Chapter 22: The Lymphatic System & Immunity

Chapter 22: The Lymphatic System & Immunity

Homeostasis Drains interstitial fluid as well as provides mechanisms for defense against disease Disease-producing microbes are called pathogens Immunity or resistance is the ability to defend ourselves against disease Vulnerability is susceptibility Have both innate (nonspecific) & adaptive (specific) immunity

Figure 22-1 An Overview of the Lymphatic System.
Lymphocyte Lymphatic Vessels and Lymph Nodes Cervical lymph nodes Thoracic duct Right lymphatic duct Lymphoid Tissues and Organs Axillary lymph nodes Lymphatics of mammary gland Tonsil Thymus Cisterna chyli Spleen Lymphatics of upper limb Mucosa-associated lymphoid tissue (MALT) in digestive, respiratory, urinary, and reproductive tracts Lumbar lymph nodes Pelvic lymph nodes Appendix Red bone marrow Inguinal lymph nodes Lymphatics of lower limb

Functions Drains excess interstitial fluid Transports dietary lipids
Returns it to blood Transports dietary lipids Carries out immune responses

Lymphatic Vessels Includes Lymphatic capillaries Lymphatic vessels
Lymph trunks Lymphatic ducts

Lymphatic Capillaries
Closed on one end More permeable than blood capillaries Endothelial cells overlap & can open like ”swinging door” to allow fluid to move in Attached to surrounding tissues by anchoring filaments Called lacteals in small intestine Carry dietary lipids Lymph here is creamy white & called chyle

Figure 22-2 Lymphatic Capillaries.
Smooth muscle Arteriole Endothelial cells Lymphatic capillary Lymphocyte Incomplete basement membrane Lymph flow Areolar tissue To larger lymphatics Interstitial fluid Venule Interstitial fluid Plasma Lymphatic capillary Interstitial fluid Lymph flow Blood capillary Blood capillaries Areolar tissue a The interwoven network formed by blood capillaries and lymphatic capillaries. Arrows indicate the movement of fluid out of blood capillaries and the net flow of interstitial fluid and lymph. b A sectional view indicating the movement of fluid from the plasma, through the tissues as interstitial fluid, and into the lymphatic system as lymph.

Lymphatic Vessels Resemble small veins but thinner walls & more valves
Interrupted by lymph nodes along the way Lymphatic vessels exit lymph nodes & join with each other forming lymph trunks

Figure 22-3 Lymphatic Vessels and Valves.
Artery Vein Artery Vein Lymphatic vessel Lymphatic vessel Toward venous system Lymphatic valve From lymphatic capillaries a A diagrammatic view of areolar connective tissue containing small blood vessels and a lymphatic vessel. The cross- sectional view emphasizes their structural differences. Lymphatic valve Lymphatic vessel b Like valves in veins, each lymphatic valve consists of a pair of flaps that permit movement of fluid in only one direction. Lymphatic vessel and valve LM × 63

Lymph Trunks & Ducts Trunks pass into lymphatic ducts
R lymphatic duct receives drainage from R side of head, neck, upper extremity, & chest L (thoracic) lymphatic duct receives drainage from rest of the body Begins as dilation called cisterna chyli Ducts drain into junction of subclavian & jugular veins Lymph trunks collect drainage from many lymphatic vessels from a particular region Principal ones are Lumbar Intestinal Bronchomediastinal Subclavian Jugular

Brachiocephalic veins
Figure 22-4 The Relationship between the Lymphatic Ducts and the Venous System. Left internal jugular vein Brachiocephalic veins Right internal jugular vein Left jugular trunk Right jugular trunk Thoracic duct Right lymphatic duct Left subclavian trunk Right subclavian trunk Left bronchomediastinal trunk Right subclavian vein Left subclavian vein Right bronchomediastinal trunk Superior vena cava (cut) First rib (cut) Azygos vein Highest intercostal vein Rib (cut) Thoracic duct Drainage of right lymphatic duct Drainage of thoracic duct Thoracic lymph nodes Hemiazygos vein Parietal pleura (cut) Diaphragm Cisterna chyli Inferior vena cava (cut) Intestinal trunk Right lumbar trunk Left lumbar trunk a The thoracic duct carries lymph originating in tissues inferior to the diaphragm and from the left side of the upper body. The smaller right lymphatic duct carries lymph from the rest of the body. b The thoracic duct empties into the left subclavian vein. The right lymphatic duct empties into the right subclavian vein.

