Pathomorphology of immune

system. Reactions and mech

anisms of hypersensitivity
 Immunogenetic organs

 Organized lymphoid tissue is divided into primary (

central) and secondary (peripheral) lymphoid orga
ns.
 The primary lymphoid organs are the thymus and
bone marrow. The thymus consists of several lobe
s, in every lobe the cortical and medullar zones ar
e present. Epithelial cells are the basic structure el
ements of the lobe. These cells produce peptide h
ormones, which stimulate T-lymphocyte (or T-cells
) differentiation.
 Coming from the bone marrow to the thymus, pret
hymocytes (prethymic T-cells) are deposited in the
cortical layer and then they migrate into the medull
ar layer. As they migrate, their differentiation takes
place. Cells are being divided into T-helpers, T-kill
ers, T-suppressors. Maturing of B-lymphocytes (or
B-cells) takes place in the bone marrow, and later
they migrate to the secondary lymphoid organs.
 The indicated stages of T- and B-lymphocytes mat
uring are called antigen-independent, i. e. they do
not depend on contacts with the antigens.
 To the secondary lymphoid organs belong lymphat
ic nodes, the spleen, lymphoid tissue of the mucou
s membranes. Interaction processes between the i
mmunocompetent cells take place, i. e. objective i
mmune reactions (or responces) are formed.
 Alien or foreign agents, which have penetrated the
bodily tissues, are caught by the lymphatic nodes.
The lymphatic node is covered by a dense capsule
of connective tissue under which the friable reticul
ar tissue is located. This reticular tissue forms the
border and medullar sinuses. B-lymphocytes are f
ound between the sinuses, T-lymphocytes (thymu
s-dependent zone) are in the paracortical zone.
 If the lymphatic nodes are in rest the B-lymphocyte
s form primary follicles in the B-zone. After an anti
genic stimulation, B-lymphocytes form secondary f
ollicles, where there is the dense ring of B-lympho
cytes on the peryphery, and the gerninal center is i
n the middle, where macrophages and proliferatin
g B-lymphocytes are found. Plasmatic cells are for
med out of them which migrate to the lymphoid tis
sues of the medullar zone.
 Under antigenic stimulation of the T-dependent zo
ne, a well-expressed T-lymphocyte proliferation is
observed in the T-zone of the lymphatic node.
 Spleen (or lien) consists of white and red pulp. Th
e lymphoid tissue forms the white pulp. B-depende
nt zone is a peripheral zone of lymphoid follicles; t
he T-dependent one is a periarterial zone.
 Lymphoid tissue is associated with mucous memb
ranes. It is located in the epithelium and does not
have a connective tissue capsule. Lymphocytes ar
e either diffusly spread or presented by diffuse acc
umulations together with macrophages and plasm
atic cells.
 Besides, humans have even more organized struc
tures with well-formed follicles – such as pharynge
al, palatine, and lingual tonsils, Peyer's patches, a
nd lymphoid structures of the appendix.
Types of the lymphocytes and th
eir role in the development of the
immunity reactions
 Specific immune reactions (responces) are produc
ed by the lymphocytes. The lymphatic nodes are
mainly of two types of lymphocytes, which differ as
to their origin and functional peculiarities: T- and B
-lymphocytes, and natural killer-cells (NK-cells) in
small quantity.
 T-cells (lymphocytes)
 The peripheral blood contains 65-80% of all T-lym
phocytes. These cells are divided into effector-cell
s and regulator-cells.
 Effector-cells are killers which have specific cytoto
xicity to the alien cells. T-killers destroy target cells
without the help of antibody complement. T-cell re
ceptor kinds with the antibody of the target cells, w
hich is a signal to lymphocytes to discharge the su
bstances that destroy the target cell. Besides, T-kil
lers produce lymphokins, which activate and attrac
t the macrophages, natural killers and other cells.
 Subpopulation of T-cells, that is T-helpers and T-s
uppressors, perform the main regulatory function.
T-helpers stimulate the proliferation and differentia
tion of B-lymphocytes.
 T-suppressors suppress the immune response. Ac
tivated T-suppresors suppress the T-suppresors a
ctivity and the immune response proper.
 B-lymphocytes compose 8-15% of all the lymphoc
ytes of the peripheral blood. B-lymphocytes format
ion takes place in the red bone marrow from the st
em cell. Mature B-lymphocytes populate the secon
dary lymphoid organs. Under antibody influence a
nd its interaction with T-lymphocytes and macroph
ages, B-lymphocytes start differentiating into lymp
hoblasts, divide and transform into young plasmati
c cells.
 The main function of the plasmatic cells which are
the successors of B-cells is the synthesis which ta
kes place without specific immunoglobulin (antibod
ies).
 At present, 5 classes of immunoglobulin hav
e been discovered and studied. They are: Ig
A, IgD, igE, IgM, IgG.
 Natural killers or normal killers (NK-cells) co
mprise up to 5% of all the lymphocytes, and
are formed in the red bone marrow from T-ly
mphocyte precursors. NK-cells mature in the
red bone marrow and then migrate to differe
nt tissues. Their main function is cytotoxic ef
fect toward an alien cell, including tumor cell
s.
Morphologic basis of the humoral
and cell-mediated immunity
 All living processes are supported by the co
nstant functioning of the main physiologic sy
stems including the immune one. The immu
ne system functioning is manifested in 2 for
ms:
 1. Normal functioning
 2. Active functioning
 So, 1. The immune system cannot rest, bec
ause old cells die, faulty appear, viruses and
bacteria penetrate through skin and mucous
membranes, they all get destroyed by the im
mune system cells.
 2. System active functioning is presented by
the immune reaction of two types:
 a. humoral immunity
 and b. cell-mediated immunity
 Humoral immunity reactions are responses
of the immune system to a definite antibody,
which is characterized by B-lymphocyte clon
e proliferation, their differentiation into plasm
atic cells that synthesize immunoglobulins (a
ntigens).
 Cell-mediated immune response is formed a
s a result of a number of immune-competent
cell interactions and that leads to the clone fi
lling with T-lymphocyte-effectors which are s
ensitized to that particular antibody.
Immunopathologic processes. De
finition. Classification.
 Immunopathologic processes are the ones the dev
elopment of which is connected with the immunoc
ompetent (lymphoid) tissues function.

