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Semiolog y of immune system. Department of pediatrics. No t i o n. Immune system reunites the organ s , tissues and cells , which ensure the defense of h uman organism against the genetically strange substances (antigen s ) by exogenous and endogenous origin . Immune system.

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semiolog y of immune system

Semiologyof immune system

Department of pediatrics

no t i o n


Immune system

reunites the organs, tissues andcells, which ensure the defense ofhuman organism against the geneticallystrange substances (antigens) by exogenous and endogenous origin.

immune system

Immune system

Two possibilities of IS response manifesting were distinguished for to understand how the organism succeedsto put up resistance to the external medium factors (infectious agents) :

elimination ofpathogenic agents with the

nonspecific means of IS response or

producing of some cellular and molecular componentsfor adopting the pathogenic agent

(specific means).

physiologic importance

Physiologic importance

The function of IS consists in the Ag identifying and generation of specific response –


accumulation of sensibilized lymphocytes, which will



eliminated the Ag from organism.

components of immune system

Components of immune system

1. Lymphoid organs:

a) Central

b) Peripheral

2. Humoral components

a) Nonspecific

b) Specific

3. Cellular components

a) Nonspecific

b) Specific

central lymphoid organs

Central lymphoid organs

The central lymphoid organs (primary) are represented by:

hematogene marrow


central lymphoid organs1

Central lymphoid organs

The central lymphoid organs have a major significance inimmunitybecause they represent theplace oflymphopoiesis.

At their level, the cellular components of IS: B lymphocytes and T lymphocytes, aredifferentiatingfrom derived precursors originated from stem cell, proliferatingand se maturating in functional cells.

hematogene marrow

Hematogene marrow

Hematogene marrow is localizing in the trabeculae of osseos spongious tissue fromlong bones epiphyses, from flat bones and from short bones. From the histologic point of view, it is formed from stroma, blood, lymphatic vesselsand nerves. The stroma is formed from conjunctive reticular cells, forminga network where are sitting the stem cells. Here the B lymphocytes are differentiating.



The thymus is sitting retrosternally.

From the anatomic point of view, the thymus is formed from two lobes connected by isthmus.

Each lobe is formed from lobules delimitedby conjunctive septa whichproceed fromthe capsula covering the entire organ.

Two zones are described in the thymic lobule: corticaland medullar.

The thymic cells are lymphocytes, epithelial and non-epithelial cells.

The process of differentiation is developing under the influence of local hormones (thymosine, thymopoietine, thymuline) secretedespecially by subcapsular and subtrabecular epithelium.



The thymus is forming at the end of first month of intrauterine development.

It is positioned retrosternally.

It is covered by conjunctive tissue capsulawhichseparates the organ in lobules.

Each lobulehas cortical and medullar layer. The cortical layer contains T-lymphocytes, and epithelial cells of medullar layer form the Gassale corpuscles.



The thymus releases in the systemic circulation


hormones (thymosine, thymopoietine, thymic factor etc.) whichregulates the proliferationand differentiation of lymphocytes.

The thymus achieves the maximal degree of development in early childhood.

In the period of 3 – 13-15 yrsthe stabilizationof gland mass has place, and ulterior it involutes.

The cortical layer becomesmore poor in T-lymphocytes, the Gassale corpuscles from medullar layer disappear, thesestructures beingreplacedwith conjunctiveand adipose tissue.



In rare cases the physiologic involutionis not producing.

These clinical situationsusuallyare associatedwithdiminishing of GCS secretionby cortical layer of suprarenal glands. Such patientsare more receptiveto intercurrent infections, have increased risc forneoplastic processes appearance.

peripheral lymphoid organs

Peripheral lymphoid organs

Peripheral (secondary) lymphoid organs are represented by:


Lymph nodes

Lymphoid tissue from mucosae



The spleen is situatedin the left superior part of abdomen.

It has exterior capsulafrom conjunctive tissuewhichsendsin parenchymaprolongationsforming trabeculae. Thesetogetherwith the reticular cells network form a support for agreat lot of cells.