Lymphatic Organs Primary lymphatic organs Secondary lymphatic organs
Sites were stem cells divide & become immunocompetent (mount an immune response) Includes Red bone marrow Thymus Secondary lymphatic organs Sites where most of the immune responses occur Lymph nodes Spleen Lymphatic nodules

Figure 22-6 The Origin and Distribution of Lymphocytes (Part 1 of 3).
Red Bone Marrow One group of stem cells remains in the red bone marrow, producing daughter cells that mature into NK cells and B cells. Multipotent hemopoietic stem cell Interleukin-7 Lymphoid stem cells Lymphoid stem cells NK cells B cells

Figure 22-6 The Origin and Distribution of Lymphocytes (Part 2 of 3).
Thymus The second group of stem cells migrates to the thymus, where subsequent divisions produce daughter cells that mature into T cells. Thymic hormones Lymphoid stem cells Production, selection, and differentiatiion of T cells Mature T cells Mature T cells

Thymus Bilobed organ consisting of divisions called lobules
Each lobule has a cortex & medulla In the medulla, thymic corpuscles or Hassall’s corpuscles Assists in maturation of the T cells

Anatomical landmarks on the thymus.
Figure 22-9 The Thymus. Thyroid gland Trachea Right lobe Left lobe Thymus Right lobe Left lobe Septa Left lung Right lung Heart Lobule Diaphragm b Anatomical landmarks on the thymus. a The appearance and position of the thymus in relation to other organs in the chest. Medulla Septa Cortex Lymphocytes Lobule Thymic corpuscle Thymic epithelial cells Lobule A thymic corpuscle LM × 550 The thymus gland LM × 50 d Higher magnification reveals the unusual structure of thymic corpuscles. The small cells are lymphocytes in various stages of development. c Fibrous septa divide the tissue of the thymus into lobules resembling interconnected lymphoid nodules.

Lymph Nodes Usually occur in groups Cortex has lymphatic nodules
Filters lymph & carries out immune responses

Figure 22-8 The Structure of a Lymph Node.
Lymphatic vessel Lymph nodes Efferent vessel Lymph node artery and vein Hilum Lymph nodes Trabeculae Medulla Medullary sinus Cortex Outer cortex (B cells) Subcapsular space Subcapsular space Germinal center Outer cortex Capsule Deep cortex (T cells) Dividing B cell Capsule Medullary cord (B cells and plasma cells) Afferent vessel Dendritic cells Nuclei of B cells Capillary

Spleen Organized into white pulp, which is mostly lymphocytes & macrophages, & red pulp, which is blood filled venous sinuses Functions include Removal of worn-out, ruptured, or defective RBCs & platelets Storage of platelets Hemopoiesis during fetal life Immune responses

Figure The Spleen. Parietal peritoneum Visceral peritoneum Stomach Diaphragm Spleen Rib Gastrosplenic ligament Liver Pancreas Gastric area Diaphragmatic surface Aorta Spleen Hilum Renal area Kidneys SUPERIOR a A transverse section through the trunk, showing the typical position of the spleen projecting into the peritoneal cavity. The shape of the spleen roughly conforms to the shapes of adjacent organs. White pulp of splenic nodule Gastric area Capsule Hilum Red pulp Splenic vein Renal area Splenic artery Trabecular artery Splenic lymphatic vessel Central artery in splenic nodule The spleen LM × 50 INFERIOR c Spleen histology. White pulp is dominated by lymphocytes; it appears purple because the nuclei of lymphocytes stain very darkly. Red pulp contains a large number of red blood cells. b A posterior view of the surface of an intact spleen, showing major anatomical landmarks.

