\
The Lymphatic
System and
Immunity
‘The environment in which we live i filled with microbes that have
the ability to cause disease if given the right opportunity. we did
Not resist these microbes, we would be ill constantly or even die.
Fortunately, we have a number of defenses that either keep
‘microbes from entering our bodies or combat them if they do gain,
‘entrance. The lymphatic (lymphoid) system is one of the principal
body systems that helps to defend us against disease-producing
microbes. In this chapter you will earn about the organization and
components of the lymphatic system and its role in keeping us
healthy,
Looking Back to Move Ahez
+ Circulatory (Section 16.3)
+ Cancer (chapter 3, Common Disorders)
+ Epidermis of Skin (Section .1)
+ Mucous Membranes (Section 44)
+ Phagocytosis (Section 33)
Maintaining homeostasis in the body requires continual combat against
harmful agentsinourinteraland extemal environments Despite constant
‘exposure to a varity of pathogens (PATH é-ens)—
bative action should begin. Buta T cell becomes activated only if its
antigen receptor binds tothe foreign antigen (antigen recognition)
while atthe same time it receives a second simulating signa, 2 pro-
‘ess known as costimulation (Figure 17). common costimulator
|sinterleukin-2 (2). The need fortwo signals isa litle ke starting
and arvingacar. When you insertthe correct key (antigen inthe ign-
tion (eel receptor) and tur it the car starts (recognition of specfc
antigen), butitcanact move forwarduntilyou move the gear shi into
drive (costimulation) The need for costimulation probably helps
prevent immune responses from occurring accidentally.
Once aT ell has been activated, it undergoes clonal selection.
Recall that clonal selections the process by which alymphocytepro-
Iierates (divides several times) and differentiates (forms more highly
specialized cells) in response toa specific antigen. The result of clonal
selection isthe formation of aclone of cellsthatcanrecognzethesame
antigen a the original ymphocyte (see Figure 17.6). Some ofthe cells
‘of aT cell clone become effector cells, while other cells ofthe lone
become memory cells The effector calls ofa T call lone cary out
immune responses that ultimately resuttin elimination ofthe intruder
‘As you have already leamed there are two major types of mature
Tells helper Tcellsand cytotoxic Tells Activation of ahelper Tell,
resultsin the formation ofa clone of active helper T cells and memory
helper T cells (Figure 17.9). The active helper Tcellshelp other cells of
the adaptive immune system combat intruders. Fo instance, helper
FF cells release the protein interieukin2, which acts as acostimulator
‘resting helper Tcellsor cytotoxic T cells, anditenhances activation
‘nd proliferation of cls, B cells, and natural kiler cls. The memory
telperT cells of a helper T cell clone ate not activ cells. However if
the same antigen enters the body again in the future, memory helper
cellscan quickly proliferate and diferentiate into more active helper
cells and more memory helper T cells.
Clinical Connection
‘Organ Transplantation
‘Przan transplantation involves the replacement ofan injured or diseased
‘Ban, such a5 the heart, tver, kidney, lngs, or pancreas, with an oan
‘onated by anather individual. To reduce the rik freecion recipients of
‘gan transplants receive immunosuppressv drugs One such dugis lo-
orig, derived from a fungus, which inhibits secretion of ieleuki-2 by
#Haer Tells but has ony a minimal effect on B cel. Thus, thers of ee:
tis diminished while resistance to some diseases smaieained
TIEMITETEY Activation endclonatsteton ota helper Tee
‘Once a eipr Yen sce Aforms wane facie Piper T |
andmamonytiger Teal
Toot antigen
teeepior
‘tonal selection
(Goterion and
terectiaon)
ze o,
‘Ace helper calls Memory helper Tees
(cecrte 2). (ongived)
Q What are some of the functions of an active helper T Cell?
Activation of cytotoxic T cell results inthe formation ofa clone of
cftotore T cll that consists of active cytotoxic T ces and memory
‘ytotoric Tells (Fre 17.10). Active ototoxic Tees attackotherbody
‘eels that have been infected with the antigen. Memory toto Tells
do not atack infected body cel. Instead, they can quickly proliferate
and diferentite into more active cytotoxic T cells and more memory
‘ytotorcT cells ifthe same antigen enters the body at future time.