Two types of tissue enterin the spleen structure : the tissue responsibleforgrown old blood cells destruction and urgent generation of new erythrocytes, plateletsand granulocytes (red pulp) and tissue populatedbyimmune competent cells (white pulp).



Spleen white pulp is a lymphoid tissue situatedin two zones:

T-dependent zone, situatedaround central arteriolaand

B-dependent zone, whichsurroundsthe T-zone, as a muff.

In B-zone thecells are organizedinprimary follicles (non stimulated) and in secondary follicles (stimulated).

At the periphery of B-zone, to the exterior,the splenic macrophages are sitting.

lymph nodes

Lymph nodes

The lymph nodes are oval

formations by different dimensions, situated in theconfluence placeofgreat lymph vessels.

lymph nodes1

Lymph nodes

The forming of LN begins in the 2-ndmonth of

intrauterine developmentand is finishing in thepostnatal period.

In new-born the LN capsula is very thin and

fine, the trabeculae are weakly differentiated, and

their palpationis difficult. LN are soft and they are includedin good developed adipose tissue at this age.

At 1 year age theLNcan be palpated at the majority ofchildren.

Parallel with their growing their differentiation has place.

lymph nodes2

Lymph nodes

In the 3 yrs age the capsula is good


At 7-8 yrstheforming of trabeculae in the

interior ofLN begins.

At 12-13 yrs the structure of LNisdefinitized, being good differentiated all theirstructures:

capsula, trabeculae, follicles, sinuses.

lymph nodes3

Lymph nodes

In the puberty period the LN growing

is finishing, and sometime evenpartially regresses.

The maximal number of LN is achieved

around10 years age.

The mature has approximatively

460 LN, having total mass by1%

from corporal mass (500 – 1000g).

lymph nodes4

Lymph nodes

Each lymph node (LN) is covered at surface with

conjunctive tissue capsule, and in interior contains

lymphoid tissue.

The lymphoid tissue of LN isseparated in two



Cortical layer isformedfromfollicles–

conglomeratesof B lymphocytes.

Inparacorticallayer the T-lymphocytes are placed

Inmedullarlayer the plasmocytes, secreting

immunoglobulins are placed.

lymph nodes5

Lymph nodes

LNareplaced in groups, throughthem the lymph

drainage from distinct anatomic zones has place.

Due to theirstructure and localization theLN

have a roleofbarrierin the pathway of infection

spreading, preventing its generalization.

LNfilter the particleswith antigenic properties,

and the lymphocytesand plasmocytesfrom

LN ensure the synthesis of antibodies.

The lymphoid system of respiratoryand digestive

tract ensures the good functioning of local

immunity at the level of their mucosa.

lymph nodes6

Lymph nodes

The reaction of LN at different stimuli, especially

infectiouscan be observed from 3 months age.

In 1-2 yrs age children thebarrier function of LN

is not good expressed, therefore in this age the

infections easily are generalized (septicemia,

meningitis, generalized forms of TBC).

Immaturity of lymphoid system at the level of

digestive tubepredisposes thesuckling babiesat

intestinal infectionsand allergization of organism on

enteral pathway.

lymph nodes7

Lymph nodes

In the antepreschool age theLNare still

good structuredand can serveas

mechanicalbarrier against the infection


In this age the lymphadenites, including

these purulent and caseous (TBC) are


In the age of 7-8 years the LNbecome

functional and can suppress the infection

through immunologic mechanisms.

lymph nodes8

Lymph nodes

Occipital– placedon occipital tuberozities – they collect the lymphfrom the scalp skinand cervical posterior region.

Mastoidian– placedin region of mastoid apophises, retroauricular – placed postrior fromears pavilion – both groups collect the lymphfrom medium ear, external auditive conduct, ears pavilion, paraauricular teguments.

Submandibular – placedunder inferior bundlesof mandiba – collect the lymphfrom face skin andgums mucosa.

Mentoniar– placedone self bilaterallyin the region ofchin – collect the lymphfrom the inferior lip skin, mucosa of gumsand from inferior incissives.

lymph nodes9

Lymph nodes

Anterior cervical and tonsilar – placed anterior from the sternocleidomastoidian muscle, in superior cervical triangle– collect the lymphfrom face teguments, from parathyroid gland, nasal, faringealand buccalmucosa.

