UNIT 4 - CHAPTER 16: LYMPHATIC SYSTEM AND IMMUNITY LEARNING OUTCOMES: 1. Describe the general functions of the lymphatic system.

Transcription

1 LEARNING OUTCOMES: 16.1 Intrductin 1. Describe the general functins f the lymphatic system Lymphatic Pathways 2. Identify and describe the parts f the majr lymphatic pathways Tissue Fluid and Lymph 3. Describe hw tissue fluid and lymph frm, and explain the functin f lymph Lymph Mvement 4. Explain hw lymphatic circulatin is maintained, and describe the cnsequence f lymphatic bstructin Lymph Ndes 5. Describe a lymph nde and its majr functins. 6. Identify the lcatins f the majr chains f lymph ndes Thymus and Spleen 7. Discuss the lcatins and functins f the thymus and spleen Bdy Defenses Against Infectin 8. Distinguish between innate (nnspecific) and adaptive (specific) defenses Innate (Nnspecific) Defenses 9. List seven innate bdy defense mechanisms, and describe the actin f each mechanism Adaptive (Specific) Defenses r Immunity 10. Explain hw tw majr types f lymphcytes are frmed and activated and hw they functin in immune mechanisms. 11. Identify the parts f an antibdy mlecule. 12. Discuss the actins f the five types f antibdies. 16-1

2 LEARNING OUTCOMES: 13. Distinguish between primary and secndary immune respnses. 14. Distinguish between active and passive immunity. 15. Explain hw allergic reactins, tissue rejectin reactins, and autimmunity arise frm immune mechanisms Life-Span Changes 16. Describe life-span changes in immunity. 16-2

3 16.1 INTRODUCTION The lymphatic system is clsely assciated with the cardivascular system. The primary rgans f the lymphatic system are the bne marrw and thymus gland, and the secndary lymphatic rgans include the lymph ndes and spleen. These rgans wrk tgether t transprt excess tissue (interstitial) fluid t the bld stream, transprt dietary fat, and help defend the bdy against disease-causing agents (pathgens) LYMPHATIC PATHWAYS Lymphatic pathways begin as lymphatic capillaries, which cme tgether t frm afferent lymphatic vessels, which lead t lymph ndes. The vessels that leave the lymph ndes are called efferent lymphatic vessels, which cme tgether t frm lymphatic trunks, which lead t tw cllecting ducts, which finally jin the subclavian veins, where the lymph enters the cardivascular system. See General Overview Figure 16.1, page 617 and Fig 16.7, page 620. A. Lymphatic capillaries: See Fig 16.2, page 618 and Fig 16.8, page are micrscpic clsed-ended tubes that extend int interstitial spaces 2. receive lymph thrugh their thin walls 3. are assciated with anchring filaments, which serve an imprtant functin during edema (discussed later) 4. are lcated thrughut the bdy, except in: a. avascular tissues b. central nervus system c. splenic pulp d. bne marrw 5. include lacteals that are lymphatic capillaries within villi f the small intestine B. Lymphatic vessels (LV): See Fig 16.4 & 16.5, page are frmed by the merging f lymphatic capillaries 2. have walls similar t veins and pssess valves that prevent backflw f lymph. See Fig 16.3, page lead t lymph ndes as "afferent" LVs; leave lymph ndes as "efferent" LVs, and then merge int lymphatic trunks. 16-3

4 16.2 LYMPHATIC PATHWAYS C. Lymphatic trunks: See Fig 16.4, page drain lymph frm relatively large bdy regins 2. Principal lymphatic trunks include the fllwing: a. lumbar trunk b. intestinal trunk c. brnchmediastinal trunk d. subclavian trunk e. jugular trunk f. intercstal trunk 3. pass their lymph int venus bld by jining ne f tw cllecting ducts. D. Cllecting ducts: See Fig 16.6, page Tw within the thracic cavity: a. Right lymphatic duct drains the right upper bdy (25% f ttal bdy). b. Thracic (left lymphatic) duct drains the remaining 75% f the bdy's lymph. 2. jin the subclavian veins. See the abve figures t study the relatinship f lymphatic system t cardivascular system. See Summary Figure 16.7, page