Elimination of Invaders cytotoxic T cells are the soldiers
that march forth to do battle with foreign invaders in cell-mediated
immune responses. The name cytotoxic reflects their function—
Kalin cells. They leave secondary lymphatic organs and tissues and
Scanned with CamScanner173 haven mmanty 19
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Formation of ote Tel lone: Satenunapiponemenea = conser
@ Isebes a rsope by apne
a @ @ Besides cells infected by microbes, whatother types of
ae @O_ cells do eytotoxie T cell attack?
a” @° ‘on their surface. The cytotoxic T cell then releases granzymes,
wy brotenigesting enzymes that vigae’ apoptosis, the fragmenta
score eytoxe Tela Memory evetole Tels tion af ear contents (Figure 1-11). Once the infected el is
feast teed tey "fone dertroyed the related microbes are kil by phagocytes.
ea A.Atematively, cjotove T eels bind to infected body cells and
What is the function of a memary eytotonieT cl? release two proteins from their granules: perforin and gronu-
Iysin. Perforn inserts into the plasma membrane of the target,
mig to seck out and destroy infected tage calls, cancer cels, ell and creates channel nthe membrane (Figure 17-120)
nd ransplanted cel igure 17.41). Cytotove Tcellsrecognize and AS a result extracellular fluid flows into the target cell and
atioch otargetcels Then te cjtotoe Tees deliver 2“lthathie Toss (cll bursting) occurs. Other granules in cyttore
onion Teall release granulysin, which enters though the channels and
Gytotowe Tels il nfected target body cells much ke natural destroys the microbes by creating holes in thei plasma mem-
bileccatisdo: the mojor ierence is thateytotoiTcelishaverecep- anes. CytotorcT cell may also destroy target cellsby releasing a
tors specif for a particular microbe and thus kil only target body 1024 molecule called iymphetaxio which activates enzymesin the
cells infected with one paricular typeof microbe; natural kilercells__'"GEt cell. These enzymes cause the target cells DNA to fragment,
[sn dostcy a wide vonety of mecrobeinfected body cls, Cytotoxic 24 the cell dies. In addition, ctoto T cells secrete gamma
Tells have two principal mechanisms for kling infected targtcals: ‘interferon, which attracts and activates phagocytic cells, and mac.
rophage migration inhibition factor, which prevents migration of
ytotorc Teel, using receptors on ther surfaces, recognize and phagocytes from the infection ste. Ater detaching from a target.
» bind to infected targetelsthat have microbial antigens displayed call, acyttoxic Teel can seek out and destroy another target cel
Scanned with CamScanner420. CHAPTER 17 Tetymphac Sytem an erty
Checkpoint
“7. wnatis tbe normal function f major histocompatbiy complet
protein etantges)?
1. Hom do antigens ave at ymphate sues?
9. How do anger presenting els process angers?
130, vnataetneunconsot nee eto, and meron Tet?
21, How do notices htt?
B Cells and Antibody-mediated Immunity
‘The body contains not only millions of eilferent T cells ut aso mil
lions of ciferentB cells, each capable of responding ta specific ant-
‘8. Cytotorc Tells leave lymphatic tissues to seek out and destroy
‘foreign antigen, but cells stay put. Inthe presence of afreignati-
en, aspeciicBcellinalymph node, the spleen, ormucosa-associated
Iymphatic tissue becomes activated. Then it undergoes clonal selec
tion, forming a clone of plasma ces and memory els. Plasma cells
‘are the effector cells ofa 8 cell clone they secrete specific antibodies,
‘hich in tum circulate in the lymph and blood to reach the site of
During activation of a8 cellantigen receptors onthe ellsurface
‘of 2B cal bind to an antigen (Figure 17.12).B cell antigen receptors
{are chemically similar tothe antibodies that eventually are secreted
by the plasma cells. Although B cells can respond to an unprocessed
_ntigen present in lymph or interstitial Mud, their response is much
‘more intense when they process the antigen. Antigen processing ina
‘8 cell ocursin the following way: the antigen i taken into the 8 cll,
broken down into fragments and combined with MHC protein, and
‘moved to the 8 cell surface. Helper T calls recognize the processed
antigen-MHC protein complex and deliver the costimulation needed
for B cell division and diferentiation. The helper T cell releases
Jnterleukin-2 ond other proteins that function as costimulators to
activate B cells
Once activated, 2 B cell undergoes clonal selection
Figure 17.12). The results the formation ofa cione of 8 cells that
Consists of plasma cells and memory B cells. Plasma cells secrete
intibodies. A few days ater exposure to an antigen, a plasma cell
.2cretes hundreds of millions of antibodies each day for about 4or
‘days, until the plasma cell dies. Most antibodies travel in lymph
1 Blood to the invasion site. Memory 8 cells do not secrete anti-
‘dies. instead, they can quichly proliferate and differentiate into
‘re plasma cells and more memory B cells should the same ant-
‘reappear ata future tim
‘Although the functions of the five classes of antibodies differ
“sewhat, all attack antigens in several ways:
Yeutralize antigen. The binding of an antibody to its antigen
leutralizes some bacterial toxins and prevents attachment of
tome viruses to body cells.