Posterior cervical – placed posterior fromthe sternocleidomastoidian muscle, anterior fromtrapezium muscle, in cervical superior triangle – collect the lymphfrom cervical region and partiallyfrom larynx.

The LNfrom above mentioned groups are

frequently cataloguedas a unique group –

cervical LN.

lymph nodes10

Lymph nodes

Supraclavicular– placedin supraclavicular fossa – collect the lymphfrom superior partofthorax, pleural domes and pulmonary apexes.

Subclavicular– placedin infraclavicular fossa – collect the lymphfrom the thoracic walland pleura.

Axillary – placed în axillary fossa – collect the lymphfrom superior members (exceptionfingers V, IV, III and palm).

Thoracic– placedon the inferior margin ofbig pectoral muscle – collect the lymphfrom thoracic wall teguments, parietalpleura, partiallyfrom lungs and mammal glands.

lymph nodes11

Lymph nodes

Cubital – placed in the cubital regionat the level of bicepstendon – collect the lymphfrom V, IV, III fingers and palm.

Inguinal – placedonline of inguinal ligament– collect the lymphfrom the teguments of inferior member, hypogastrium, buttocks, anal region, perineum, genital organs.

Popliteal– placedin the popliteal fossa – collect the lymphfrom the teguments ofleg.

lymph nodes12

Lymph nodes

The knowledge of LN localizationand of their draining zoneshas a major role in theidentifying ofinfectiongateway, especially in the case when the modificationsof infection gateway are minimal oreven absent, but regional LNwill reactin the all cases.

the semeiology of ln affection

The semeiology of LN affection


In the case of LN marked enlargement, the child or the

parents can remark this modificationand can present the respective complaints.

In the case of lymphadenitis thechild canaccusepain, tumefactionand hyperemiaat the level of affected LN.

sem e iolog y of ln af f ect ion

Semeiology of LN affection


Only LN which are placed superficially and are very enlarged in volume (lymphogranulomatosis, infectious mononucleosis) can be observed.

In lymphadenitisthe hyperemia of tegumentscovering theinvolved LN, which usually is tumefied and painful at palpation can be observed.

sem e iolog y of ln af f ect ion1

Semeiology of LN affection

Palpation. At palpation the LNthe following

Characteristics are appreciated:

Dimension – usually theLNhave a diameter

around 0,3-0,5 cm (pea seed).

The dimension of LNisgradated as the following:

I degree – dimension of millet seed

II grad – dimension oflentil seed

III grad – dimension of pea seed

IV grad – dimension ofhorse bean

V grad – dimension of peanut

VI grad – dimension of pigeon egg.

Increasing of LN dimension poate can be isolated or in group, symmetrical or unilateral.

sem e iolog y of ln af f ect ion2

Semeiology of LN affection


If in each group 3 or less LN are palpable – they are considered solitary,

If in some group more than 3 LNare palpated – they are considered multiple.

sem e iolog y of ln af f ect ion3

Semeiology of LN affection


Can be soft, elastic, hard.

It depends from the oldness and nature of process:

in chronic pathology the LN are hard,

in the case of recent affectionthey have soft consistence.

Physiologically the consistence of LN is elastic.

sem e iolog y of ln af f ect ion4

Semeiology of LN affection

Mobility – usually the LN are mobile.

Reportwith teguments, adipose subcutaneous tissue, other LN. Physiologically the LN don’tconnectwith adiacent tissuesand not between them.


LN are painless at palpation.

The presence of pain at palpation indicates an acute inflammatory process at the level of LN.

sem e iolog y of ln af f ect ion5

Semeiology of LN affection

The palpation of symmetrical LN isperforming with both hands concomitantly.

(exception – cubital LN).

In healthy children until 3 groups of LN are palpable.