5 16.3 TISSUE FLUID AND LYMPH A. Tissue Fluid Frmatin 1. Tissue fluid is bld plasma that has passed thrugh cardivascular capillary walls int interstitial spaces, minus large plasma prteins. 2. Recall the cnstituents f plasma frm Chapter 14: a. primarily water b. disslved substances including small plasma prteins, nutrients, wastes, gases, electrlytes, enzymes, and hrmnes. B. Lymph Frmatin 1. As prtein cncentratin in interstitial spaces increases, its pressure increases. 2. Increasing pressure frces tissue fluid int lymphatic capillaries. 3. This fluid is nw called lymph. 4. Lymph frmatin prevents accumulatin f excess tissue fluid (i.e. prevents edema). C. Lymph Functin 1. returns small leaked plasma prteins back t the bld stream 2. transprts freign particles t the lymph ndes 3. transprts lipids and lipid-sluble vitamins absrbed in GI tract t bldstream 16.4 LYMPH MOVEMENT A. Lymph Flw 1. Lymph is under lw pressure and may nt flw readily withut aid frm external frces (similar t venus return). a. The squeezing actin f skeletal muscles aids mvement. b. The lw pressure in the thracic cavity created by breathing mvements, mves lymph up frm abdminal t thracic regin. c. Recall the presence f ne-way valves. 2. Obstructin f lymph mvement a. Any cnditin that interferes with the flw f lymph results in edema. Edema = accumulatin f excess interstitial fluid leading t swelling f tissues. b. Tissue swelling pulls n anchring filaments making penings between cells even larger s mre fluid can mve int the lymphatic capillary (i.e. reducing swelling). See Fig 16.8, page c. The surgical remval f lymph ndes causes bstructin and results in edema (i.e. accmpanying mastectmy). 16-5

6 16.5 LYMPH NODES A. Structure f a Lymph Nde. See Fig 16.9, page 621, and Fig 16.10, page Overview: Lymph ndes are lcated alng lymphatic pathways; cntain lymphcytes, and macrphages, which destry invading micrrganisms. 2. Size is usually less than 2.5 cm, and shape is bean-like, with bld vessels, nerves, and efferent lymphatic vessels attached t the indented regin (hilum). a. Afferent lymphatic vessels enter at pints n the cnvex surface. 3. Nde is enclsed in a dense CT capsule that extends int the nde and subdivides it int ndules. 4. Outer regin = crtex cntains germinal centers f densely packed B cells (+ macrphages) in spaces called lymphatic ndules (r fllicles). 5. Inner regin = medulla cntains T cells (+ macrphages and plasma cells) arranged as medullary crds (spaces thrugh which lymph flws). B. Flw f Lymph thrugh Lymph Nde: See Fig 16.10, page ne-way directin nly 2. Lymph enters the nde thrugh ne f several afferent lymphatic vessels n cnvex surface. 3. Lymph flws inward thrugh sinuses (between medullary crds), and 4. exits the nde via ne f tw efferent lymphatic vessels at the hilum. C. Lcatins f Lymph Ndes See Fig 16.11, page Lymph ndes generally ccur in grups r chains alng the paths f larger lymphatic vessels. 2. They ccur primarily in the fllwing regins: a. cervical b. axillary c. supratrchlear d. inguinal 3. They als ccur within the fllwing bdy cavities: a. pelvic b. abdminal c. thracic D. Functins f Lymph Ndes 1. Remval and destructin f ptentially harmful freign particles frm lymph. a. Accmplished thrugh phagcytsis by macrphages. 2. Centers fr the prductin f lymphcytes that act against freign particles. * See bx n page 622 re: lymphangitis. 16-6