mobilize bacteria. Some antibodies cause bacteria to lose
«tie motility, which limits the spread of bacteria into nearby
sues.
Acton and clonal selection of cls. Plasma ces
re acuay much lrgerthan Beas
A
Plume celesscte abode
Beet agen
rece
Dpeteron?
shdeter pans
cot isplaying processed
repens copes
ByreperTect: wien
‘leases cosimalaor:
99
Memery Beals
(eestearbosies)
ongaves)
@ How many diferent kinds of antibodies willbe secreted by
‘te plasma cells in the clone shown here?
‘3. Agglutinate antigen. Binding of antiboges to antigens may co-
rect pathogens to one another, causing agglutination, the clump:
ing together of particles. Phagocytic cells ingest agglutinated m-
robes more readily.
4.Activate complement. Antigen-antibody complexes activate
complement proteins, which then work to remove microbes
‘through opsonization and cytolysis
5. Enhance phagocytosis. Once antigens have bound to an antibody’
‘arable region the antibody actsasa “fog that attracts phagocytes
‘Antibodies enhance the activity of phagocytes by causing agalutina
tion, byactvating complement, and by coating microbes otha they
‘are more susceptible to phagocytosis opsonization).
‘Table 17.3 summarizes the functions of cells that participate in
adaptive immune responses.
|
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‘Summary of Cell Functions ln Adaptive Immune Responses
Antigen presenting Cell (APC) Processes and presen foreign artgen oT els incldes macrophages, 8 ces, and enc cals
Helper ¥ cat ‘eps cite els of mrnane sytem eb rude by reaaang striae een Peiecn?
(2, wich enhances acvaton and @vsion of ais cher prota aac phagocyes and ease
‘hago abity of macrophages: aa stimulates Gevelogmert of 8 els Int artbady Posen
plasma eels and eveopmert of atra Klee
fotone Teall ‘ls ost target cls by leasing ganzymes tat induce apoptass, perfor tat forms Canoes
to cause fois, ranulysn that Gestroys micobes nphotoun ak Sess a ce OMA,
{Eamma-neferon that tracts macophoges and incesses the pragacyc avy, and maCoeNagE
Innbtion factor that prevents macrophage migration rom eo fection
Memory T call ‘Remains in phat tsue ard recognizes orignal nvacingaign, ven yeas ae sk
cat Dierenttes nto antibody preducng plasma call
Plasma elt Descendant of Bclthat produces and secretes artbodies
Memory Ball Remains ead to produce amore rapid and foreul secondary response should the same age
eter the body nthe future
TT clinical Connection ‘ytotoxc T cells or plasma cll within hours the next time the same
Monoclonal Antibodies
‘An anibody mediated response typically produces many diferent ent
bodies that recogniaeciferen.pasf an arin or ferent artigensof2
foreign cll By contrast, amonoconal antibody (MAB) is2 pure antibedy
produced from a single clone of identical els gown in the laboratory,
CUrical uses Abs include he diagnosis of pregnancy alles, andi
eases such a strep throat, hepatitis abies, and some sewvaly transmited
‘iseases. MAbs hve also been used to detect cancer at an etl sage and
todetermine the estentof metastasis Theymayalsabe weulin preparing
‘vaccines to counteract the rejection associated with transplants to est
‘autoimmune dzeaes and perhaps to teat ADS.
antigen appears.