Lymphatic Nodules Masses of lymphoid tissue scattered throughout lamina propria of GI, urinary, reproductive, & respiratory systems Known as mucosa-associated lymphatic tissue (MALT) Some occur in large aggregations such as Peyer’s patches , in the appendix, & the tonsils

Figure 22-7 Lymphoid Nodules.
Pharyngeal epithelium Pharyngeal tonsil Palate Germinal centers within nodules Palatine tonsil Lingual tonsil Pharyngeal tonsil LM × 40 a The locations of the tonsils Intestinal lumen Mucous membrane of intestinal wall Germinal center Aggregated lymphoid nodule in intestinal mucosa Underlying connective tissue b Diagrammatic view of aggregated lymphoid nodule Aggregated lymphoid nodules LM × 20

Innate Immunity Includes external physical & chemical barriers & various internal defenses Skin & mucous membranes Antimicrobial substances Natural killer cells Phagocytes Inflammation Fever

Figure 22-11 Innate Defenses.
Physical barriers Duct of eccrine sweat gland keep hazardous organisms and materials outside the body. Hair Secretions Epithelium Phagocytes engulf pathogens and cell debris. Fixed macrophage Free macrophage Neutrophil Eosinophil Monocyte Immune surveillance is the destruction of abnormal cells by NK cells in peripheral tissues. Lysed abnormal cell Natural killer cell Interferons are chemical messengers that coordinate the defenses against viral infections. Interferons released by activated lymphocytes, macrophages, or virus-infected cells Complement is a system of circulating proteins that assist antibodies in the destruction of pathogens. Lysed pathogen Complement Inflammation Blood flow increased Phagocytes activated Capillary permeability increased Complement activated Clotting reaction walls off region Regional temperature increased Adaptive defenses activated is a localized, tissue-level response that tends to limit the spread of an injury or infection. Mast cell Fever is an elevation of body temperature that accelerates tissue metabolism and body defenses. Body temperature rises above 37.2C in response to pyrogens

Skin 1st lines of defense
Provide both physical & chemical barriers to prevent entry of pathogens & foreign substances Characteristics of skin that make it a good physical barrier Many layers of closely packed cells Keratinized Periodic shedding Chemically, the skin provides Sebum from sebaceous glands Unsaturated fatty acids inhibit certain bacteria due to acidity Sweat from sweat glands Helps to flush from surface

Mucous Membranes Secrete mucus which is thick & sticky trapping microbes Respiratory Guard hairs Cilia Coughing Sneezing GI tract Saliva Defecation Vomiting Acidity of gastric juice Urinary Flow of urine Lacrimal apparatus Washing action of tears Lysozyme Enzyme with antibacterial properties

Figure 22-11 Innate Defenses (Part 1 of 2).
Physical barriers Duct of eccrine sweat gland keep hazardous organisms and materials outside the body. Hair Secretions Epithelium Phagocytes engulf pathogens and cell debris. Fixed macrophage Free macrophage Neutrophil Eosinophil Monocyte Immune surveillance is the destruction of abnormal cells by NK cells in peripheral tissues. Lysed abnormal cell Natural killer cell Interferons are chemical messengers that coordinate the defenses against viral infections. Interferons released by activated lymphocytes, macrophages, or virus-infected cells

2nd Lines of Defense Engage once 1st lines of defense have been breached Includes Antimicrobial substances Phagocytes Natural killer cells Inflammation Fever

Antimicrobial Substances
4 main types that discourage microbial growth Interferons Produced when cells infected with viruses Stimulate neighboring cells to produce antiviral proteins that interfere with viral replication 3 types Alpha Beta Gamma

Figure Interferons. Interferon alpha (α) is produced by cells infected with viruses. They attract and stimulate NK cells and enhance resistance to viral infection. Interferon beta (β) is secreted by fibroblasts and slows inflammation in a damaged area. Interferon gamma () is secreted by T cells and NK cells and stimulates macrophage activity.