In physiological conditions the

The chin, supra- and subclavicular,

thoracal, cubital and poplitealLN

are not palpating.

sem e iolog y of ln af f ect ion6

Semeiology of LN affection

The LN can be considered normal, if:

their dimension does notexceed the

dimension of pea seed,

are solitary,

by elastic consistence,


don’t adherebetween them and

adjacent tissues,

are not painful.

sem e iolog y of ln af f ect ion7

Semeiology of LN affection

For the performing of certain diagnosis, the clinical examination ofLN is supplementedat necessitywith special paraclinicalexaminations:

puncture of LN,

biopsy of LN,


sem e iolog y of ln af f ect ion8

Semeiology of LN affection

In children the modifications of LN both local andgeneralized are frequently observed.

Local/regional enlargementof LN accompanies the suppurative processesat the level of teguments: folliculites, pioderma, furunculosis, miliary multipleabscesses , infected sores, hydroadenitis etc.

sem e iolog y of ln af f ect ion9

Semeiology of LN affection

Lymphadenopathy – enlargement of LN in dimensions, sometimes with modification of their consistence.

Polyadenia – increasing of number of palpable LN.

sem e iolog y of ln af f ect ion10

Semeiology of LN affection

In diphtheria, scarlet fever, tonsillitis the cervical LN react.

În felinosisthe cubital and/or axillary LN are modified.

sem e iolog y of ln af f ect ion11

Semeiology of LN affection

TBC of peripheral LN usuallyislimiting at the affection of one group ofLN, most often cervical.

The LN represent a voluminous, hard, painless conglomerate (packet).

They are adherent between them and

adjacent tissues.

They have tendency of evolution to the

caseous necrosis, with forming of

local fistula, after that the „ stellated scars” remain.

sem e iolog y of ln af f ect ion12

Semeiology of LN affection

In theinfectious mononucleosis all groupsof peripheral LN are affected, but the affection of cervical posterior LN predominates.

In rujeolathe occipital LN are affected.

For rubeola the diffuse LN affection, more pronounced in cervical,

occipital and axillar LN groups is characteristic.

sem e iolog y of ln af f ect ion13

Semeiology of LN affection

In adenoviral and paragrippal infection

the anterior and posterior cervical and occipital LN are predominantly involved.

In mumps the auricular LNare palpating as

firm formations which are placed

superiorly to parotidian tumefiated glands.

In toxoplasmosismost frequently

thegroups of cervical,

axillary, inguinal LN are affected. The LN have the dimensionsof a nut, sometimes can have a form of pockets, but each node can be palpated separately.

sem e iolog y of ln af f ect ion14

Semeiology of LN affection

In HIV/AIDS thegeneralized lymphadenopathyis a precociousand constant symptom.

The diameter of LN is 2-3 cm, the contur net delimitated, hard atpalpation, not adhere between them and not to adjacent tissues, usuallyare sensibleat palpation, sometimes painful.

sem e iolog y of ln af f ect ion15

Semeiology of LN affection

Lymphosarcoma ismanifesting by

affectionof isolated LN group,

usually cervical or supraclavicular.

LNare very hard, painlessatpalpation,

the local signs of inflammation are


The generalized lymphadenopathy can

be present in a lot of acute or chronic

infectious pathologies and in

noninfectious pathologies.

sem e iolog y of ln af f ect ion16

Semeiology of LN affection

The diffuse diseases of conjunctive tissue can be around the noninfectious causes of generalized lymphadenopathy.

Lymphogranulomatosisas a rule beginswith

peripheral LN affection, more frequently cervical or/and mandibular. In the same timewithdisease evolution the LN grow in conglomerates.

LN are painless, atpalpationcreates a sensation of „sackofpotatoes”. The diagnosis is confirmed by the hystologic examination of LN (Berezovski-Sternberg cells).

In ALL (acute lymphoblastic leukaemia) all

groups of LN are rapidly growing in

dimensions. They are soft and painless atpalpation.

lymphoid tissues as s ociate d to mucos a e

Lymphoid tissuesassociated to mucosae

The lymphoid tissues associated to mucosae also enter in the category of secondary lymphoid organs.