‘One measure of immunological memory is the amount of anti
body in blood plasma. After an intial contact with an antigen, no
antibodies are present fora few days. Then, the levels of antibodies
slowly rise, fist lgM and then IgG, followed by a gradual decline
(Figure 17.13). Thisisthe primary response. Memory cells may lve
for decades. Every new encounter withthe same antigen causes a
secretion of antibodies. The primary response aker
Ftstepesre) mer than the secondary response ake seondor
subsequent exposure toa ven antigen
Immunological Memory
[Ahallmark of adaptive immune responsesis memory for specific ant-
‘gens that have triggered immune responses inthe past. mmunolog-
‘cal memory due to the presence oflonglasting antibodies and very
long:tved lymphocytes that arise during division and diferentiation
of antigen stimulated B cells and T cells.
Primary and SecondaryResponses _Adapveimmune
responses, whether ellmedated or anibody-medlate, are much
‘quicker and more Intense aera second or subsequent exposure
to an antigen than ater the frst exposure. italy, ony afew cls
have the correct antigen receptors to respond, and the immune
response may tahe several days to buld to maximum intensity.
Because thousands of memory ells exist aker an inital encounter
tnth an antigen they can divide and diferente into helper Tels,
‘immunological memory i the bass for sucesfl mmurizaton by
vcinton.
@ Which type of antibody responds most strongly during the
secondary response?
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‘rapid division of memory cells The antibody level ater subsequent
‘encounters is fa greater than during a primary response and con-
sists mainly of IgG antibodies. This accelerated, more intense re-
sponse is called the secondary response. Antibodies produced dut-
ing a secondary response are even more effective than those
produced duringa primary response. Thus, they are more successful
In disposing ofthe invaders
Primary and secondary responses occur during microbial infec
tion. When yourecoverfrom an infection without taking antimicrobial,
‘drugs, itis usualy becouse ofthe primary respons. Ifthe same mi-
‘robe infects you later, the secondary response could be so swt that
‘the microbes are destroyed before you eaibit any sins or symptoms
of infection,
Naturally Acquired Immunity and Artificially
Acquired Immunity immunological memory provides the
bass for immunization by vecination agaist certain diseases, for
instance, polo. When you receive the vccne, which may contain
weakened or killed wiole mizrobes or parts of microbes, your 8
Calls and calls are actnate, Should you subsequently encounter
the Uving pathogen a an infecting microbe, your body inates 3
secondary response. However, booster dotes of zme immunising
agents must be ven periodically to mainsin adequate protection
against the pathogen, Table 17.4 summarize the various types of
antigen encounters that provide nturaly and atl acquired
munity.
TABLE 17.4 Types of Adaptive Immunity
Naturally acquired Following exposure toa microbe antigen
setive immunity recognition by Bclls and Tels and
‘ontimolton leno antbody secreting plasma
ls, enotonT el and Band Timemory cls
Waturally equired Trlr ogg antibodies from mother tus
‘atsivelmmonity across the placenta, of pA antibodies rom
other to baby nmi during rest feeding
“anigensieguced dung vaccination
‘Simulte celtmedated and antibody mediated
immune response, indingto production of
‘memory cls The antigens are pereated tobe
Immunogens but not pathogen; hat they
ails a immune response but not cause
Senifeareiiness
‘iat acqlred
Active Immnity
‘ariiclaly acquire
passive immunity
Tnravenons jection af mmunoglobullns
(amiboces)
Checkpoint
12, How ore cel mediated and antibody mated rune esorses
‘ima? How cosh er?
12, whaticnederence between the secondary tesponse 18"
antigen andthe primar response?
174
Aging and the Immune
System
‘OBJECTIVE
+ Deteribe the effet of aging on the immune system
With advancing age, most people become more susceptible tal
‘types of infections and malignancies. Their response to vaccines is
‘decreased, and they tend to produce more autoantibodies (antibod-
les against ther bodys onn molecules). In addition, the immunesys-
tem exhibits lowered levels of function. Fr example, Tcelis become
less responsive to antigen, and fewer T cals respond to infections.