4 main types that discourage microbial growth Interferons Complement Group of inactive proteins in plasma that enhance or “complement” certain immune reactions C1-C9 & factors B, D, & P (properdin) Causes Cytolysis Promotes phagocytosis Contributes to inflammation

Complement Activation
Classical pathway Antigen-antibody complex activates C1 Eventually leads to activation of C3 Alternative pathway Interaction between lipid-carbohydrate complexes on microbial surface & complement factors B, D, & P It then activates C3 Lectin pathway Proteins produced by liver which bind to surface of microbe causing the activation of C3

Figure 22-14 Pathways of Complement Activation.
Alternative Pathway The alternative pathway begins when several complement proteins, notably properdin, interact in the plasma. This interaction can be triggered by exposure to foreign materials, such as the capsule of a bacterium. The end result is the attachment of an activated C3b protein to the bacterial cell wall. C3 The alternative pathway is important in the defense against bacteria, some parasites, and virus-infected cells. Properdin Factor B Factor D C3b Bacterial cell wall Classical Pathway Cell Lysis by Pore Formation The most rapid and effective activation of the complement system occurs through the classical pathway. C3b Attachment (alternative pathway) Once an activated C3b protein has attached to the cell wall, additional complement proteins form a membrane attack complex (MAC) in the membrane that destroys the integrity of the target cell. C5-C9 Antibody Binding and C1 Attachment MAC Antibody binding C3b Antibodies Bacterial cell wall Activation and Cascade C3b Attachment (classical pathway) C4 C2 C3 C1 C3b C3b Multiple pores in bacterium Cell lysis Enhanced Phagocytosis A coating of complement proteins and antibodies both attracts phagocytes and makes the target cell easier to engulf. This enhancement of phagocytosis, a process called opsonization, occurs because macrophage membranes contain receptors that detect and bind to complement proteins and bound antibodies. C1 must attach to two antibodies for its activation. The attached C1 protein then acts as an enzyme, catalyzing a series of reactions involving other complement proteins. The classical pathway ends with the conversion of an inactive C3 to an activated C3b that attaches to the cell wall. Histamine Release Release of histamine by mast cells and basophils increases the degree of local inflammation and accelerates blood flow to the region.

Complement C3 C3a C3b C5 C5a C5b MAC Phagocytosis Inflammation
Joins with C6, C7, C8, C9 MAC

Figure 22-14 Pathways of Complement Activation (Part 3 of 3).
Cell Lysis by Pore Formation Once an activated C3b protein has attached to the cell wall, additional complement proteins form a membrane attack complex (MAC) in the membrane that destroys the integrity of the target cell. C5-C9 MAC Multiple pores in bacterium Cell lysis Enhanced Phagocytosis A coating of complement proteins and antibodies both attracts phagocytes and makes the target cell easier to engulf. This enhancement of phagocytosis, a process called opsonization, occurs because macrophage membranes contain receptors that detect and bind to complement proteins and bound antibodies. Histamine Release Release of histamine by mast cells and basophils increases the degree of local inflammation and accelerates blood flow to the region.

Complement is a system of circulating proteins that assist antibodies in the destruction of pathogens. Lysed pathogen Complement Inflammation Blood flow increased Phagocytes activated Capillary permeability increased Complement activated Clotting reaction walls off region Regional temperature increased Adaptive defenses activated is a localized, tissue-level response that tends to limit the spread of an injury or infection. Mast cell Fever is an elevation of body temperature that accelerates tissue metabolism and body defenses. Body temperature rises above 37.2C in response to pyrogens

4 main types that discourage microbial growth Interferons Complement Iron-binding proteins Inhibit growth of bacteria by reducing available Fe2+ Includes Transferrin Lactoferrin Hemoglobin

4 main types that discourage microbial growth Interferons Complement Iron-binding proteins Antimicrobial proteins Can kill a wide range of microbes Can also attract dendritic cells & mast cells Includes Dermicidin Defensins Cathelicidins

Natural Killer (NK) Cells
Lymphocyte Can kill wide range of infected body cells & certain tumor cells Attack any cell that displays abnormal or unusual membrane proteins Releases perforin, which pokes holes in cell membrane causing cytolysis Also releases granzyme which induce cell to undergo apoptosis

Figure 22-12 How Natural Killer Cells Kill Cellular Targets.
Recognition and adhesion 2 Realignment of Golgi apparatus 3 Secretion of perforin 4 Lysis of abnormal cell NK cell Golgi apparatus Abnormal cell Perforin molecules Pores formed by perforin complex NK cell Abnormal cell

Phagocytes Perform phagocytosis 2 major cells 5 phases Chemotaxis
Neutrophils Macrophages Wandering Fixed 5 phases Chemotaxis Adherence Ingestion Forms phagosome Digestion Phagosome merges with lysosome forming phagolysosome Phagocyte forms lethal oxidants in process called oxidative burst Killing

