Activation Figure 12.11, step 1b Site of lymphocyte origin KEY: Site of antigen challenge and final differentiation to mature B and T cells Sites of development of immunocompetence as B or T cells; primary lymphoid organs Lymphocytes destined to become T cells migrate from bone marrow to the thymus and develop immunocompetence there. B cells develop immuno-competence in the bone marrow. and Bone marrow Immature lymphocytes Circulation in blood Thymus

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Lymphocyte Differentiation and Activation Figure 12.11, step 2 Site of lymphocyte origin KEY: Site of antigen challenge and final differentiation to mature B and T cells Sites of development of immunocompetence as B or T cells; primary lymphoid organs Lymphocytes destined to become T cells migrate from bone marrow to the thymus and develop immunocompetence there. B cells develop immuno-competence in the bone marrow. After leaving the thymus or bone marrow as naive immunocompetent cells, lymphocytes “seed” the infected connective tissues (especially lymphoid tissue in the lymph nodes), where the antigen challenge occurs and the lymphocytes become fully activated. and Bone marrow Lymph nodes and other lymphoid tissues Immature lymphocytes Circulation in blood Immunocompetent, but still naive, lymphocytes migrate via blood Thymus

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Lymphocyte Differentiation and Activation Site of lymphocyte origin KEY: Site of antigen challenge and final differentiation to mature B and T cells Sites of development of immunocompetence as B or T cells; primary lymphoid organs Lymphocytes destined to become T cells migrate from bone marrow to the thymus and develop immunocompetence there. B cells develop immuno-competence in the bone marrow. After leaving the thymus or bone marrow as naive immunocompetent cells, lymphocytes “seed” the infected connective tissues (especially lymphoid tissue in the lymph nodes), where the antigen challenge occurs and the lymphocytes become fully activated. Activated (mature) lymphocytes circulate continuously in the bloodstream and lymph, and throughout the lymphoid organs of the body. and Bone marrow Lymph nodes and other lymphoid tissues Immature lymphocytes Circulation in blood Immunocompetent, but still naive, lymphocytes migrate via blood Mature immunocompetent B and T cells recirculate in blood and lymph Thymus

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Verbal Summary of the 3 Previous Slides  Lymphocytes must be immunocompetent to work  Must respond to a specific antigen  All lymphocytes originate from hemocytoblasts in the red bone marrow  B lymphocytes become immunocompetent in the bone marrow (remember B for B one marrow)  T lymphocytes become immunocompetent in the thymus (remember T for T hymus)

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Functions of Cells and Molecules Involved in Immunity Table 12.3 (2 of 2)

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings B cell activation  leads to a humoral response

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings B cell activation  leads to a humoral response

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings B cell activation  leads to a humoral response

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings *** Events of the Humoral/Antibody Mediated Immune Response *** 1.A B lymphocyte with binds to its specific antigen 2.The binding event attracts a helper T cells which activates the B cell with chemicals 3.The B cell undergoes clonal selection (fancy way of saying the B cell divides) 4.Many clones are produced  MOST go on to make antibodies  fight this infections

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings B cell activation  leads to a humoral response  B cells can become antibody-making plasma cells (most do) BUT some become memory B cells…

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Figure Humoral Immune Response Primary Response (initial encounter with antigen) Antigen Antigen binding to a receptor on a specific B cell (lymphocyte) (B cells with non-complementary receptors remain inactive) Proliferation to form a clone B lymphoblasts Plasma cells Secreted antibody molecules Clone of cells identical to ancestral cells Subsequent challenge by same antigen Memory B cell Memory B cells Plasma cells Secreted antibody molecules Secondary Response (can be years later) hill.com/sites/ /student_view0/chapter22/animati on__the_immune_response.html

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Humoral Immune Response  Most B cells become plasma cells  Produce antibodies to destroy antigens  Activity lasts for 4 or 5 days  Some B cells become long-lived memory cells (secondary humoral response)

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Humoral Immune Response  Secondary humoral responses  Memory cells are long-lived  A second exposure causes a rapid response  The secondary response is stronger and longer lasting

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Figure Humoral Immune Response Primary Response (initial encounter with antigen) Antigen Antigen binding to a receptor on a specific B cell (lymphocyte) (B cells with non-complementary receptors remain inactive) Proliferation to form a clone B lymphoblasts Plasma cells Secreted antibody molecules Clone of cells identical to ancestral cells Subsequent challenge by same antigen Memory B cell Memory B cells Plasma cells Secreted antibody molecules Secondary Response (can be years later)

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings NOTELESS REVIEW  In groups no larger than 3 people flow chart & describe the events that cause B cell activation  Use the terms  Plasma cell  Memory B cell  Immunocompetent  Explain why in a secondary response the immune system reacts rapidly and intensely  Clonal selection  Helper T cell  Antibody

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Figure Humoral Immune Response

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Types of Acquired Immunity Figure ch?v=gZFp3l9rHKU

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Antibodies (Immunoglobulins)  Soluble proteins secreted by B cells (plasma cells)  Carried in bodily fluids (to look for invaders  Capable of binding specifically to an antigen

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Figure 12.15a Antibodies

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Antibody Structure  Four amino acid chains linked by disulfide bonds  Two heavy chains  Two light chains  Specific antigen- binding sites are present where heavy & light chains interact

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Antibody function  BOTH of these allow phagocytosis to occur 1. Precipitation- when soluble antigens are clustered together get so big they become solids 2. Agglutination- clumping of anitgens with antibodies

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings

Antibody function  Besides recruiting macrophages antibodies can Complement fixation – complement proteins activated, cause Neutralization- prevent antigen’s use of toxic chemicals Hy8THENXo

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Antibody Function Figure com/watch?v=lrYlZ Jiuf18

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings What do you think these are? What do you know about this type of cell?