‘This may recut from age elated atrophy ofthe thymus o decreased
production of thymic hormones. Because the cell population
decreases with age, 8 cals are also less responsive. Consequently,
antibody levels donot increase as rapidly in response toa challenge
by an antigen, resulting in increased susceptibit to various infec-
tions es for this key eason tha elderly individual ae encouraged
to get influenza fu) vacinations each yea.
‘Checkpoint
14, What arethe consequences decreasesin the numberof cls
and Beelswin advancing ge?
To appreciate the many ways thatthe lymphatic system and immu-
nity contribute to homeostasis of other body systems, examine
Focus on Homeostasis: The Lymphatic System and Immunity. Next,
in Chapter 18, we wil explore the steuctur and function of the es:
piratory system and see how is operation's regulated by thenervous
system. Most importantly, the respiratory system provides for gas
‘exchange=taking in oxygen and blowing of carbon dioxide. The
cardiovascular system aids gas exchange by transporting blood
containing the gases between the lungs ad tissue cls.
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Common Disorders
AIDS: Acquired Immunodeficiency
Syndrome
‘Acquired immunodeficiency syndrome (A105) sa condition in which
‘2 person experiences 2 teltale assortment of infections due to the
progressive destruction of immune system cells by the human immu-
Iodefciency virus (HI). AIDS represents the end stage of infection
by HIV.A person who is infected with HIV may be symptomtee for
‘many year, even while the virus is actively attacking the immune sys-
tem. nthe wo decades after the ist fivecases were reportedin 1981,
22 milion people died of AIDS. Worldwide, about 3 milion people
are currently infected with HV.
HIV Transmission secause HiVispresentin the blood and
‘some body fluid, it ie most effectively transmitted (spread from
‘one person to another) by practices that involve the exchange of
blood or body fluids, HI i transmitted in semen or vaginal id
during unprotected (without @ condom) anal, vaginal, or oral sex.
HIV also is transmitted by direct blood-to-blood contact, such as
‘occurs in intravenous drug users who share hypodermic needles
or health-care professionals who may be accidentally stuck by
Hiv-contaminated hypodermic needles. In addition, HIV can be
transmitted from an Hivinfected mother to her baby at birth or
during breast feeding
“The chances of transmitting or of beinginfected by HIV during
vaginal or anal intercourse can be greatly reducedalthough not
climinated—by the use of latex condoms. Public health programs
aimed at encouraging drug users notto share needles have proved
effective at checking the Increase in new HIV infections in this
population. Also, giving certain drugs to pregnant HiVinfected
‘women greatly reduces the risk of transmission of the virus to
their babies.
HIVis a very fragile virus; it cannot survive forlong outside the
human body. The virus is not transmitted by insect bites. A person
‘cannot become infected by casual physical contact with an HIV:
infected person, such as by hugging or sharing household items.
The vius can be eliminated from personal care items and medical
equipment by exposing them to heat (135°F for 10 minutes) or by
‘leaning them with common disinfectants such as hydrogen pe
‘oxide, rubbing alcohol, household bleach, or germicidal cleansers
such as Betadine* or Hbiclens. Standard dishwashing and clothes
washing also kil HIV
HIV: Structure and Infection Hiv consists of an inner
core of ribonucleic acid (RNA) covered by a protein coat (capsid)
surrounded by an outer layer (envelope), composed of a lipid
ilayer penetrated by proteins. Outside a living host cel, virus is
sunable to replicate, However, when the virus infects and enters a
hhost cell Its RNA uses the host cell's resources to make thousands
va rage tee
nent any eminent
ieee eee
Signs, Symptoms, and Diagnosis of HIV Infection
Soon afer being infected with MW, most people experience a brief
ft illness, Common signs and symptoms ae fever, fatigue rash,
headache, joint pain, sore throat, and swollen lymph nodes. About
50% of infected people have night sweats. As early as three to four
weeks ater HIV infection, plasma cells begin secreting antibodies
‘against HIV These antibodies are detectable in blood plasma and
form the bass for tome ofthe screening tests for HW. When people
test “HIV-positive? it usually means they have antibodies to HIV
antigensi their bloodstream,
Progression to AIDS Mer 2 period of 2 to 10 years, the
Virus destroys enough helper Tcels that most infected people begin
to experience symptoms of Immunodeficiency. HNinfected people
‘commonly have enlarged lymph nodes and experience persistent
fatigue, involuntary weight los, night sweats, skin rashes, iarhea,
and various lesions ofthe mouth ané gums. In addition, the virus may
begin to infect neuronsin thebrainafecting the person's memory and
producing visual disturbances.