7 16.6 THYMUS AND SPLEEN A. Thymus See Fig page sft, bilbed rgan lcated within the mediastinum 2. decreases in size (atrphy) after puberty; See Fig 16.13, page cmpsed f lymphatic tissue that is subdivided int lbules 4. Each lbule cntains an uter (dark-staining) crtex filled with densely packed lymphcytes arund a central medulla (light staining) filled with swirled epithelial cells. See Fig 16.12b, page Functins: a. immature (undifferentiated) T cells migrate frm the bne marrw t the thymus (via) the bld. The thymus is the site f maturatin f T cells (which will leave the thymus and prvide immunity) b. The epithelial cells secrete a hrmne called thymsin, which stimulates further maturatin f T cells after they leave the thymus and migrate t ther lymphatic tissues. B. Spleen See Figure page lcated in the upper left prtin f the abdminal cavity (behind stmach) 2. resembles a large lymph nde that is encapsulated and subdivided int lbules by cnnective tissue 3. cntains tw types f tissue. See Fig 16.14b, page 625. a. White pulp = lymphcytes arranged arund central arteries. b. Red pulp = bld filled sinuses (venus bld that als serves as bld reservir). 4. Functins: a. Remval and destructin f freign particles and wrn bld cells frm bld. Macrphages remve and destry bacteria and damaged r wrn red bld cells and platelets thrugh phagcytsis. b. stres and releases bld during hemrrhage c. in immunity as a site f B cell prliferatin int plasma cells * See summary Table 16.1, page 625, which summarizes the lcatins and majr functins f lymph ndes, thymus, and spleen. 16-7

8 16.7 BODY DEFENSES AGAINST INFECTION A. Intrductin: Infectin is caused by the presence and multiplicatin f pathgens. Pathgens are viruses and micrrganisms (bacteria, fungi, prtzans, parasites) that cause disease. The bdy is equipped with tw types f defense mechanisms t fight infectin: 1. Innate (nnspecific) resistance = 1 st and 2 nd lines f defense. 2. Adaptive (specific) resistance, r immunity = 3 rd line f defense INNATE (NONSPECIFIC) DEFENSES = prtectin against a wide range f pathgens. Mechanisms include species resistance, mechanical barriers, chemical barriers, fever, inflammatin and phagcytsis. A. Species Resistance Each species is resistant t certain diseases that may affect ther species. This is because its cells d nt have receptrs fr the pathgen r its tissues d nt prvide the temperature r chemical envirnment that a particular pathgen requires. Hwever, that species may be susceptible t diseases that ther species may be able t resist. Examples: Humans are infected by measles, mumps, gnrrhea, and syphilis; ther animal species are nt. B. Mechanical barriers: First Line f Defense 1. include the skin and mucus membranes 2. As lng as mechanical barriers remain unbrken, they prevent the entrance f sme pathgens. C. Chemical Barriers: First and Secnd Lines f Defense 1. Enzymes a. The enzyme in gastric juice (i.e. pepsin) is lethal t many pathgens. b. The enzyme in tears (i.e. lyszyme) has antibacterial actin. 2. Acid a. Lw ph in stmach (hydrchlric acid) prevents grwth f sme bacteria. 3. Salt a. High salt cncentratin in perspiratin kills sme bacteria. 16-8