Inflammation Dispose of microbes, toxins, or foreign material at site of injury, prevent spread to other tissues, & prepare site for repair 3 basic stages Vasodilation & increased permeability of blood vessels Emigration Tissue repair Cardinal signs of inflammation Redness Heat Pain Swelling

Tissue Damage Mast Cell Activation Chemical change
Figure Inflammation and the Steps in Tissue Repair (Part 1 of 2). Tissue Damage Chemical change in interstitial fluid Mast Cell Activation Release of histamine and heparin from mast cells

Vasodilation & Increased Capillary Permeability
Promoted by Histamine Kinins Prostaglandins Leukotrienes Complement Vasodilation allows greater blood flow while increased capillary permeability allows defensive mechanisms to enter into damaged area

Tissue Repair Phagocyte Attraction Attraction of phagocytes,
Figure Inflammation and the Steps in Tissue Repair (Part 2 of 2). Redness, Swelling, Heat, and Pain Phagocyte Attraction Attraction of phagocytes, especially neutrophils Dilation of blood vessels, Increased blood flow, increased vessel permeability Release of cytokines Clot formation (temporary repair) Removal of debris by neutrophils and macrophages; stimulation of fibroblasts Activation of specific defenses Tissue Repair Pathogen removal, clot erosion, scar tissue formation

Emigration Depends on chemotaxis
Neutrophils respond first followed by macrophages Accumulation of dead bacteria, debris, & dead phagocytes forms pus

Tissue Repair Phagocyte Attraction Attraction of phagocytes,
Figure Inflammation and the Steps in Tissue Repair (Part 2 of 2). Redness, Swelling, Heat, and Pain Phagocyte Attraction Attraction of phagocytes, especially neutrophils Dilation of blood vessels, Increased blood flow, increased vessel permeability Release of cytokines Clot formation (temporary repair) Removal of debris by neutrophils and macrophages; stimulation of fibroblasts Activation of specific defenses Tissue Repair Pathogen removal, clot erosion, scar tissue formation

Fever Hypothalamic thermostat is reset to higher temperature due to microbial toxins or other pyrogens Intensifies effects of interferon, inhibits growth of some microbes, & speeds up body reactions

Adaptive Immunity Also known as specific or acquired immunity
Different from innate immunity Specificity Must be able to distinguish self from non-self Memory Substance that provokes an immune response is known as an antigen

Figure 22-5 Classes of Lymphocytes.
subdivided into T Cells B Cells NK Cells Approximately 80% of circulating lymphocytes are classified as T cells. B cells make up 10–15% of circulating lymphocytes. NK cells make up the remaining 5–10% of circulating lymphocytes. differentiate into Cytotoxic T Cells Helper T Cells Suppressor T Cells Memory T Cells Plasma Cells Cytotoxic T cells attack foreign cells or body cells infected by viruses. Helper T cells stimulate the activation and function of both T cells and B cells. Suppressor T cells inhibit the activation and function of both T cells and B cells. Memory T cells are a subset of T cells that respond to a previously encountered antigen. When stimulated, B cells can differentiate into plasma cells, which produce and secrete antibodies.

Figure 22-6 The Origin and Distribution of Lymphocytes.
Red Bone Marrow Thymus One group of stem cells remains in the red bone marrow, producing daughter cells that mature into NK cells and B cells. The second group of stem cells migrates to the thymus, where subsequent divisions produce daughter cells that mature into T cells. Multipotent hemopoietic stem cell Migrate to thymus Thymic hormones Interleukin-7 Lymphoid stem cells Lymphoid stem cells Lymphoid stem cells Production, selection, and differentiation of T cells NK cells B cells Mature T cells Mature T cells B cells and NK cells enter the bloodstream and migrate to peripheral tissues. Mature T cells enter the bloodstream and migrate to the lymph nodes, spleen, and other lymphoid tissues. Peripheral Tissues All three types of lymphocytes circulate throughout the body in the bloodstream, establishing immunity. Immune surveillance Antibody-mediated immunity Cell-mediated immunity NK cells attack foreign cells, body cells infected by viruses, and cancer cells. They secrete chemicals that lyse the plasma membrane of the abnormal cells. When stimulated, B cells can differentiate into plasma cells, which produce and secrete antibodies. These antibodies attach to pathogens. This starts a chain reaction that leads to the destruction of the pathogen. One type of mature T cell, called cytotoxic T cells, plays a role in cell-mediated immunity. These cells attack and destroy foreign cells or body cells infected by viruses. NK cells B cell Cytotoxic T cell Abnormal cell Abnormal cell Plasma cell Cell destroyed Antibodies Cell destroyed

