Chapter 43 THE IMMUNE SYSTEM

Disease-causing microorganisms are called pathogens.

They include bacteria, viruses, protozoans and fungi.
Immunology is the study of specific defense mechanisms.
Two maor !inds of defense have evolved to counter the thread of infection.
". Innate immunity# rapid response to a broad range of microbes.
$. Acquired immunity# slower response to specific microbes% it is also called adaptive immunity%
it includes lymphocytes and antibodies.
There are specific defense mechanisms and nonspecific defense mechanisms also !nown as innate
immune response.
INNATE IMMUNITY
&t provides a wide range of defenses. These defenses are not specific for a type of pathogen.
Eternal !efense Mechanisms
These mechanisms are nonspecific and include mechanical and chemical barriers.
Mechanical "arriers include s!in, hair, mucous.
#hemical "arriers include sweat, sebum, tears, and stomach acid% lyso$ymes digest the cell wall
of bacteria.
&ntact s%in is barrier that prevents pathogens from penetrating into the body.
Secretions from sweat and sebaceous glands give the s!in a p' of 3 to (, which is acidic enough to
prevent colonization by many microbes.
)aliva, tears and mucus also !ill bacteria.
&yso$ymes are enzymes found in tears, sebum and tissues that attac! the cell wall of bacteria.
*cid secretions and enzymes in the stomach !ill most ingested pathogens.
Internal #ellular And #hemical !efenses'
&nvading organisms are ingested and destroyed trough phagocytosis.
+hite blood cells or leu%ocytes are involved in this process.
(' )hagocytes destroy bacteria and other cells.
There are four types of white blood cells ,leu!ocytes- that are phagocytes.
Neutrophils are the first phagocytes to arrive usually within an hour of inury.
.eutrophils ma!e about /01-201 of all white blood cells.
Damaged cells secrete chemical signals that attract neutrophils# chemotais.
Monocytes arrive ne3t and become large macrophages.
4onocytes ma!e about (1 of +5C.
4acrophages are long-lived cells.
&ngest the bacterium into a food vacuole that fuses with a lysosome which secrets supero3ide
ions, 6$
-
, and nitric o3ide, .6, both strong antimicrobial substances% hydrolytic enzymes digest
the microbial components.
4acrophages are found in the lungs, liver, lymph nodes, !idney, brain, spleen, and connective
tissues.
5oth phagocytize pathogens, their products and dead and inured cells.
* neutrophil can phagocytize about $0 cells and a macrophage "00 cells before they become
inactive and die.
7us consists of dead phagocytic cell, fluid and proteins lea!ed out of capillaries.
)ome bacteria are resistant to macrophage digestion.
Eosinophils ma!e about ".(1of all leu!ocytes.
They attac! large parasitic invaders li!e blood flu!es.
They discharge hydrolytic enzymes on the surface of the parasite.
They have limited phagocytic activity.
*' Antimicro"ial proteins
#omplement system proteins are regulatory proteins secreted by cells of the immune system.
There are about 30 of these serum proteins.
Two types of interferon provide innate defense against viral infection.
)ome lymphocytes secrete a third type of interferon that activates microphages.
They are important signaling cells during immune responses and lead to the lysis of the viruses,
yeast and bacteria, and enhance their phagocytosis by macrophages.
They are inactive until an infection occurs.
!efensins are secreted by activated macrophages.
Interferons are proteins produced by virus infected cells. They signal other cells to produce chemicals
that inhibit viral replication.
+' Inflammation is a protective mechanism.
Damage to tissue by physical inury or by infection triggers the inflammatory response.
&t is regulated by proteins in the plasma, by cyto!ines, and by substances called histamines
released by platelets, by basophils ,+5C-, and by mast cells.
5lood flow increases bringing phagocytic cells to the site of infection. This is probably the most
important element of inflammation.
Histamines released in response to inury cause vasodilation and ma!e capillaries more
permeable allowing antibodies to enter the tissues% postcapillary venules constrict.
'istamines are released by circulating leu!ocytes called "asophils and by mast cells found in
connective tissue.
8eu!ocytes and damaged cells release prostaglandins that increase blood flow to the inured
area.
#hemo%ines secreted by flood vessel endothelial cells and monocytes attract phagocytes to the
inured area.