9 16.8 INNATE (NONSPECIFIC) DEFENSES C. Chemical Barriers: First and Secnd Lines f Defense 4. Interferns a. Interfern is a grup f hrmne-like peptides prduced by certain uninfected cells in respnse t the presence f viruses. b. These antiviral prteins interfere with the prliferatin f viruses, stimulate phagcytsis, and enhance the activity f cells that help resist infectins and the grwth f tumrs. 5. Defensins a. Destry bacteria by making hles in their cell walls and/r membranes. 6. Cllectins a. Prtect by attaching themselves t a variety f micrbes. Prvide brad prtectin against them. 7. Cmplement a. A system f 11 prteins that wrk t lyse infected cells. b. Als attracts phagcytes t the area. D. Natural Killer Cells (NK cells) 1. special lymphcytes 2. attack freign material micrbes, cancer cells, ther abnrmal cells 3. use perfrins t rupture cell membranes 4. enhance inflammatin E. Inflammatin: Secnd Line f Defense See Table 16.2, page Inflammatin is a tissue respnse t damage, injury, r infectin. 2. Bld vessels dilate, increasing capillary permeability. a. The respnse includes lcalized tissue redness (rubr), swelling (tumr), heat (calr), and pain (dlr). 3. Chemicals released by damaged tissues attract varius white bld cells t the site f injury. a. Pus may frm as WBC s, bacterial cells, and debris accumulate. 4. Tissue fluid leaks int area. a. A clt (fibrin) may frm in affected tissues. 5. Fibrblasts arrive. a. A fibrus cnnective tissue sac may frm arund the injured tissue and thus prevent the spread f pathgens. 16-9

10 16.8 INNATE (NONSPECIFIC) DEFENSES F. Phagcytsis: Secnd Line f Defense G. Fever 1. Definitin: Phagcytsis is the prcess by which specialized cells engulf and ingest freign particles in rder t destry them. a. Recall functin f lyssmes. 2. The mst active phagcytes in the bld are neutrphils and mncytes. 3. Mncytes give rise t macrphages (thrugh diapedesis, Chap 14) that migrate t varius bdy tissues. 4. Phagcytic cells assciated with the linings f bld vessels in the bne marrw, liver, spleen, and lymph ndes cnstitute the reticulendthelial tissue. 5. Phagcytes remve and destry freign particles frm tissues and bdy fluids. 1. Infectin (by bacteria and viruses) causes sme lymphcytes t prduce Interleukin I, which increases bdy temperature. 2. Other factrs can als increase bdy temperature, including expsure t heat, UV light, acids, and bases. 3. Increased bdy temperature decreases bld irn levels, which increases phagcytic activity. * See Summary Table 16.3, page 627 t review nnspecific resistance mechanisms ADAPTIVE (SPECIFIC) DEFENSES OR IMMUNITY Adaptive (Specific) Defenses (Immunity) are (is) prtectin against particular diseasecausing agents. It is ur third line f defense against infectin. See Figure 16.15, page 628. A. Antigens (Ag's) 1. Definitin: An antigen is a substance (usually a prtein) that causes the frmatin f an antibdy and reacts specifically with that antibdy. 2. Hw des this prcess ccur? a. Befre birth, bdy cells inventry the prteins and ther large mlecules present in the bdy (i.e. self prteins). b. After the inventry, lymphcytes develp receptrs that allw them t differentiate between freign (nn-self) antigens and self-antigens. c. When nn-self r freign antigens (Ag's) enter human tissues, they cmbine with T cell and B cell surface receptrs, and stimulate these cells t cause an immune respnse/reactin (IR) against them

11 16.9 ADAPTIVE (SPECIFIC) DEFENSES OR IMMUNITY B. Lymphcyte Origins: See Fig 16.17, page Lymphcytes riginate in red bne marrw and are released int the bld befre they becme differentiated. 2. Abut half f these undifferentiated lymphcytes reach the thymus where they are prcessed int T cells. 3. Sme undifferentiated lymphcytes are (prbably) prcessed in the bne marrw and becme B cells. 4. Bth T cells (70%-80% f circulating lymphcytes) and B cells (20%- 30%) are transprted thrugh the bld t the lymphatic rgans (lymph ndes, spleen, and thymus) where they reside and act in immune respnses against freign antigens. 5. See SEM f circulating lymphcyte, a B cell in Fig 16.16, page Lymphcyte Functin a. Antigen-Presenting Cells Begin the Immune Respnse. b. A macrphage is typically the first cell t respnd t an antigen. It then alerts lymphcytes t the invader. c. After digestin f the antigen (by the macrphage), a self-prtein attaches a cpy f the freign antigen t the cell membrane f the macrphage. A gene f the majr histcmpatibility cmplex (MHC) cdes fr this self-prtein. d. A lymphcyte nw recgnizes and binds t the antigen-presenting cell. T cells and then B cells are activated and begin a chain f reactins that ultimately destry/neutralize the invading antigen