Immunocompetence Both B cells & T cells must develop immunocompetence before they leave their sites of maturation Ability to carry out immune response Consists of placing proteins into & onto cell membrane some which are the antigen receptor capable of recognizing a specific antigen

Figure 22-17 An Overview of the Immune Response.
Cell-Mediated Immunity Direct Physical and Chemical Attack Activated T cells find the pathogens and attack them through phagocytosis or the release of chemical toxins. Adaptive Immunity Antigen presentation triggers specific defenses, or an immune response. Phagocytes activated T cells activated Communication and feedback Destruction of antigens Antibody-Mediated Immunity Attack by Circulating Antibodies Activated B cells give rise to cells that produce antibodies

Clonal Selection (Expansion)
When a B cell or T cell encounters its antigen, it proliferates & differentiates This results in clones that also recognize this same antigen Most of the clones become effector cells meaning that they seek out the antigen; the others become memory cells

Antigens Have 2 important characteristics
Immunogenicity Can provoke an immune response Reactivity Ability of antigen to react specifically with the antibodies or cells that it provoked Has epitopes or antigenic determinants that are what our immune system recognizes & reacts to Large, complex molecules that are usually proteins Smaller substances that lack immunogenicity are called haptens

MHC Antigens Major histocompatibility complex “self antigens”
Glycoproteins located in our cell membranes Unique to each individual except identical twins 2 types MHC-I All nucleated cells of the body MHC-II On surface of antigen presenting cells

Exogenous Antigen Presentation
Plasma membrane 5 1 Antigenic fragments are displayed by Class II MHC proteins on the plasma membrane. Phagocytic APCs engulf the extracellular pathogens. 4 Antigenic fragments are bound to Class II MHC proteins. 2 Lysosomal action produces antigenic fragments. 3 The endoplasmic reticulum produces Class II MHC proteins. Nucleus Endoplasmic reticulum Lysosome c Phagocytic antigen-presenting cell.

Endogenous Antigen Presentation
1 Plasma membrane 5 Antigen presentation by Class I MHC proteins is triggered by viral or bacterial infection of a body cell. The abnormal peptides are displayed by Class I MHC proteins on the plasma membrane. Viral or bacterial pathogen 2 The infection results in the appearance of abnormal peptides in the cytoplasm. Transport vesicle 4 After export to the Golgi apparatus, the MHC proteins reach the plasma membrane within transport vesicles. 3 The abnormal peptides are incorporated into Class I MHC proteins as they are synthesized at the endoplasmic reticulum. Endoplasmic reticulum Nucleus a Infected cell.

Cytokines Small proteins used for cellular communication
Can stimulate or inhibit normal cell function

Figure 22-28 Cytokines of the Immune System.

Cell-Mediated Immunity
Involves T cells T cells have MHC-I antigens but also have another known as a CD receptor CD8 Found on cytotoxic T cells Recognizes MHC-I CD4 Found on helper T cells Recognizes MHC-II

Antigen Recognition & Costimulation
T cells have to have antigen recognition meaning that they must have a receptor that recognizes the antigen & they have a CD4 or CD8 receptor that recognizes the MHC-I or MHC-II receptor Costimulation can involve either cytokines or membrane molecules

Figure 22-20 Antigen Recognition and Activation of Helper T Cells.
Antigen Recognition by CD4 T Cell Foreign antigen Antigen-presenting cell (APC) APC Class II MHC Antigen Costimulation Inactive CD4 (TH) cell CD4 protein T cell receptor TH cell CD4 T Cell Activation and Cell Division Memory TH cells (inactive) Active TH cells Cytokines Cytokines Active helper T cells secrete cytokines that stimulate both cell-mediated and antibody-mediated immunity. Cytokines