5lood flow to the inured area brings clotting elements to initiate tissue repair, ma!es the s!in feel
warm, and may causes redness.
Edema ,swelling- occurs.
&nured cells put out chemical signals that cause the release of leu!ocytes from the bone marrow.
,' Natural -iller #ells
Natural %iller cells .N-/ are large, granular lymphocytes that originate in the bone marrow.
*ttac! cancer cells, infected cells and pathogens including certain fungi.
9elease proteins that destroy target cells by lysing the cells.
.: cells trigger apoptosis of infected cells.
0' Inverte"rate Immune System
&nvertebrates depend mostly on innate, non-specific mechanisms of defense.
&nvertebrates apparently lac! cells e;uivalent to lymphocytes responsible for specific immune response.
&nsects defend themselves by mechanisms similar to those of vertebrates.
Hemocytes of insects ingest bacteria and damaged cells.
&nvertebrates have a simple defense system. Their system is nonspecific.
&nvertebrates in general do not have immunological memory.
<arthworms have immunological memory.
<chinoderms have coelomocytes that phagocytose foreign cells, and produce interleu!ins.
Cyto!ines have been found in some invertebrates.
A#1UI2E! IMMUNITY 3 &YM)H4#YTES
7athogens always come in contact with lymphocytes when they invade a vertebrate.
7hagocytes secrete cyto%ines that activate lymphocytes when they phagocytose microbes.
7athogens have macromolecules on their cell surfaces that the body recognizes as foreign.
These foreign substances stimulate an immune response. They are called antigens.
8ymphocytes recognize and bind to a small portion of the antigen called the epitope.
*n antigen that is a protein has a specific se;uence of amino acids that ma!es up the epitope or antigenic
determinant.
*n antibody interacts with a small, accessible portion of the antigen, the epitope.
*n epitope interacts with a specific antibody and is capable of inducing the production of the specific
antibody.
These antigen determinants vary in number from ( to more than $00 on a single antigen.
The shape of the epitope can be recognized by the antibody or a T cell receptor.
ANTI5EN 2E#45NITI4N 6Y &YM)H4#YTES
Cells of the immune system include lymphocytes# T lymphocytes or T cells, 6 lymphocytes or 6 cells7
natural %iller .N-/ cells and phagocytes.
These cells circulate throughout the body in the blood and lymph, and are concentrated in the spleen,
lymph nodes and other lymphatic tissues.
T lymphocytes and 6 lymphocytes target specific invaders.
5 cells and T cells recognize antigens by means of antigen-specific receptors embedded in their plasma
membranes.
<ach of these cells bears about "00,000 of these antigen receptors.
*ll the receptors on a single cell are identical, that is, they all recognize the same epitope.
<ach lymphocyte displays specificity of a particular epitope on an antigen and defends against that
antigen or a small set of closely related antigens.
6 #ells 2eceptors 8or Antigens
* typical 63cell receptor or anti"ody is a =-shaped molecule consisting of four polypeptide chains#
Two identical heavy chains and two identical light chains oined by disulfide "ridges to
form the Y3shaped molecule'
The transmembrane region of the tail portion anchors the receptor in the plasma membrane
and a short portion penetrates into the cytoplasm.
The tips of the = are the variable regions, 9 regions, of the heavy and light chains.
The tail of the = shaped antibody is made of the constant or C regions of the heavy chains.
The interaction between the antigen-binding site and its corresponding antigen is stabilized by multiple
noncovalent bonds between chemical groups on the respective molecules.
The receptor binds to molecules that are on the surface of the infectious agent.
They recognize intact antigens.
*ntibodies have two main functions#
". Combine with antigen and labels it for destruction.
$. *ctivates processes that destroy the antigen that binds to it.
*ntibodies do not destroy the antigen. &t labels the antigen for destruction.
)ecreted antibodies are serum globular proteins also !nown as immunoglo"ulins, &g.
T #ell 2eceptors 8or Antigens And The 2ole 4f The MH#
T cell receptors consist of two polypeptide chains, > and ? chains lin!ed by disulfide bridge.
They have a straight shape, not a = shape li!e the 5-cell receptors.
The transmembrane region anchors the antibody to the plasma membrane.
The variable @ regions at the other end of the antigen form a single antigen-binding site.
The remainder of the molecule is made up of the constant C region.
The T cell receptors bind with antigens li!e the 5 cell receptors.