12 16.9 ADAPTIVE (SPECIFIC) DEFENSES OR IMMUNITY C. T cells and the Cellular Immune Respnse (CMI): 1. T cells respnd t antigens directly (by cell-t-cell cntact). 2. T cells secrete cytkines (lymphkines) t enhance ther immune respnses t antigens. See Table 16.5, page 630. a. Clny stimulating factrs stimulate bne marrw t prduce lymphcytes. b. Interferns blck viral replicatin, stimulate macrphages t engulf viruses, stimulate B cells t prduce antibdies, attack cancer cells. c. Interleukins cntrl lymphcyte differentiatin. d. Tumr necrsis factr stps tumr grwth, etc. 3. Types f T cells: a. Helper T cells (CD4) becme activated when they encunter a displayed antigen (n macrphage) fr which it is specialized t react (see previus page). i. Once activated, helper T cells stimulate B cells t prduce antibdies (see belw). ii. CD4 Helper T cells stimulate Antibdy Mediated Immunity (AMI) and secrete cytkines (CMI). iii. The HIV virus cripples these cells. b. Memry T cells are prduced upn initial expsure t an antigen. i. They allw fr immediate respnse against subsequent expsure(s) t the same antigen. c. Cyttxic T cells (CD8) recgnize freign antigens n tumr cells and virus-infected cells. i. Stimulated cyttxic T cells prliferate int a large clne f cells that secrete perfrin t destry target cells. d. Natural Killer Cells als use perfrins t destry tumr cells. i. Bth cyttxic T cells and natural killer cells can lyse antigens in ther ways als

13 16.9 ADAPTIVE (SPECIFIC) DEFENSES OR IMMUNITY D. B cells and the Humral Immune Respnse (Antibdy mediated immunity, AMI): 1. B cells interact with antigen-bearing agents indirectly, by secreting prteins called antibdies. 2. B Cell Activatin a. B Cell becmes activated when it binds t an activated T cell. b. Once activated, a B cell prliferates, enlarging int its clne. c. Activated B cells specialize int plasma cells that secrete antibdies. d. Antibdies react against the specific antigen-bearing agent that stimulated its prductin. 3. A diverse ppulatin f B cells defends ne against a large number f pathgens. See bx n page 633. See Fig 16.18, page 631 and Fig 16.19, page 632, t see the cmplex cascade f CMI and AMI events invlved in an immune respnse. 4. Antibdy mlecules: See Figure 16.20, page 633. a. Antibdies are prteins called immunglbulins. b. They cnstitute the gamma glbulin fractin f plasma. c. Each immunglbulin mlecule cnsists f fur chains f amin acids linked tgether. tw heavy chains tw light chains d. Variable regins at the ends f these chains are specialized t react with antigens. cmprise antigen-binding sites 16-13

14 16.9 ADAPTIVE (SPECIFIC) DEFENSES OR IMMUNITY D. B cells and the Humral Immune Respnse (Antibdy mediated immunity, AMI): 5. Types f immunglbulins: See Table 16.6, page 633. The five majr types f immunglbulins are IgG, IgA, IgM, IgD, and IgE. a. IgG mst abundant circulating antibdy (80% f ttal) ccurs in plasma and tissue fluids defends against bacterial cells, viruses and txins activates cmplement nly antibdy t crss placenta; See bx n page 634. b. IgA abut 13% f circulating antibdies ccurs in excrine gland secretins (i.e. tears, saliva, breast milk, etc.) defends against bacterial cells and viruses Levels decrease during stress, lwering resistance t infectin. c. IgM abut 6 % f circulating antibdies first antibdies t be secreted after initial expsure t an antigen ccurs in plasma prduced in bld transfusins activates cmplement. d. IgD less than 1% f antibdies ccurs n the surface f mst B cells invlved in activatin f B-cells. e. IgE Less than 0.1 % f antibdies ccurs in excrine gland secretins prmtes inflammatin and allergic reactins because it causes the release f histamine frm mast cells (basphils)