Figure 22-19 Antigen Recognition and Activation of Cytotoxic T Cells.
Activation and Cell Division Destruction of Target Cells Antigen recognition occurs when a CD8 T cell encounters an appropriate antigen on the surface of another cell, bound to a Class I MHC protein. Antigen recognition and costimulation result in T cell activation and cell division, producing active TC cells and memory TC cells. The active TC cell destroys the antigen-bearing cell. It may use several different mechanisms to kill the target cell. Infected cell Active TC cells Inactive CD8 T cell Viral or bacterial antigen Lysed cell Memory TC cells (inactive) Costimulation Perforin release Costimulation activates CD8 T cell Destruction of plasma membrane Before activation can occur, a T cell must be chemically or physically stimulated by the abnormal target cell. Cytokine release CD8 protein Stimulation of apoptosis Class I MHC T cell receptor Disruption of cell metabolism Antigen Lymphotoxin release Infected cell CD8 T cell

Antibody-Mediated Immunity
1 2 3 Sensitization Activation Division and Differentiation Antigens Class II MHC T cell receptor ANTIBODY PRODUCTION Antigen Class II MHC Antibodies B cell Inactive B cell T cell Antigens bound to antibody molecules Stimulation by cytokines Cytokine costimulation Plasma cells Antigen binding Activated B cells Sensitized B cell Helper T cell Sensitized B cell Memory B cells (inactive)

Antibodies Belong to a group of glycoproteins known as globulins so also called immunoglobulins (Ig) 4 polypeptides 2 heavy 2 light

Figure 22-23 Antibody Structure and Function.
Antigen binding site Heavy chain Antigen binding site Antigenic determinant sites Disulfide bond Variable segment Light chain Complement binding site Antigen Antibodies Constant segments of light and heavy chains Site of binding to macrophages c Antibodies bind to portions of an antigen called antigenic determinant sites, or epitopes. a A diagrammatic view of the structure of an antibody. Light chain Antigen binding site Complete antigen + Heavy chain Hapten Carrier molecule d Antibody molecules can bind a hapten (partial antigen) once it has become a complete antigen by combining with a carrier molecule. b A computer-generated image of a typical antibody.

Table 22-1 Classes of Antibodies (Part 1 of 2).

Table 22-1 Classes of Antibodies (Part 2 of 2).

Antibody Actions Neutralizes antigen Immobilizes bacteria
Agglutinating or precipitating antigen Activates the complement Enhances phagocytosis opsonization

Immunological Memory The primary response takes about two
SECONDARY RESPONSE IgG Antibody level in plasma IgG IgM IgM 1 2 3 4 1 2 3 4 Time (weeks) Time (weeks) a The primary response takes about two weeks to develop peak antibody levels (titers). IgM and IgG antibody levels do not remain elevated. b The secondary response has a very rapid increase in IgG antibody concentration and rises to levels much higher than those of the primary response. Antibody levels remain elevated for an extended period after the second exposure to the antigen.

Figure 22-16 Forms of Immunity.
Ability to resist Infection and disease Adaptive (Specific) Immunity Innate (Nonspecific) Immunity Adaptive immunity is not present at birth. You acquire immunity to a specific antigen only When you have been exposed to that antigen or receive antibodies from another source. Genetically determined— no prior exposure or antibody production involved Active Immunity Passive Immunity Develops in response to antigen exposure Produced by transfer of antibodies from another source Naturally acquired active immunity Artificially induced active immunity Naturally acquired passive immunity Artificially induced passive immunity Develops after exposure to antigens in environment Develops after administration of an antigen to prevent disease Conferred by transfer of maternal antibodies across placenta or in breast milk Conferred by administration of antibodies to combat infection