‘As the immune system slowly collapses, an Hivinfected person
becomes susceptible to a host of opportunistic infections. These are
infections caused by microorganisms that are normally held in check
‘but now proliferate because ofthe defective immune system. AIDS is
ciagnosed when the helper T cell count drops below 200 cells per mi
craliter(= cublemilimeter ofbloodor when opportunistic infections
arise, whichever occurs ist atime, opportunistic infections usually
are the cause of death.
Treatment of HIV Infection atpresent, infection with HN
cannotbe cured, Vaccines designed to blocknewHIVinfections and to
reduce the viral oad (the numberof copies of HIVRNA in a microliter
of blood plasma) in those who are already infected are in clinical
tral, Meanwhile, three categories of drugs have proved successful in
extending the life of many HiV.nfected people:
A. Reverse transcriptase inhibitors interfere with the action of
‘everse transcriptase the enzyme thatthe virus uses to conver its
RNA into DNA copy. Among the drugsin this category are zidowu-
dine (Z0v, previously called AZT), didanosine (ddl), and stavudine
(GAT), Tzivie®, approved in 2000 fr treatment of HIV infection,
‘combines three reverse transcriptase inhibitors in one pill.
2. integrase inhibitors block the enzyme integrase, which inserts the
HIV NA copy into host cell ONA. The drug altegraviris an example
of an integrase inhibitor,
Scanned with CamScanner3. Protease inhibitors interfere with the action of protease, avira en-
Zyme that cuts proteins into pieces to assemble te protein coat of
newly produced HW particles. Orugs inthis category include neli-
Navir,saquinawir rtonavi, and indinavie
‘The recommended treatment for HIV-infected patients it Nghly
ctive antiretroviral theropy (HAART)—2 combination of the
‘ore antiretrow
inhibitor drug classes. Most HIV-infected individual
HAART experience a drastic reduction in vial lo
inthe number of helper T cells in their blood, Not only does HAART
elay the progression of HIV infection to AIDS, but many individu-
als with AIDS have seen the remission or disappearance of oppor-
{unisticinfections and an apparent return to heath, Unfortunately,
HAART is very costly (exceeding $10,000 per year), the dosing
Schedule is grueling, and not all people can tolerate the toc side
‘effects of these drugs. Although HIV may vitually disappear from
the biood with drug treatment (and thus a blood test may be
“negative” for HIV), the vieus typically stil lurks In various Iym>
‘hati tissues. In such cates, the infected person can still transmit
the vius to another person.
Allergic Reactions
‘A perton who is overly reactive o a substance that is tolerated by
‘most other people is s3id tobe allergic. Whenever an allergic reaction
‘takes place, some tissue injury occurs. The antigens that induce on
‘allergic reaction are termed ollergens. Common allergens include
Certain foods (milk, peanuts, shellfish, eggs), antibiotics (peniclin,
tetracycline), vaccines (pertussis, typhoid), venoms (honeybee, SP,
snake), coumetics, chemicals in plants such a8 poison ivy, pollens,
ust, molds, jodine-containing dyes use in certain tay procedures,
‘and even microbes.
Type 1 (anaphylactic) reactions are the most common and
typically occur within 2 to 30 minutes after a person who was pre-
Vioutly sensitized to an allergen is reexposed toi. In response to
‘certain allergen, some people produce IgE antibodies that bind to
the surface of mast cells and batophils The next time the same al-
lergen enters the body, it attaches to the Igé antibodies already
present. In response, both the mast cells and basophils rele
histamine, prostaglandins, and other chemicals. Collectively,
these chemicals cause vatodilation, increased blood capillary p
‘meability, increased smooth muscle contraction inthe airways of
the lungs, and increased mucus secretion, As a result, @ person
may experience inflammatory responses, difcuty in breathing
through the narrowed airways, and 2 runny nose from excess mur
us secretion, In anophylactle shock or anaphylaxis, which may
‘occur in a susceptible individual who has ust received a triggering
‘drugor been stung by 8 wasp, wheezing and shortness of breath a
airways constrict are usually accompanied by shock due to vasodi-
lation and uid loss from blood. Injecting epinephrine to dilate the
snd strengthen the heartbeat usually is elfectve in this
Ie: threatening emergency.