T cell receptors are capable of recognizing small fragments of the antigen that are bound to normal cell-
surface proteins called 4'C molecules.
5 cell receptors recognize intact antigens on the surface of the pathogen.
T cell receptors recognize fragments of antigens presented by the 4'C comple3.
MA:42 HIST4#4M)ATI6I&ITY #4M)&E; .MH#/
The ability to distinguish self from non-self depends largely on a group of cell surface proteins !nown as
MH# antigens.
These proteins are synthesized by a group of genes called the ma<or histocompati"ility comple, 4'C.
The principal function of the 4'C is to present antigens on the surface of cells recognition by T
lymphocytes# cytoto3ic T cell ,Tc- and helper T cells ,T'-.
Class & 4'C molecules and Class && 4'C molecules mar! body cells as AselfA.
&t permits recognition of self, a biochemical AfingerprintA.
The 4'C antigens are a group of membrane glycoproteins that act as mar!ers on the surface of the cells
of the individual.
Blycoproteins are proteins with a sugar chain attached to it.
Antigen presentation#
+hen a cell is infected or a macrophage engulfs a pathogen, antigen protein fragments are combined with
Class & or && 4'C proteins and transported to the surface of the cell to be presented to a nearby T cell.
There are two sets of 4'C genes that code for proteins.
#lass I MH# molecules. Cound on all nucleated cells. Distinguish self from non-self. Corms 4'C-
antigen comple3 with fragments of proteins made by the infecting microbe, usually a virus, on the
surface of the cell surface. These 4'C-antigen comple3es are recognized by a subgroup of T cells
called cytotoic T cells.
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#lass II MH# molecules. Cound on specialized antigen-presenting cells including macrophages, 5
cells, dendritic cells, activated T cells, spleen cells, lymph node cells, and the cells in the interior of
the thymus. Class && 4'C molecules form comple3es with antigens from protein fragments of
digested bacteria that have been digested after being ta!en in by phagocytosis. These comple3es
stimulate helper T cells to form interleu!ins and activate 5 cell. These phagocytic cells are called
antigen-presenting cells.
The class && 4'C antigens regulate the interaction between 5 cells, T cells and antigen-presenting
cells.
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*n engulfed bacterium...
4acrophage engulfs bacterium.
*ntigen forms comple3 with the class && 4'C protein.
4acrophage displays 4'C-antigen comple3 on its cell surface.
Helper T cells are activated when their receptors combine with the 4'C-antigen comple3.
*n infected body cell...
7athogen invades the body and infects cells.
4acrophage engulfs pathogen.
*ntigen forms comple3 with the class & 4'C protein.
4acrophage displays 4'C-antigen comple3 on its cell surface.
Helper T cells recognize the foreign antigen-4'C comple3.
<ach vertebrate species possesses numerous different alleles for each class & and class && 4'C gene.
* group of closely lin!ed polymorphic genes, e.g. multiple alleles for each locus% sometimes up
to $00 alleles for one gene determine these glycoproteins.
They are located on chromosome / in humans.
&ymphocyte development'
T lymphocytes or T cells are responsible for cellular immunity.
6riginate in the bone marrow.
&n the thymus they become immunocompetent that is capable of immune response.
&n the thymus they divide many times and some develop specific surface proteins with receptor
sites. These cells are selected to divide# positive selection.
The T of T cells comes from FthymusG.
6 cells are responsible for anti"ody3mediated immunity.
7roduced in the bone marrow daily by the millions.
They mature in the "one marro=.
Carry specific glycoprotein receptor to bind to a specific antigen.
+hen a 5 cell comes into contact with an antigen that binds to its receptors, it clones identical
cells, and produces plasma cells that manufacture antibodies.
*lso produce memory 6 cells that continue to produce small amounts of antibody after an
infection.
The 5 of 5 cells comes from Fbursa of CabriciusG and organ uni;ue to birds where the cells were
first found. =ou may associate the 5 with Fbone marrowG.
&ymphocyte diversity "y gene rearrangement
The se;uence of amino acids at the tip of the variable regions of the receptor determines the specificity of
an antigen receptor.
During the early development of the 5 and T cells, genes are rearranged under the influence of enzymes
called recom"inases.
4aturing lymphocytes have genes that code for antigen receptor chains, @ regions.