 Immunopathologic process may be a manifestatio

n of:

 1. Immunogenetic disturbance (antigenic stimulati

on or immunedeficiency)
 2. Local immune reaction in the sensitized body, i.
e. hypersensitivity reaction
 So, immunogenetic disturbances may be co
nnected with :
 a) thymus
 b) peripheral lymphoid tissue

 They are connected with the two types of th

e immune reactions – humoral and cell-medi
ated.
 Thymus pathology is manifested by:

 - aplasia
 - hypo- and dysplasia
 - atrophy
 - accidental involution
 - thymus and lymphoid follicles hyperplasia
 - thymomegalia
 Aplasia – is the absence of the thymus; hypo- or d
ysplasia – the thymus is decreased in size, divisio
n between cortical and medullar substances and n
umber of lymphocytes is decreased. These are co
ngenital development defects, accompanied by th
e deficiency of cell-mediated immunity or combine
d immune deficiency.
 Accidental involution is a quick decrease of the thy
mus mass and bulk under glucocorticoid influence
in different stress situations, infections, intoxication
, traumas. The majority of T-lymphocytes is subjec
ted to disintegration (apoptosis).
 Thymus atrophy develops as an unfavorable outco
me of the accidental involution and is the reason f
or a few acquired immunedeficiency syndromes.
 Thymomegalia is characterized by the parenchym
a mass and bulk increase with the preservation of
normal structure of the organ. Congenital thymom
egalia, found in children, is accompanied by the de
velopment defects of the internal organs, congenit
al suprarenal and sexual gland dysfunction. In infe
ctious diseases it is accompanied by lymphoid tiss
ue hyperplasia. Production of the thymus hormone
s is decreased, cell-mediated immunity is disturbe
d.
 Acquired thymomegalia is found in adults in chroni
c insufficiency of the suprarenal (adrenal) glands.
Death cause in thymomegalia can be infectious di
seases, while endocrine system disturbance can l
ead to sudden death in surgical intervention.
 Hyperplasia of the thymus with the lymphoid follicl
es is typical for autoimmune diseases. B-lymphocy
tes gather in the dilated intralobular perivascular s
paces and lymphoid follicles appear. Thymus hor
mone production is decreased or increased.
Thymus of a child, low magnification
Thymus of an adult, low magnification
Bone marrow, high magnification
Changes in the peripheral lymph
oid tissue
 These changes are the most characteristic in antig
enic stimulation and hereditary insufficiency.
 In antigenic stimulation (sensitization), the macrop
hage reaction and lymphocytic hyperplasia develo
p with their subsequent plasmocytic transformation
. Changes are supplemented by an increased micr
ovascular permeability and interstitium edema. Ly
mphatic nodes are increased in size, plethora and
edema develop; many plasmoblasts are found in t
he cortical layer of the light follicular centers and in
the medullar zone.
 The spleen is increased, plethotic, plasmatization
of the red pulp in follicular peripheral zone is obser
ved. If cell-mediated immune reactions develop in
response to the antigen stimulation, so sensitized l
ymphocytes proliferate in the lymphatic nodes and
spleen, T-zones become wider.
 Hereditary insufficiency of the lymphoid tissue in th
e spleen is characterized by follicle size decrease,
light centers are absent. Follicles and the cortical l
ayer (B-dependent zones) are absent in the lymph
atic nodes. These changes are characterestic of th
e hereditary immune-deficiency synderomes, conn
ected with the humoral immunity defect.
Development mechanisms of the
hypersensitivity reactions of the d
elayed-type and immediate type