Type (ytotore)reactlons ae caused by antibodies directed
against antigens. ona peron’sbloodcelisor tissue calls Typelreations,
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which may occur in incompatible blood Uanshusion reactions,
damage cela by causing hy,
Type il (immune-compler reoctloms invohve antigens. antibod
les, and complement. Glomeritonephits and theumatind arthrs
(2) aie in his wo.
Type WV (cell-mediated) reactions ot delayed hypersensitivity
reactions ususlly appear 12-72 hours after exposure to an
Allergen. Type 1 reactions occur when allergens are taken up by
site of allergen entry into the body, where they produce gamma
Interferon, which activates macrophages, and tumor necrosis fe
tor, which stimulates an inflammatory response, intrac
bacteria such as Mycobacterium tuberculosis wiager this type of
cell mediated immune response, as do certain haptens, such as
pozon ivy toxin, The shin test for tuberculosis alsa is a delayed
hypersensitivity reaction,
Autoimmune Diseases
In an ovtolmmune dizeose (aw: MON) or autoimmunity, the
immune system fails to display selftolerance and attacks the
person's own tesues. Autoimmune diseases usually arise in early
‘adulthood and are common, afflicting an estimated 5% of adults in
North America and Europe. Females sufer autoimmune diseases
‘more often than males, Sereactive Bclls and T cells normally are
Geleted of inactivated during negative selection. Apparently, this
process not 100% elective. Under the influence of unknown en
onmental triggers and certain genes that make some people more
susceptible, self-tolerance breaks down, leading to activation of
selereactve clones of T cells and B cells. These cells then gene!
cellmediated of antibody-mediated immune responses against
seltantigens.
‘variety of mechanisms produce diferent autoimmune dis:
‘eates. Some involve production of autoantibodies, antibodies that
bind to and stimulate or block self-antigens. For example, autoan
bodies that mimic TSH (thyroid-stimulating hormone) ae present
In Graves disease and stimulate secretion of thyroid hormones
(thus producing hyperthyroidism); autoantibodies that bind to and
block acetylcholine receptors cause the muscle weakness charac-
teristic of myasthenia gravis. Other autoimmune diseases involve
activation of cytotoxic T eels that destroy certain body cells. Exam
ples include type 1 diabetes mellitus, in which T cells attack the
Insulin-producing pancreatic beta cells, and multiple sclerosis),
Jn which T calls attack myelin sheaths around axons of neurons.
Inappropriate activation of helper T cells or excessive production of
gamma-interlron also occur in certain autoimmune diseases.
Other autoimmune disorders include rheumatoid arthritis (RA),
systemic lupus erythematosus (SLE), rheumatic fever, hemolytic
‘and pernicious anemias, Addison's disease, Mashimote's thyroiditis,
‘and ulcerative colts.
‘Therapies for various autoimmune diseases include removal of
‘the thymus gland (thymectomy), injections of bets.interferon
immunosuppressive drugs, and plasmapheresis, in which the426 CHAPTER LT The lymphatic Ssem on immanny
fitered to remove antibodies and antigen:
person's blood plasma
antibody complexes
Infectious Mononucleosis
Infectious mononucleess or “mono" sa contagious disease caused
by theEpsten-Borr vis (EBM. occurs manly inchildren and young
dls, and more often in ferales than in males. The virus commonly
enters the body through intimate oral contact suchas hissing which
‘accounts foritbeing called the “hissing disease” EBY then multiplies
in lymphatic issues and spreads ito the blood, where it infects and
‘mkiplesin 8 cells, the primary host cells. Because ofthis infection,
the 8 cells become enlarged and abnocmalin appearance so that hey
resemble monocytes, the primary reason forthe term mononucleoss,
Besides an elevated white blod cll eount with an abnormally high
percentage of lymphocytes, signs and symptoms include fatigue,
headache, iziness, sore throat, enlarged and tender lymph nodes,
and fever. There is no cure for infectious mononucleosis, but the
disease usualy uns its coursein afew weeks.