These can be:

good individualized anatomically structures


lympho-epithelial diffuse structures.

lymphoid tissues as s ociate d to mucos a e1

Lymphoid tissuesassociated to mucosae

The individualized anatomically structures are:

1. Componentele of Valdayer lymphatic ring

a) lingual tonsils

b) palatine tonsils

c) tubar tonsils

d) faringean tonsils

2. Payer’s patches

3. Vermiform appendix

lymphoid tissues as s ociate d to mucos a e2

Lymphoid tissuesassociated to mucosae

The diffuse lympho-epithelial tissues

Are localized at the level of digestive, respiratory, genito-urinary tracts etc.

After their localizationthese tissues were named:

MALT – mucosae associated lymphoid tissue

SALT – skin associated lymphoid tissue

BALT – bronchia associated lymphoid tissue

GALT – gut associated lymphoid tissue

i s nonspecific immunity

IS. Nonspecific immunity

The factors of nonspecific protectionhave a large spectrumof action, that is possessa high specificity.

Thenonspecificforces of protection are sufficient for to combat the majority of pathogen agents.

Nonspecific reactions are at the basis of natural immunity and offer to organism the immunityeven against the pathogen agents which the organismdidn’t anteriorly met.

i s nonspecific immunity1

IS. Nonspecific immunity

These factors beingphylogeneticallyolder have a decisive role

In the protection of nevborns

until the maturation of specific immune mechanisms.

i s nonspecific immunity2

IS. Nonspecific immunity

Nonspecific protection

is ensured by the

physiologic barriers and

humoral nonspecific factors.

i s nonspecific immunity3

IS. Nonspecific immunity

In the physiologic barriers enter:

tegumentsand intact mucosae,


ciliary epithelium,

acid gastric medium,

Hematoencephalic barrier,

kidneys (which excretesome

microorganisms, especially viruses).

i s nonspecific immunity4

IS. Nonspecific immunity

Nonspecific humoral protection isensured by:


properdin, present inbloodand other BL,


complementsystem ,


The last two componentshave special statusbeing mechanismsof nonspecific and specific protectionin the same time.

i s nonspecific immunity5

IS. Nonspecific immunity

Lysozyme– a protein which possesses enzymatic qualities. It destroy the structure of mucopolysacharides of cellular bacterial membranes. It isvery active on Gramm “-” bacterias.

Secretory Ig A potentiates theaction oflysozyme. The most high level oflysozymeis in newborns, and further decreases gradually.

i s nonspecific immunity6

IS. Nonspecific immunity

Properdin – a plasmaticglobulin, whichactivatesalternatively the complement and togetherensure theelimination ofviruses and bacterias from organism.

The contain de properdin in children is low, at the 1-3 weeks its level rapidly increases and remains high during all childhood.

i s nonspecific immunity7

IS. Nonspecific immunity

Interferon – a protein with antiviral action, which is manifestingin the phase of de intracellular virus replication.

It can be synthesized by each cellofhumanorganism, but especially by leucocytes.

i s nonspecific immunity8

IS. Nonspecific immunity

Interferon also:

blocks themultiplication of chlamidias,

plasmodium malariae, ricketsies,

increases the organism cells resistanceto

the action of exo- and endo


stimulates thephagocytosis,

increases the cytotoxicity of lymphocytes,

blocks the cangerogenesis,

Influences the antibodies forming

(small doses – stimulates it, and

high doses – inhibates it).

i s nonspecific immunity9

IS. Nonspecific immunity

In newborns the capacityof interferon synthesisis low, increases gradually and achieves the maximum at the age of 12-16 years.

i s nonspecific immunity10

IS. Nonspecific immunity

The complement (C) – enzymaticsystem, formed from plasmatic globulins, the biologic role of al which is the cellular antigens lysis (viruses, virus infected cells, bacterias, mycoplasmas, protozoa, tumoral cells) fixedby Ab.

It includes 11complement fractionsand 3 inhibitors.

i s nonspecific immunity11

IS. Nonspecific immunity

All components of complement system circulatein blood under the form of precursorswhich can be activatedon 2 pathways:

classic or


The trigger of classic activation pathwayis the Ag-Ab complex.