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Rat alveolar macrophages attach to and ingest polystyrene elliptical disk particles. The macrophage cells are ~15 µm in diameter, and the polystyrene particles are 3 µm long, 1 µm wide, and 0.1 µm thick. Interactions of the peculiarly shaped particles and the macrophages provide insight into phagocytosis and the functioning of the immune system.  Arise from monocytes when exposed to chemicals  Widely distributed in lymphoid organs  Tend to remain fixed in the lymphoid organs Macrophages

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings I LIED to you ALL  When I told you macrophages were not lymphocytes I told the truth  When I told you macrophages are not involved in the adaptive/specific immune system I told a BIG FAT LIE… it was to HELP YOU… to SAVE YOU from going crazy and getting mucho confused!!!

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Cellular (Cell-Mediated) Immune Response  Antigens must be presented to T cells  Presenters: macrophages OR cells infected by an antigen (antigen presentation)  T cells must recognize non-self and self molecules  After T cells bind to antigen and self- antigen MANY clones form (like with B cells) and different cells are produced hill.com/sites/ /student_view0/chapter2 2/animation__the_immune_response.html

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Cellular (Cell-Mediated) Immune Response Figure 12.17

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings T cell clones 1. Cytotoxic (killer) T cells  Kill virus-infected, cancer- infected, or foreign cells from a graft or transplant  Insert a toxic chemical (perforin) then release enzyme-degrading chemicals (granzymes) 2. Memory T cells  Remember invader for next time

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Cellular (Cell-Mediated) Immune Response Figure 12.18

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings B cell activation T cell activation

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings

Figure ww.yout ube.com/ watch?v= CeVtPDj JBPU

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Organ Transplants and Rejection  Major types of grafts  Autografts—tissue transplanted from one site to another on the same person  Isografts—tissue grafts from an identical person (identical twin)  Allografts—tissue taken from an unrelated person  Xenografts—tissue taken from a different animal species Best Donors Never work Can work w/ close match

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings

Immune System Disorders  Autoimmune diseases  Rneumatoid Arthritis  Graves Disease  Multiple Sclerosis  Systemic Lupus  Immunodeficiencies  HIV  Allergies

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Rheumatoid Arthritis

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Graves Disease

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Multiple Sclerosis

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Systemic Lupus

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Immunodeficiencies  Condition that is inherited or acquired, marked by abnormal production or function of the immune cells  HIV/AIDS  Virus that attacks and destroys helper T cells (CD4)  Killer T cells can’t be activated (humoral response is affected too)  Healthy person T cells/volume (500 or above is normal)  CD4 count of 200 or less means you have AIDS

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings HIV/AIDS  Treated with meds  Reverse transcriptase inhibitors  viral RNA can’t become DNA and insert into host’s DNA  Protease inhibitors  Cuts proteins to make the mature protein components of an infectious HIV viron; if no protease doesn’t work no new virons.  Drugs that prevent HIV from entering a cell DNA  HIV vaccines (in development, FDA approved vaccine to begin human trials in January 2012)

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Allergies  Many small molecules (haptens or incomplete antigens) are not antigen by themselves  When haptens link up with our own proteins they can however cause an immune response  The immune response is harmful rather than protective because it attacks our own cells

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Allergies (Hypersensitivity)  Abnormal, vigorous immune responses  Types of allergies  Immediate hypersensitivity  Triggered by release of histamine from antibodies binding to mast cells (contain histimine)  Reactions begin within seconds of contact with allergen  Anaphylactic shock—dangerous, rare systemic response after allogen enters into blood

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Allergy Mechanisms Figure Antigen (allergen) invades body Plasma cells produce large amounts of class IgE antibodies against allergen Mast cell with fixed IgE antibodies Granules containing histamine IgE IgE antibodies attach to mast cells in body tissues (and to circulating basophils) Sensitization stage More of same allergen invades body Allergen binding to IgE on mast cells triggers release of histamine (and other chemicals) Histamine causes blood vessels to dilate and become leaky, which promotes edema; stimulates release of large amounts of mucus; and causes smooth muscles to contract Subsequent (secondary) responses Antigen Histamine Mast cell granules release contents after antigen binds with IgE antibodies Outpouring of fluid from capillaries Release of mucus Constriction of bronchioles

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Allergy Mechanisms Figure 12.20, step 1 Antigen (allergen) invades body Sensitization stage