Lymphomas
Lymphomas (im-F0-mas;ymph- = clear water;-oma = tumor) ae
cancers of the lymphatic organ, especialy the lymph nodes. Most
hhaverio known cause, The twomaintypesof lymphomas areHodgkin
isease and non-Hodgkin lymphoma.
‘Hodgkin dzeate (HO) is characterized by painless, nontender
enlargement of one ar more lymph nodes, most commonly in the
neck, ches, and axillae (armpits). If the disease has metatasied
from these sites, fevers, night sweats, weight os, and bone pain also
‘occur. MO pmariy aflets individuals betwen ages 15 and 35 and
‘those ove ti more common in males éagnosed early, MO has
990-99% cure rate.
Non-Heéghia lymphoma (MHI), which & more common than
oO, occurs in al age groups. MHL may start the same way a3 HD but
‘may alt include an enlarged spleen, anemia, and genera malaise.
Upto half of al individuals with NHL ae cured or survive for alengthy
period. Treatment options for both HD and NMI include radiation
therapy, chemotherapy, and red bone marrow transplantation.
‘Systemic Lupus Erythematosus
Systemic lupus erythematous (SL erethém-+-T0-u),0F pus
{pus » wal) sa ehronc autoimmune disease that affects mut
ple body systems Most caes of SLE acu in women between the
‘sgesof 15 and 25, more oken in blacks than in whites. Although the
aus of SLE i not known, both a genetic predisposition tthe ds
fate and environmental factors contibute Females arene ines
tore likely than males to suf from SLE. The dsorderohen occurs
infemales who exhibit extremely low levels androgens (male sex
hormones).
Signs and symptoms of SLE include joint pan, sight fever,
fatigue, oral ulcers, eight os, enlarged lymph nodes and splen,
photosensity, rapid loss of large amounts of scalp ha, and
sometimes an eruption across the bridge ofthe nose and cheeks
called a "butterfly ash The erosive nature some ofthe SLEskin
lesions was thought ta resemble the damoge inflicted by the bi
ofa wot-thus the term lupus, Kidney damage occurs a antigen
antibody complexesbecometrappedin kidney cpilaies, thereby
obstructing blood fering. Renal failure isthe most common
couse of death
Medical Terminology and Conditions
Adenitis (2-25; aden = plan) is = nflammation of)
Enlarge, tender, ad lames yh nodes sung from aninfecton
‘Allegra (AL 6-gaalo-= other) Axransplant between genetical d=
{erent indviduas ofthe same species. Skin transplants rom otter people
‘and blood tanshsions are allopat.
‘Autograft (at6-ar;outo- = sal A transplant in which ones own
tisue is grated to another part the Body suc ssn gras for bur
treatment or plastic surgen)
‘Chronic fatigue syndrome CFS) Aciorder, essay occuringin young
female aduts, chracterae by (t) extreme fatigue that impairs normal
‘activities for at lassie months and [2 the absence of ether known ds
teases (cancer, infection, dive abuse, toy, or psychiatre disorders)
‘that might produce simiar symptoms.
Gamma globulin (GLOB.O‘in) Suspension of immunoglobulins fom
blood consisting of antibodies that reat witha speciicpathogen.Rispre-
pared by injecting the pathogen into armas, removing bleed rom the
armas ae antibodies hove Been produced, olating the antibodies,
Sndineting them toa human o provide short emmy,
Graf dnytsue or ogan sed orvansparation or atransplantofsieh
yperspenim (iperSPLENam; hyper: = ve) Abnomalspencac
thy dueto splenic enlargement and associated wih an increased rate
esruction of ara bode
Lymphadenopathy fim fal-eNOP.a th; mph = cer Mui potty =
sease) Enlarge, sometimes tender Iymph glands 35a response to
Infection alsocalledaneten land.
Splenomegalyspl-nO EG, mego:= large) Enlapesplen.
‘Tonsiectomy tor’ sb LEK 6m ectomy = exon Removal of ators
enoyat(ZE¥-6-gat:rero-=srangeorforeign)Atansplnt between
animals of ciferent species, enogats from porcine (pig) ar bovine
(com) sue maybe wsedin people a 2 physiological desing for severe
burs.
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