15 16.9 ADAPTIVE (SPECIFIC) DEFENSES OR IMMUNITY D. B cells and the Humral Immune Respnse (Antibdy-mediated immunity, AMI): 6. Antibdy Actins: See Table 16.8, page 635. Antibdies attack antigens directly, activate cmplement, and stimulate lcal tissue changes that hinder antigen-bearing agents. a. Direct attachment invlves the fllwing: agglutinatin precipitatin neutralizatin b. Activatin f cmplement (a psitive feedback mechanism) invlves the fllwing: psnizatin hemtaxis inflammatin lysis * See Table 16.6, page 633, which summarizes the steps in antibdy prductin and cmpares T & B cell activity. E. Immune Respnses (IR): See Fig 16.21, page 636. a. When B cells r T cells first encunter an antigen fr which they are specialized t react, the reactin is called a primary IR. 1. During this respnse, antibdies are prduced fr several weeks (IgM). 2. Sme B cells and T cells remain drmant as memry cells. b. A secndary IR ccurs rapidly if the same antigen is encuntered at a later time (IgG)

16 16.9 ADAPTIVE (SPECIFIC) DEFENSES OR IMMUNITY F. Practical Classificatin f Immunity See Table 16.9, page 637. a. A persn wh encunters a live pathgen, which stimulates a primary IR, and suffers symptms f a disease, develps naturally acquired active immunity. b. A persn wh receives a vaccine cntaining a dead r weakened pathgen. Hwever, stimulatin f the IR causes the persn t develp artificially acquired active immunity. * See bx n page 636 re: Vaccines. c. A persn wh receives an injectin f gamma glbulin that cntain ready-made antibdies has artificially acquired passive immunity. In this instance, the patient des nt have time t develp active immunity (i.e. hepatitis), n IR ccurs, and the immunity prvided is nly shrtterm. d. When antibdies (IgG) pass thrugh a placental membrane frm a pregnant wman t her fetus, the fetus develps naturally acquired passive immunity. This prvides shrt-term immunity withut develpment f an IR

17 16.9 ADAPTIVE (SPECIFIC) DEFENSES OR IMMUNITY G. Allergic Reactins 1. Allergic reactins invlve antigens cmbining with IgE antibdies. The resulting IR is likely t be excessive r vilent and may cause tissue damage. 2. Types f allergic reactins: a. Immediate-reactin allergy (type I), which is inherited, causes the prductin f an abnrmally large amunt f IgE (animal dander, pllen, etc.). See Fig 16.22, page 638, which summarizes steps invlved. Allergic reactins result frm mast cells (recall frm Chapter 14 that mast cells are basphils that have traveled frm the bld int tissues) bursting and releasing allergy mediatrs, such as histamine and sertnin. In anaphylactic shck, these allergy mediatrs are respnsible fr the symptms f the allergic reactin, including decreased bld pressure (vasdilatin) and difficulty breathing (brnchcnstrictin). i. See Intrductin n page 617, Peanut Allergy. ii. See bx n page 637 re: thery f rigin f allergies due t skin eczema in childhd. Suppressr cells that inhibit the prductin f IgE usually terminate an allergic reactin. b. Antibdy-dependent cyttxic allergic reactins (type II) ccur when bld transfusins are mismatched (review incmpatible dnrs frm Chapter 14). See bx n page 639 re: tuberculin skin test. c. Immune cmplex allergic reactins (type III) invlve autimmunity, which is an IR against self-antigens (see belw). d. Delayed-reactin allergy (type IV), which can ccur in anyne and can cause inflammatin f the skin, results frm repeated expsure t antigenic substances (i.e. husehld detergents, csmetics)