 At the second contact with an antibody, the immun
e system reacts upon it with a stronger immune re
sponse, the allergic or hypersensitivity reaction de
velops.
 The same mechanisms of cellular interactions, as i
n the humoral and cell-mediated immunity reaction
s, lie in the basis of allergic reactions.
 Hypersensitivity reactions are the local immune re
actions in the sensitized body.
 There are 5 mechanisms of the hypersensiti
vity reactions:
 The 1-st mechanism (anaphylactic allergy of
the immediate type) – antibodies (reagent, I
gE) are produced and fixed on the cell surfa
ce (on labrocytes, basophils), they specifical
ly react with antibodies, that leads to the exc
retion of the biologically active substances c
alled mediators. This is accompanied by the
acute inflammation (rhinitis, allergic eruption
s, bronchial asthma) development.
 The 2-nd mechanism (humoral cytotoxic immune r
eactions or cytotoxic hypersensitivity) is cytolysis, i
t may be provided by the complement, which is act
ivated when an antibody is connected with an anti
gen, or with other antibodies. Examples of such ty
pe reactions are: reactions in blood transfusion, R
h-factor incompatibility (i. e. haemolytic disease of
the newborn) intolerance to some drugs.
 The 3-rd mechanism is connected with the toxic ac
tion of the circulating immune complexes (also call
ed: immune complex hypersensitivity) (antibody+a
ntigen) on the cells and tissues, that leads to comp
lement component action (for example: serum dise
ase, Arthus phenomenon).
 The 4-th mechanism is stipulated by the effe
ctor k-cell (lymphocytes) – and macrophage
action on the tissues. The sensitized T-effec
tors affect the antigens and cytolysis develo
ps. Such mechanism is characteristic of aller
gy in infectious diseases.
 The 5-th mechanism is granulomatosis.
 Some of the mechanisms are the expressio
n of the humoral immunity, others of the cell-
mediated immunity. The reactions connecte
d with the immunopathologic reactions of th
e humoral immunity are called immediate ty
pe hypersensitivity (ITH) reactions; those re
actions, which are connected with the immu
nopathologic mechanisms of the cell-mediat
ed immunity are called delayed-type hypers
ensitivity (DTH) reactions. Besides those, th
ere are also transplant rejection reactions.
Lymphatic node, low magnification
Lymphatic node, high magnification
Spleen, low magnification
Spleen, high magnification
Morphologic characteristic of the
hypersensitivity reactions
 Immediate type hypersensitivity reactions (ITH) –
have the morphology of an acute inflammation. Th
ey develop quickly, and have alterative and exudat
e, and vascular changes, reparation processes are
very slow. Alterative changes are expressed by th
e plasmatic infiltration, mucoid and fibrinois swellin
g, fibrinoid necrosis of the vascular walls. Fibrin, n
eutrophils, erythrocytes are found in the focus of th
e immune inflammation; fibrinous or fibrinous-hem
orrhagic exudate is also observed.
Contact dermatitis
 Proliferative reactions develop later, they are poorl
y expressed, but endothelium and perithelium proli
feration exists.
 ITH reactions in Arthus phenomenon (in sentisized
animals after injecting all the corresponding antige
n dose)
 In human it arises in tuberculosis, syphilis, rheuma
tism, systemic lupus erythematosus, croupous pne
umonia.
 Delayed-type hypersensitivity (DTH) reactions. Tw
o types of cells take part in this reaction; they are s
ensitized lymphocytes and macrophages.
Affection of salivary gland in Sjogren syn
drome
Islet of Langerhans. Insulitis in diabetes mellitus o
f 1st type. Lymphocytal infiltration suggests autoi
mmune affection
 REJECTION OF TRANSPLANT