In the absence of Ab the complement system can be activated through alternative pathway – properdinic.

i s nonspecific immunity12

IS. Nonspecific immunity

Phagocytosis – a processof capture anddigestionof Ag by tissular macrophages (monocytes) and circulant macrophages (neutrophilsand monocytes). The phagocytesare the first cells whichenter in contact with exo- or endogenous Ag.

i s nonspecific immunity13

IS. Nonspecific immunity

The immune protection isensuredby 2 specific mechanisms :

cellular and


whichare differing from one another by the mechanismsof

neutralization and

Ag elimination.

cellular immunity

Cellular immunity.

The immune response is ensured by

T-lymphocytes (thymodependent) and

B-lymphocytes (bursodependent).

The both cellular lines have a common predecessor –stem cell, whichmigratesfrombone marrowin thymus and in analog of Fabricius burse, when the differentiation and theirmaturation have place.

Thenthese cells populate the T şi B zones of LN. Here, at the first meeting with Ag their sensibilizationand ulterior differentiationinanother 2 subpopulations have place:

effector cells and

memory cells.

cellular immunity1

Cellular immunity

Effector cells – participate directly in the „liquidation” of antigenic aggressor. In the cell immunity there are cytotoxic T-lymphocytes (T-killer). They neutralize the antigen directlyorthroughsome special biologic active substances – lymphokines.

cellular immunity2

Cellular immunity

The memory cells are the lymphocyteswhichare transforming in the inactive form, but preserve the information about the Ag. These cells are going in again in the sanguine and lymphatic circulation and „patrol” the organism.

humoral immunity

Humoral immunity

The humoral immunity is ensured by


Initially theT-lymphocytes are stimulated,

And they will be transforming in T-helpers.

These through interleukinswill stimulating the transforming of B-lymphocytesin plasmocytes, which will synthesizethe specific antibodies.

So, the effector cells of humoral immunity are plasmocytes.

B-lymphocytesreceive also informationabout the nature of Ag and from macrophageswhichcaptivatethese antigensandremakethem primarly.

is specific immunity

IS. Specific immunity

In this way for good functioning of IS anharmoniouscollaboration between these three types of immunocompetent cells is necessary:

T-, B-lymphocytesand macrophages.

In the same time during antigenic stimulation the T-suppressors are forming. Theyblock T-helperis, in this wayblocking the Ab synthesisby B-lymphocytes.

This capacity of the organism is the basis of immunotolerance.

c y tokine s


There are the soluble molecules, synthesizedby a great varietyof cells, inclusively by lymphocytes, with the roleofhumoral messengers, which realize thecommunicationbetweendifferent cells, controlling theirgrowing, differentiation, maturation, division, metabolism, functions.

is specific immunity1

IS. Specific immunity

T- and B-lymphocytescan be foundfrom the age of 10-12 weeks of intrauterine development.

T-lymphocytesbecome functionally afterthe age of 14-15 weeks of intrauterine development.

The newbornshave a more number of

T- and B-lymphocytescomparatively with another age andadults, but these cells are notcompletelyfunctional.

is specific immunity2

IS. Specific immunity

B-lymphocytessynthesizemore classesof Ig: G, M, A, D, E.

In each antigenic aggressiona lot of Ig classes are synthesized

As a response to primary contactwith Ag the Ig M, after that IgG, ulterior IgA are synthesized.

At repeated contact with Ag the IgG from start is synthesized.

humoral immunity1

Humoral immunity

IgG constituies 70-80% from the totality of plasmatic Ig.

It is the self Ig which passes the placentar barrier, ensuringthe passive immunity of thenew-born.

Transmission of IgG from mother to fetus has place more actively in the last weeks of pregnancy, thus the level of IgG in premature babiesis less thanin term born baby.

humoral immunity2

Humoral immunity

During the time the level of maternal IgG in blood plasma of suckling babydecreases, and achieves the minimum at 6-9 months.

At the age of one year the intensity of proper IgG synthesis constitutes 50% from that of adult.

At 4-6 yearsthe level of IgG in children achievesthe IgG level at adult.

humoral immunity3

Humoral immunity

IgM constitutes 5-10% from total plasmatic Ig. They constitute the first lineof defensive taking partin the complement activationon classic pathway, agglutinationand opsonization of Ag, lysisofalien cells.