18 16.9 ADAPTIVE (SPECIFIC) DEFENSES OR IMMUNITY H. Transplantatin and Tissue Rejectin 1. There are fur types f tissue transplants: See Table 16.10, page 639. a. Isgrafts ccur between identical twins. i.e. bne marrw transplant frm a healthy twin t ne with leukemia b. Autgrafts are self grafts. i.e. skin graft frm ne part f the bdy t anther c. Allgrafts ccur between individuals f the same species. i.e. kidney transplant frm a relative d. Xengrafts ccur between individuals f different species. i.e. pig heart valve int a human 2. A transplant recipient s immune system may react with dnated (nn-self) tissue in a tissue rejectin reactin. 3. Matching cell surface mlecules f dnr and recipient tissues (MHC) and using immunsuppressive drugs can minimize tissue rejectin. 4. Immunsuppressive drugs increase the recipient s susceptibility t infectin (decreases resistance)

19 16.9 ADAPTIVE (SPECIFIC) DEFENSES OR IMMUNITY J. Autimmunity 1. In autimmune disrders, the bdy prduces antibdies against self antigens, resulting in an attack n ne s wn tissues. 2. The cause f autimmune disrders is unknwn, but researchers feel that they may be caused by: a. a previus viral infectin, b. faulty T cell develpment, c. reactin t a self antigen that is clse in structure t a nn-self antigen, d. by persistent fetal cells, where fetal cells persist in the female s circulatin as an adult. Fr sme unknwn reasn, these hiding fetal cells in tissues such as skin, emerge stimulating antibdy prductin. This mechanism called micrchimerism may explain why s many mre females are stricken with autimmune disrders than males. In sclerderma, which means hard skin, patients are typically diagnsed between ages Symptms include fatigue, swllen jints, stiff fingers and mask-like face. Hardening may als affect bld vessels, lungs, and esphagus. 3. Sme Autimmune Disrders are presented in Table 16.11, page 640. a. Glmerulnephritis where antibdies attack kidney cells that resemble streptcccal antigens. See Clinical Applicatin 20.2, page 779. b. Grave s Disease where antibdies attack thyrid gland. See Table 13.8 and Fig 13.22, page 506. c. Type I Diabetes (IDDM) where antibdies attack beta cells f Islets f Langerhans f pancreas. See Clinical Applicatin 13.4, page 516. d. Hemlytic anemia where antibdies attack erythrcytes. e. Myasthenia Gravis where antibdies attack acetylchline receptrs in skeletal muscle. See Clinical Applicatin 9.1, page 299. f. Pernicius Anemia where antibdies attack the vitamin B binding sites in gastric mucsa. See bx n page 531 and Table 14.2, page 532. g. Rheumatic Fever where antibdies attack heart valves that resemble streptcccal antigens. h. Rheumatid arthritis where antibdies attack synvial membranes. See Clinical Applicatin 8.2, page 288. i. Systemic Lupus Erythematsus (SLE) where antibdies attack DNA, neurns, and bld cells

20 16.10 LIFE SPAN CHANGES A. The immune system declines early in life, partially due t the decreasing size f the thymus. B. The activity level f T cells and B cells declines as we age. C. The prprtins f the five types f immunglbulins shift as we age. OTHER INTERESTING TOPICS: A. Frm Science t Technlgy 16.1, Immuntherapy. See pages 634. B. Clinical Applicatin 16.1, page 641, Immunity Breakdwn: HIV/AIDS. INNERCONNECTIONS OF THE LYMPHATIC SYSTEM - See page 643. CHAPTER SUMMARY see pages 642, CHAPTER ASSESSMENTS see pages INTEGRATIVE ASSESSMENTS/ CRITICAL THINKING see page