 Prevalence of operations on transplantation of tiss

ues (organs) has significantly increased in clinical
practice for the last two decades. Presently operati
ons are successfully conducted on transplantation
of cornea, skin and bones. Transplantation of kidn
eys is executed with high success in many large m
edical centers.
 Transplantation of heart, lungs, liver and marrow a
re still experimental procedures, but success of th
ese operations is increased every day.
 Factors, limiting transplantation of tissues, are im
munological reactions against the transplanted cell
s and presence of the proper donor organs.
 Autotransplantation does not cause the immunolo
gical reactions of rejection, which is transplantatio
n of the patient's own tissues from one part of orga
nism to the other (for example, skin, bones, veins),
and also transplantation of tissues between geneti
cally identical twins (isotransplantation), because t
he tissue is perceived as "own".
 At transplantation of non-vascular transplants (for
example, corneas) the reaction of the immunologic
al rejection fails to appear, because absence of cir
culation of blood in a transplant prevents the conta
ct of immune cells with antigens, and for developm
ent of immune answer contact of antigen with the
cells of the immune system is needed.
 Transplantation of tissue between genetically hete
rogeneous people causes an immunological answ
er which can lead to rejection. The expressed reac
tion of rejection is increased along with growth of g
enetic distinctions between donor and recipient. Pr
esently almost all organs are transplanted from pe
ople.
 Transplantation of organs between genetical
ly different members of the same kind is call
ed allotransplantation.
 Xenotransplantation is transplantation of org
ans between the individuals of different kind
s (for example, the case of transplantation of
heart of baboon to the child is known); such
type of transplantation is accompanied a he
avy immunological reaction and is not utillize
d practically.
Clinical types of rejection of trans
plant
 There are a few forms of rejection of transpl
ant: from transient reaction, occuring in a fe
w minutes after transplantation, to the slow r
eactions, showing up violation functions of t
he transplanted tissues over years after tran
splantation. Mechanisms, engaged in these
different types of rejection, are also different.

 Acutest rejection: the acutest rejection is a quick a
s lightning reaction, occuring within the limits of a f
ew minutes after transplantation and characterized
by heavy necrotic vasculitis ischemic damage of di
splanted organ. The accumulation of immune com
plexes and activating of complement in the wall of
the involved vessels can be determined by immun
ological methods.
 The acutest rejection is being caused by presenc
e in the blood of recipient of high levels of pre-exis
tent antibodies against antigens on the transplante
d cells. The reaction of antibodies with antigens ca
uses immunecomplex (the phenomenon of Arthus)
damage in the vessels of transplant.
 After the beginning of application of technique of di
rect determination of compatibility of tissues the ac
utest rejection became rare.