These genes consist of numerous coding gene segments that undergo random, permanent
rearrangement, forming functional genes that can be e3pressed as receptor chains.
The @ coding genes are separated by an intron from an e3on that codes for the constant chain C.
7ortions of the D.* between segment genes ,@- are deleted and the new segments of D.*
reoined including the e3on C.
The new gene is then transcribed and introns are removed during processing of the pre-m9.*.
7oly * and cap are added to the m9.* and processing is finished.
The m9.* is translated into variable and constant regions.
)ee Cig 43."", page E0/.
The rearrangement of genes occurs at random during maturation, and by chance a chain may end up being
able to recognize a particular antigen.
Immune responses and immunological memory
*ntigens cause the lymphocytes to form two clones of cells# effector cells and memory cells.
". *ntigen molecules bind to the antigen receptors of a 5 cell.
$. The selected 5 cell multiplies and gives rise to a clone of identical cells bearing receptors for the
selecting antigen.
3. )ome proliferating cells develop into short-lived plasma cells that secrete antibody specific for the
antigen.
4. 6ther cells develop into long-lived memory cells that can respond rapidly upon subse;uent e3posure
to the same antigen.
9esponse caused by the first e3posure to an antigen is called the primary immune response'
During the primary immune response, antibody-producing 5 cells called plasma cells and
effector T cells multiply.
<3posure to the same antigen at a later time causes a more rapid and effective response called secondary
immune response.
*ntibodies produced in the secondary immune response are more numerous and have greater
affinity for the antigen.
This is called immunological memory.
#E&&3ME!IATE! IMMUNITY
Cytoto3ic T lymphocytes and macrophages are responsible for cell-mediated immunity.
Cytoto3ic T cells destroy infected cells and cells altered in some way li!e cancer cells.
Cytoto3ic T cells recognized antigens only when they are presented forming the 4'D-antigen comple3.
#yto%ines are proteins and peptides that stimulate other lymphocytes.
Helper T #ells
+hen a helper T cell encounters and recognizes a class && 4'C molecule-antigen comple3 on an antigen
presenting cell, the helper T cell proliferates and differentiates into a clone of activated helper T cells and
memory helper T cells.
7athogen invades the body and infects cells.
4acrophage engulfs pathogen.
*ntigen forms comple3 with the class II MH# protein.
4acrophage displays 4'C-antigen comple3 on its cell surface.
CD4 proteins enhance the recognition of the 4'C-antigen comple3 by helper T cells.
'elper T cells recognize the foreign antigen-4'C comple3 and secrete the cyto!ine &8-$.
Competent T cells are in turn activated, increase in size and divide mitotically.
Clones of competent T cells are produced.
Clones differentiate into memory T cells, cytoto3ic T cells and other types of cells.
Cytoto3ic T cells leave the lymph nodes and migrate to the area of infection.
#ytotoic T cells
Cytoto3ic T cells are the effectors of cell-mediated immunity.
They destroy pathogens, cancer and transplanted cells.
*t the site of infection,
*ll nucleated cells have class I MH# proteins on its surface.
&n infected cells, cancer cells and foreign cells, their proteins are bro!en down and carried by
newly made class & 4'C proteins to the surface of the cell.
The infected cell displays class & 4'D-antigen comple3 on its surface.
Cytoto3ic T cells recognize the displayed comple3 and binds to the infected cell with the help of
CDH proteins.
Cytoto3ic T cells release proteins ,lymphoto3ins, perforins- in the site of infection and destroy
pathogens by lysing.
4acrophages are attracted to the site to ingest pathogens.
4'C proteins have the ability to bind to different antigenic peptides displayed by the macrophage. )hort
peptides are fle3ible in solution and can adapt to the binding site of the 4'C protein. *lso, the 4'C
binding site is somewhat fle3ible and can accommodate a variety of peptides with not the e3act
homology.
6 cells
5 cells are responsible for antibody-mediated immunity, also called humoral immunity.
*ntibody molecules serve as cell surface receptors that combine with antigens.
6nly 5 cells bearing a matching receptor on its surface can bind a particular antigen.
*ntigens that cause helper T cells produce cyto!ines and stimulate the production of memory cells and
plasma cells, are !nown as T3dependent antigens. They can be produced only with help from a helper T
cell.