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Allergy Mechanisms Figure 12.20, step 2 Antigen (allergen) invades body Plasma cells produce large amounts of class IgE antibodies against allergen Sensitization stage

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Allergy Mechanisms Figure 12.20, step 3 Antigen (allergen) invades body Plasma cells produce large amounts of class IgE antibodies against allergen Mast cell with fixed IgE antibodies Granules containing histamine IgE IgE antibodies attach to mast cells in body tissues (and to circulating basophils) Sensitization stage

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Allergy Mechanisms Figure 12.20, step 4 More of same allergen invades body Subsequent (secondary) responses Antigen

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Allergy Mechanisms Figure 12.20, step 5 More of same allergen invades body Allergen binding to IgE on mast cells triggers release of histamine (and other chemicals) Subsequent (secondary) responses Antigen Histamine Mast cell granules release contents after antigen binds with IgE antibodies

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Allergy Mechanisms Figure 12.20, step 6 More of same allergen invades body Allergen binding to IgE on mast cells triggers release of histamine (and other chemicals) Histamine causes blood vessels to dilate and become leaky, which promotes edema; stimulates release of large amounts of mucus; and causes smooth muscles to contract Subsequent (secondary) responses Antigen Histamine Mast cell granules release contents after antigen binds with IgE antibodies Outpouring of fluid from capillaries Release of mucus Constriction of bronchioles

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Allergy Mechanisms Figure 12.20, step 7 Antigen (allergen) invades body Plasma cells produce large amounts of class IgE antibodies against allergen Mast cell with fixed IgE antibodies Granules containing histamine IgE IgE antibodies attach to mast cells in body tissues (and to circulating basophils) Sensitization stage More of same allergen invades body Allergen binding to IgE on mast cells triggers release of histamine (and other chemicals) Histamine causes blood vessels to dilate and become leaky, which promotes edema; stimulates release of large amounts of mucus; and causes smooth muscles to contract Subsequent (secondary) responses Antigen Histamine Mast cell granules release contents after antigen binds with IgE antibodies Outpouring of fluid from capillaries Release of mucus Constriction of bronchioles

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Types of allergies (continued)  Delayed hypersensitivity  Caused by substances that are haptens and come in contact w/ skin (poison ivy)  Triggered by the release of cytokines () from activated helper T cells  Symptoms usually appear 1–3 days after contact with antigen  Need corticosteroids to provide relief  Anti-inflammatory medication

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Disorders of Immunity: Immunodeficiencies  Production or function of immune cells or complement is abnormal  May be congenital or acquired  Includes AIDS (Acquired Immune Deficiency Syndrome)

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Disorders of Immunity: Autoimmune Diseases  The immune system does not distinguish between self and nonself  The body produces antibodies and sensitized T lymphocytes that attack its own tissues

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Disorders of Immunity: Autoimmune Diseases  Examples of autoimmune diseases  Multiple sclerosis—white matter of brain and spinal cord are destroyed  Myasthenia gravis—impairs communication between nerves and skeletal muscles  Type I diabetes mellitus—destroys pancreatic beta cells that produce insulin

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Disorders of Immunity: Autoimmune Diseases  Examples of autoimmune diseases  Rheumatoid arthritis—destroys joints  Systemic lupus erythematosus (SLE)  Affects kidney, heart, lung and skin  Glomerulonephritis—impairment of renal function

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Self Tolerance Breakdown  Inefficient lymphocyte programming  Appearance of self-proteins in the circulation that have not been exposed to the immune system  Eggs  Sperm  Eye lens  Proteins in the thyroid gland

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Self Tolerance Breakdown  Cross-reaction of antibodies produced against foreign antigens with self-antigens  Rheumatic fever

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Developmental Aspects of the Lymphatic System and Body Defenses  Except for thymus and spleen, the lymphoid organs are poorly developed before birth  A newborn has no functioning lymphocytes at birth, only passive immunity from the mother  If lymphatics are removed or lost, severe edema results, but vessels grow back in time

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Figure 12.12, step 1 Humoral Immune Response Primary Response (initial encounter with antigen) Antigen Antigen binding to a receptor on a specific B cell (lymphocyte) (B cells with non-complementary receptors remain inactive)

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Figure 12.12, step 2 Humoral Immune Response Primary Response (initial encounter with antigen) Antigen Antigen binding to a receptor on a specific B cell (lymphocyte) (B cells with non-complementary receptors remain inactive) Proliferation to form a clone B lymphoblasts

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Figure 12.12, step 3 Humoral Immune Response Primary Response (initial encounter with antigen) Antigen Antigen binding to a receptor on a specific B cell (lymphocyte) (B cells with non-complementary receptors remain inactive) Proliferation to form a clone B lymphoblasts Plasma cells Secreted antibody molecules Memory B cell

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Figure 12.12, step 4 Humoral Immune Response Primary Response (initial encounter with antigen) Antigen Antigen binding to a receptor on a specific B cell (lymphocyte) (B cells with non-complementary receptors remain inactive) Proliferation to form a clone B lymphoblasts Plasma cells Secreted antibody molecules Clone of cells identical to ancestral cells Subsequent challenge by same antigen Memory B cell Secondary Response (can be years later)