 Acute rejection: the acute rejection is observed oft
en enough and can occur in from a few days to mo
nths after transplantation. It is sharp because even
if the signs of rejection appear over the months aft
er transplantation, it quickly makes progress from t
he moment of his beginning. The sharp rejection is
characterized by necrosis of cells and violation of f
unctions of organ (for example, sharp necrosis of
myocardium and cardiac insufficiency in transplant
ation of heart).

 In the acute rejection both humoral and cellular me
chanisms take part. Immune complexes are depos
ited in the shallow vessels of transplant and cause
sharp vasculitis, leading to the ischemic changes.
The cellular immune rejection is characterized by
necrosis of parenchymatous cells and lymphocytal
infiltration of tissues.
 In transplantation of kidneys the acute rejection is
seen as acute kidney insufficiency as a result of n
ecrosis of kidney tubules with lymphocytal infiltrati
on of interstitial tissue. For prevention and treatme
nt of the sharp rejection immunosuppressive medi
cations are used, for example, corticosteroids (pre
dnisolon) and cyclosporins.
 Chronic rejection: the chronic rejection is observed
in most of the transplanted tissues and causes the
progressive worsening of function of organ in mont
hs or years. Patients often have episodes of the sh
arp rejection, halted by therapy.
 In chronic rejection cellular immunity (IV type of hy
persensitiveness) is activated, that results in progr
essive elimination of parenchymatous cells. In the
staggered tissue fibrosis develops with lymphocyta
l infiltration. Occasionally presence of chronic vasc
ulitis proves the parallel influence of antibodies.
 In treatment of the chronic rejection we try to
attain balance between the damage of trans
plant and expressed toxic influencing of imm
unosuppressive medications which are usua
lly utillized for prevention of rejection.
Acute rejection in transplantation of the h
eart
Acute rejection in transplantation of the h
eart
Autoimmunization and autoimmu
ne diseases
 Autoimmunization (autoallergy, autoaggression) is
the state, characterized by appearance of reaction
of the immune system on the normal antigens of p
atient's own tissues.
 Autoimmunization is closely related to the concept
of immunological tolerance (from Lat. tolerare). It i
s characterized by the state of areactivity ("toleran
ce") of lymphoid tissue in relation to antigens, able
to cause immune answer.
 In the period of ripening of lymphoid tissue t
here is immunological tolerance to the antig
ens of all organs and tissues, except for tiss
ues of eye, thyroid, testicles, adrenal glands,
cerebrum and nerves. It is considered that t
he antigens of these organs and tissues are
bordered from lymphoid tissue by physiologi
cal barriers, which explains absence of toler
ance of the immunocompetent system to the
m.
 The immune system begins to recognize"own" and
"alien" tissue antigens in new-born in a few weeks
after birth. Thus the production of autoantibodies i
n small quantities constantly take a place on the e
xtent of all life and autoantibodies, as supposed, ta
ke part in adjusting of different functions of organis
m. Their action is under control by T-supressors a
nd anti-idiotypic antibodies, that does not allow an
autoimmune process to develop .
 Autoimmunne diseases are diseases, in basis of w
hich lies autoimmunity, that aggression of autoanti
bodies, circulatory immune complexes, containing
autoantigens, and effector immune cells (killer lym
phocytes) in regard to the antigens of own tissues
of organism.
 Therefore autoimmune diseases are also named a
utoaggressive.
 Following the mechanism of autoimmunization, we
distinguish two groups of autoimmune diseases. Fi
rst group – organ-specific autoimmune diseases w
hich develop in connection with the damage of phy
siological barriers of the immunologically isolated
organs, that allows the immune system to react on
their unchanged antigens by making of autoantibo
dies and sensibilized lymphocytes.
 Thus morphological changes, typical mainly for DT
H, develop in organs: tissue of organs is infiltrated
by lymphocytes, parenchymatous elements perish,
sclerosis develops in the end. This group includes