)ome polysaccharides and bacterial proteins can cause a 5 cell to proliferate into antibody-producing
plasma cell without the intervention of helper T cells. These antigens are called T3independent antigens.
5 cell must be activated.
4acrophage engulfs bacterium.
*ntigen forms comple3 with the class II MH# protein.
4acrophage displays 4'C-antigen comple3 on its cell surface.
'elper T cells are activated when their receptors combine with the 4'C-antigen comple3 with
the help of a CD4 protein.
*ctivated helper T cells secrete cyto!ines that activate 5 cells.
&ndependently 5 cells bind with complementary antigen and forms 4'C-antigen comple3 on its
own surface.
4'C-antigen comple3 stimulate 5 cells to divide and differentiate.
Cyto!ines also stimulate cytoto3ic T cells to become active !illers.
*ctivated 5 cells form many clones, some of which differentiate into plasma cells and some into
memory 6 cells.
7lasma cells remain in the lymph nodes and secrete specific anti"odies.
*ntibodies are transported via lymph and blood to the infected region.
*ntibodies form comple3es with antigens on the surface of the pathogen.
*ntibodies combine with antigens to forms specific comple3es that stimulate phagocytosis, inactivate the
pathogen, or activate the complement system.
4emory cells survive for a long time and continue to produce small amounts of antibody long after the
infection has been overcome.
4emory cells when stimulated can produce clones of plasma cells.
Anti"ody classes
*ntibodies are grouped into five classes of immunoglobulins or &g based on the constant region of the
heavy chains.
". &gB and &g4 defend the body against pathogens in the blood and stimulate macrophages and the
complement system.
$. &g* is present in the mucus, saliva, tears and mil!. &t prevents pathogens from attaching to epithelial
cells.
3. &gD found on 5 cells surface helps activate them following antigen binding. They are needed to
initiate the differentiation of 5 cells into plasma and memory 5 cells.
4. &g< when bound to an antigen releases histamines responsible for many allergic reactions. &t also
prevents parasitic worms.
*ntibodies combine with antigens to forms specific comple3es that stimulate phagocytosis, inactivate the
pathogen, or activate the complement system.
*ntibodies may inactivate a pathogen, e.g. when the antibody attaches to a virus, the virus may lose
its ability to attach to a host cell. This is called neutrali$ation.
The antigen-antibody comple3 may stimulate phagocytic cells to ingest the pathogen. *ntibodies
enhance macrophage attachment to the microbes for phagocytosis. This is called opsoni$ation.
Clumping of bacteria and viruses neutralizes and opsonizes the microbes for phagocytosis. This is
called agglutination.
*ntibodies can bind to soluble antigens and form immobile precipitates that can be disposed of by
phagocytes. This is called precipitation.
The antigen-antibody comple3 allows complement system proteins to penetrate the pathogenIs
membrane and open a pore that causes the lysis of the pathogenic cell. These proteins form a
mem"rane attac% comple .MA#/ that opens the pore. This is called complement fiation.
The classical path=ay is triggered by antibodies bound to antigen and is part of the humoral
response.
The alternative path=ay is triggered by substances already present in the body and does not
involve antibodies% it is part of the nonspecific defense system.
4icrobes coated with antibodies and complement proteins tend to adhere to the wall of blood vessels,
ma!ing them easy preys for phagocytes.
6psonization, agglutination and precipitation enhance phagocytosis of the antigen-antibody comple3.
Immuni$ation
Constant evolution of pathogens causes different antigens that are no longer recognizable by memory
cells and thus cause the disease again, e.g. cold, flu.
Types of immunity#
Active immunity is developed by e3posure to antigens.
Naturally induced by an infection.
Artificially induced through a vaccine.
)assive immunity is caused by the inection of antibodies produced by other organisms.
Naturally induced by the mother to the developing baby.
Artificially induced through inection of antibodies ,gamma globulin-.
5abies who are breastfed continue to receive immunoglobulins ,&g*- in the mil!.
6lood groups and "lood transfusion
The *56 system is based on the antigens found on the surface of the 95C. See Ch. 14, table 14.2.
These AantigensA are polysaccharides that if placed in the system of another person will cause a
devastating reaction% they are .6T antigens to the owner.