Figure 22-26 An Integrated Summary of the Immune Response.
Antigens Trigger Innate (Nonspecific) Immunity Complement system NK cells, Macrophages Adaptive (Specific) Immunity Antigen presentation by APCs Cell-Mediated Immunity Antibody-Mediated Immunity Antigen and Class I MHC Protein Indicates that the cell is infected or otherwise abnormal Antigen and Class II MHC Protein Indicates the presence of pathogens, toxins, or foreign proteins CD8 T cells CD4 T cells Cytotoxic T Cells Memory TC Cells Suppressor T Cells Helper T Cells Memory TH Cells Attack and destroy infected and abnormal cells displaying antigen Await reappearance of the antigen Moderate immune response by T cells and B cells Stimulate immune response by T cells and B cells Await reappearance of the antigen Inhibition Inhibition Activation of B cells Production of memory B cells Direct physical and chemical attack Production of plasma cells Direct physical and chemical attack Destruction of Antigens Secretion of antibodies Attack by circulating proteins

Figure 22-27 Defenses against Bacterial and Viral Pathogens.
VIRUSES Phagocytosis by macrophages and APCs Infection of tissue cells Infection of or uptake by APCs Antigen presentation Release of interferons Appearance of antigen in plasma membrane Antigen presentation Activation of cytotoxic T cells Activation of helper T cells Increased resistance to viral infection and spread Stimulation of NK cells Activation of cytotoxic T cells Activation of helper T cells Activation of B cells Activation of B cells Antibody production by plasma cells Antibody production by plasma cells Opsonization and phagocyte attraction Formation of antigen-antibody complexes Destruction of virus-infected cells Destruction of viruses or prevention of virus entry into cells Destruction of bacteria by cell lysis or phagocytosis a Defenses against bacteria involve phagocytosis and antigen presentation by APCs. b Defenses against viruses involve direct contact with virus-infected cells and antigen presentation by APCs.

Figure diagrams the functional relationships between the lymphatic system and the other body systems we have studied so far. SYSTEM INTEGRATOR Body System Lymphatic System Lymphatic System Body System Provides physical barriers to pathogen entry; macrophages in dermis resist infection and present antigens to trigger immune response; mast cells trigger inflammation, mobilize cells of lymphatic system Provides IgA antibodies for secretion onto integumentary surfaces Integumentary Integumentary Page 174 Lymphocytes and other cells involved in the immune response are produced and stored in red bone marrow Assists in repair of bone after injuries; osteoclasts differentiate from monocyte–macrophage cell line Skeletal Skeletal Page 285 Protects superficial lymph nodes and the lymphatic vessels in the abdominopelvic cavity; muscle contractions help propel lymph along lymphatic vessels Assists in repair after injuries Muscular Muscular Page 380 Microglia present antigens that stimulate adaptive defenses; glial cells secrete cytokines; innervation stimulates antigen-presenting cells Cytokines affect hypothalamic production of CRH and TRH Nervous Nervous Page 558 Glucocorticoids have anti-inflammatory effects; thymosins stimulate development and maturation of lymphocytes (T cells); many hormones affect immune function Thymus secretes thymosins; cytokines affect cells throughout the body Endocrine Endocrine Page 647 Distributes WBCs; carries antibodies that attack pathogens; clotting response helps restrict spread of pathogens; granulocytes and lymphocytes produced in red bone marrow Fights infections of cardiovascular organs; returns interstitial fluid to circulation Cardiovascular Cardiovascular Page 776 The LYMPHATIC System For all body systems, the lymphatic system provides adaptive (specific) immunity against infection. The lymphatic system is an anatomically distinct system. In comparison, the immune system is a physiological system that includes the lymphatic system, as well as components of the integumentary, skeletal, cardiovascular, respiratory, digestive, and other body systems. through immune surveillance, pathogens are continuously eliminated throughout the body. Respiratory Page 874 Digestive Gonads—ovaries in females and testes in males—are organs that produce gametes (sex cells). LH and FSH, hormones secreted by the anterior lobe of the pituitary gland, affect these organs. The ovaries and testes are discussed further in Chapter 28. Gonads—ovaries in females and testes in males—are organs that produce gametes (sex cells). LH and FSH, hormones secreted by the anterior lobe of the pituitary gland, affect these organs. The ovaries and testes are discussed further in Chapter 28. Page 929 Urinary Page 1010 Reproductive Page 1090

Table 22-2 Cells That Participate in Tissue Defenses (Part 1 of 2).

Table 22-2 Cells That Participate in Tissue Defenses (Part 2 of 2).

Chapter 22: The Lymphatic System & Immunity

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