thyreoiditis (disease of Khasimoto), encephalomye
litis, polyneuritis, dissipated sclerosis, idiopathic A
ddison's disease, aspermatogenia, sympathic opht
halmia.
 Second group – organ-nonspecific autoimmune di
seases. Leading to these diseases are violations o
f control of immunological homeostasis of the lymp
hoid system. Autoimmunization here develops in r
elation to the antigens of many organs and tissues
, not possessing organ specificity and incapable to
cause the products of antibodies at parenteral intr
oduction.
 Morphological changes, characteristic for the react
ions of hypersensitiveness both slow and especiall
y immediate types, develop in organs and tissues.
This group of autoimmune diseases includes syste
m lupus erythematosus, rheumatoid arthritis, syste
m sclerodermia, dermatomyositis (group of rheum
atic diseases), secondary thrombocytopenic purpl
e (disease of Moshkovich).
 There are autoimmune diseases of intermediate ty
pe, which are close to diseases of the first or seco
nd type. These are myastenia gravis, diabetes mel
litus of the I type, thyreotoxicosis, syndromes of Sj
ogren and Goodpasture and others.
 Besides autoimmune diseases, there are diseases
with autoimmune violations. Appearance of autoan
tigens at these diseases is connected to the chang
e of antigen properties of tissues and organs – de
naturation of tissue albumens (at a burn, irradiatio
n, trauma, chronic inflammation, viral infection); for
mation of autoantigen is possible at influence of ba
cterial antigen, especially cross reactive (for exam
ple, at glomerulonephritis, rheumatism).
 In formation of autoantigen a large value is given t
o gaptene mechanism, and both the products of m
etabolism and microorganisms, toxins and medicat
ions can play the role of gaptenes.
 Autoimmunization in these terms determines
not the origin of disease, but progress of typi
cal for it local (organ) changes which reflect
morphology of reactions of hypersensitivity o
f slow and immediate types.
 This group of diseases includes: certain for
ms of glomerulonephritis, hepatitis, chronic
gastritis and enteritis, cirrhosis of liver, burn
disease, allergic anaemias, thrombocytopeni
a, agranulocytosis, medicinal allergy.
 Immunodefitiency syndromes
 Immunodefitiency syndromes are the extrem
e display of insufficiency of the immune syst
em. They can be primary, conditioned by un
derdevelopment (hypoplasia, aplasia) of the
immune system, which are inherited and inn
ate immunodeficiency syndromes, or secon
dary (acquired), arising up in connection wit
h illness or conducted treatment.
 INNATE (PRIMARY) IMMUNOD
EFICIENCY
 The morphological displays of primary insufficienc
y of immune answer are linked, as a rule, with the i
nnate anomalies of thymus, or combination of thes
e anomalies with underdevelopment of spleen and
lymphatic nodes.
 Heavy combined immunodeficiency - it one of the
most heavy forms of innate immunodeficiency. It is
characterized by the defection of stem lymphatic c
ells, that results in violation of development of bot
h T-, and B-lymphocytes. The process of lowering
of thymus from neck into mediastinum is disturbed
. The amount of lymphocytes is sharply reduced in
it.
 There's also a few of them in lymphatic nodes, spl
een, lymphoid tissue of intestine and peripheral bl
ood. Immunoglobulines are absent in the serum. I
nsufficiency of both cellular and humoral immunity
is reason of various heavy infectious (viral, mycoti
c, bacterial) diseases, arising up right after birth, th
at result in early death (usually on the first year of l
ife).
 Hypoplasia of thymus (syndrome of Di-George) is
characterized by the lack of T-lymphocytesin blood
, in thymus dependent areas of lymphatic nodes a
nd spleen. The general amount of lymphocytes in
peripheral blood is diminished. For patients the sig
ns of insufficiency of cellular immunity are reveale
d, which manifests as heavy viral and mycotic infe
ctious diseases in childhood.
 Development of B-lymphocytes is usually no
t disturbed. Activity of T-helpers is almost ab
sent, however concentration of immunoglob
ulins is usually normal. In thymus hypoplasia
genetic defects are not exposed. This state i
s characterized also by absence of parathyr
oid glands, wrong development of arc of aort
a and facial skull. In absence of parathyoid g