Type * has antigen * protein in the 95C plasma membrane% Type 5 has antigen 5% Type *5 has both
antigens% and Type 6 has neither of the two antigens on its surface.
e. g. Type * blood will have antibodies against the 5 antigen. Type *5 does not have
antibodies against antigens * or 5.
The 2h factor is an antigen that can cause problem if the mother is 9h negative and the fetus is 9h
positive.
8ate in pregnancy or during delivery the 9h-positive factor of the baby can cause the formation of 9h
antibodies, anti-9h-positive &gB, in the mother that will endanger the life of future 9h positive babies by
destroying their 95C.
5rafts and organ transplants
Braft reection is an immune response against transplanted tissue.
T cells are responsible for the destruction of the transplanted organ.
The transplanted tissue has 4'C antigens that are different from those of the host that stimulate the
immune response.
Certain part of the body accepts any foreign tissue, e.g. cornea.
5ecause of the difficulty of finding a good match to transplant tissues or organs, biologists are
investigating techni;ues to transplant animal tissues and organs to humans. This procedure is called
enotransplantation.
*nimals can be genetically engineered so that they do not produce antigens that stimulate the immune
system of the host.
A"normal immune functions
Allergic reactions
Hypersensitivity is an e3aggerated immunological response to an antigen that is harmless.
4ild antigens called allergens cause allergic reactions.
&t involves sensitization, activation of mast cells and allergic response.
&t involves the production of &g< by plasma cells.
'ayfever reaction#
<3posure to pollen causes 5 cell to develop into plasma cells, which ma!e pollen specific &g<
antibodies.
&g< becomes attached to mast cells receptors.
+hen more pollen is inhaled, allergen pollen molecules attach to the &g< on the mast cells
surface.
4ast cells then release histamine and serotonin, in a process called degranulation.
These chemicals cause vasodilation, increase permeability and inflammation.
*llergic asthma occurs when the &g< becomes attached to mast cells in the bronchioles of the lungs.
Chemical released by mast cells cause smooth muscles to contract and airways narrow ma!ing breathing
difficult.
+hen the allergen reaction ta!es place in the s!in, the person develops hives.
Systemic anaphylais is hypersensitivity to a drug li!e penicillin, compounds in food, insect sting or
venom.
The reaction is widespread.
4assive amounts of histamine are released into the blood.
<3treme vasodilation and permeability follows causing a rapid drop in blood pressure, shoc! and
death.
*ntihistamine drugs ,epinephrine- bloc! the effect of histamines released by mast cells.
Autoimmune disease is a form of hypersensitivity when the body reacts against its own tissues.
<.g., 4ultiple sclerosis, insulin-dependent diabetes mellitus, rheumatoid arthritis, lupus and psoriasis.
During lymphocyte development comple3 mechanisms are developed so the +5C become self-tolerant
and do not attac! the tissues of their own body.
&t is !nown that some lymphocytes capable of attac!ing self. There is a regulatory mechanism that
prevents this from happening in healthy individuals. Cailure to regulate these lymphocytes results in
autoimmune diseases.
)rimary immunodeficiency diseases result from hereditary or congenital defects that prevent proper
functioning of innate, humoral, andDor cell mediated defenses.
*n immunodeficiency that develops later in life following e3posure to various chemical and biological
agents is classified as an ac;uired or secondary immunodeficiency.
)tress can harm the immune system. 'ormones secrete by the adrenal glands during stress affect the
numbers of white blood cells and may prepress the immune system response.
.eurotransmitters released when the person is rela3ed and happy may enhance immunity.
AI!S 3 A#1UI2E! IMMUNE !E8I#IEN#Y SYN!24ME
&t is cause by the retrovirus HI97 human immunodeficiency virus.
2etroviruses are 9.* viruses that use 9.* as a template to ma!e D.* with the help of reverse
transcriptase.
The D.* produced by the virus is inserted in the host D.* and e3ists as a provirus for the life of the
infected cell. 5ecause of its provirus e3istence, immune responses fail to eradicate the virus.
Cre;uent mutations at every viral replication compound the problem of eliminating the '&@.
'&@ destroys helper T cells and macrophages by attaching to the #!, molecules on the surface of the T
lymphocyte.
There are some evidence of destruction of the lymph nodes.
The ability of suppress infection is impaired and the patient falls victim to infectious diseases and cancer.
*JT ,acidothymidine- bloc!s the action of reverse transcriptase.