lands there is expressed hypocalcihemia, re
sulting in death in early age.
 T-lymphopenia in the syndrome of Nezelof c
ombines with violation of their function. It is
assumed that it takes place as a result of vio
lation of ripening of T-cells in thymus. The s
yndrome of Nezelof differs from syndrome of
Di-George by the typical association of dam
aging of other structures, developing from th
e third and fourth gullet pockets. Parathyroid
glands at this syndrome not damaged.
 Thymus hypoplasia is successfully treated b
y the method of transplantation of human e
mbryonic thymus, that restoring T-cell immu
nity.
 Innate agammaglobulinemia (disease of Bru
ton) - genetically conditioned recession, rela
ted to the X chromosome, disease which is
observed mainly in boys and characterized
by violation of formation of B-lymphocytes.
 Pre-B cells (CD10 positive) are found, but mature
B-lymphocytes are absent in peripheral blood and
in the B-zones of lymphatic nodes, tonsils and the
spleen. Reactive follicles and plasmatic cells are a
bsent in lymphatic nodes. Insufficiency of humoral
immunity manifests in the noticeable diminishing o
r absence of immunoglobulins in serum.
 Thymus and T-lymphocytes develop normally and
cellular immunity is not violated. General amount o
f lymphocytes in peripheral blood is within the limit
s of norm, because an amount of T-cells which ma
kes 80-90% lymphocytes of blood usually is within
the limits of norm.
 Infectious diseases in a child develop usually in th
e second half of the first year of life since level of p
assively received maternal antibodies falls. Treatm
ent of such patients is made by introduction of im
munoglobulins.
 The isolated deficiency of IgA is the most frequent
immunodeficiency, found in one of 1000 people. It
arises as result of defect of eventual differentiation
of plasmatic cells, secreting IgA. For some patient
s this defect is related to abnornal function of T-su
pressors . At most patients the deficiency of IgA ru
ns asymptomatically.
 Only a small quantity of patients has predispositio
n to the development of pulmonary and intestinal i
nfections, because for them the lack of secretory I
gA is determined in mucous membranes. At patien
ts with the expressed deficiency of IgA anti-IgA ant
ibodies are found in blood. These antibodies can r
eact with IgA, which are in the transplanted blood,
that results in development of hypersensitivity of th
e I type.
 The immunodeficiency of various degree is found
often enough. It arises as the secondary phenome
non in different diseases, or as a result of medicin
al therapy and very rarely is primary disease.
 Morphology of syndrome of the purchased i
mmunodeficiency (AIDS) does not have a s
pecific picture and differs on the different sta
ges of its development. Changes are observ
ed both in the central and in peripheral orga
ns of immunogenesis (changes are most ex
pressed in lymphatic nodes).
SECONDARY (ACQUIRED) IMM
UNODEFICIENCY
 Immunnodeficiency is always accompanied by dev
elopment of opportunistic infections and on the fin
al stage by development of malignant tumours, mo
re frequent than all sarcomas of Kaposi and malig
nant B-cellular lymphomes.
 The origin of infectious diseases depends on the t
ype of immunodeficiency:
 - the deficiency of T-cells predisposes to the infe
ctious diseases, caused by viruses, mycobacteria,
fungi and other intracellular microorganisms, like P
neumocystis carinii and Toxoplasma gondii.
 - the deficiency of B-cells predisposes to t
he festering bacterial infectious diseases.

 These infectious diseases reflect relative importan
ce of cellular and humoral answers in defence aga
inst different microbe agents.
 Sarcoma of Kaposi and malignant B-cellular lymph
omas are the most frequent malignant neoplasia w
hich develop at patients with immunodeficiency.
 The origin of malignant new formations can be con
nected to either violation of immune answer, direct
ed on the removal of developing malignant cells, w
hich appear in an organism (refuse of immune sup
ervision) or due to immune stimulation of the dama
ged immune system in which the normal mechanis
m of control of cellular proliferation is broken (it res
ults in the appearance of B-cellular lymphomas).
The lecture is over