In plasma of newborns the level of IgM is low, but increases quickly, achievingthe adult level at the1-2 years age.

humoral immunity4

Humoral immunity

IgA constitute 10-15% from total plasmatic Ig.

They aresynthesizedby plasmocytes, whichare localizedat the level of mucosaand submucosa of digestivetube and respiratory pathways.

The most partof IgA remainsin the place of synthesis(secretory IgA), ensuring the local immunity.

Secretory IgA is finding in tears, saliva, nasal andbronchial secretions, secretions of digestive tube, colostrum.

The level of secretory IgA in children is low. It increases with age and achieves the most high level at 5 years.

humoral immunity5

Humoral immunity

Seric IgA in children is less active.

In usual newborn is absent. It appearsafter first week of life.

At 1 year age the IgA level constitutes 20% from that of adult, which is achieved onlyat 10-12 years age.

humoral immunity6

Humoral immunity

IgD and IgE are containing in în non significant quantities(each - 0,2%).

IgD is a globulin by embryonic type.

It is enable to activate the complement on alternative pathway, to neutralize someviruses.

humoral immunity7

Humoral immunity

IgE constitutesthe most part of reagines – antibodies responsibleby allergic reaction releasing.

They aresynthesizedasresponseto primary contact with Ag.

IgE are fixed on the mastocytes and basophils surface, realizingthereforethe state of sensibilization.

humoral immunity8

Humoral immunity

At the repeated contact with Ag the IgE provokesthe degranlationof these cellswith eliminationfrom them of different BAS, their biologic effect being at the basis ofpathological modifications in allergic reactions.

IgE is practicallyabsentin the plasma

Of newborns.

During the time their concentrationincreasesachievingthe adult level at 10-12 years age.

is specific immunity3

IS. Specific immunity

Therefore,the IS development is an ontogenetic process genetically programmed. The forming process is initiating intrauterine.

The most important stimulusthe IS receives after birth, when the exo- and endogenous antigenic aggression, determinedespecially by digestive tube, superior respiratorypathwaysand tegumentsmicrobial population by conditioned-pathogene microflora,increases considerably.

is specific immunity4

IS. Specific immunity

Immaturity of IS in children makes them

More sensible to intercurrent infections,

favour the generalizationof infectious processwith the development of septicemiaand septicopiemia,

favour themore severe evolution of infectious pathologies.

semeiology of is affections

Semeiology of IS affections

Three types of this system functions affection are possible:

Defect of one link of IS

(primaryand secondary immunodefficiencies)

Autoaggressionagainstthe normal structuresofhuman organism

(auoimmune diseasesanddiseases due to immunocomplexes)

Dysfunctionswhen some functions of IS areexagerratedin the detriment of another (lymphoproliferative syndromes)

semeiology of is affections1

Semeiology of IS affections

The states of immunodeficiency appear as a result of oneor more links of IS function abolition.

The states of immunodeficiency are:

primary (inborn) and

secondary (acquired).

semeiology of is affections2

Semeiology of IS affections

The states of primary immunodeficiencyaredetermined by:

primaryaffection of T-lymphocytes;

primary affectionof B-lymphocytes;

combined affection of T- and B-


the summary incidence of primary

immunodeficiencystatesis by 2:1000,

50-70% beingprimary defects of

B-lymphocytar system, and

5-10% of T-lymphocytar system.

suggestive signs for a primary im m unodeficien cy are

Suggestive signs for a primary immunodeficiencyare:

The child supports frequentlyinfectious

recurrent diseasesespecially of respiratory

pathways, digestive tube, reno-urinary

system, teguments, frequently complicated

with otitis, purulent sinusitis and septicemia.

They manifest unusualreactionsat banal

infections (ex. pneumoniaat varicella).

The sufferingis determined by unusual

causal agents (ex. Pneumocystus Carinii)

suggestive signs for a primary im m unodeficien cy are1

Suggestive signs for a primary immunodeficiencyare:

Presenceof some systemic reactions

after vaccination with live viral

attenuated vaccines or BCG

Bizarre hematologic deficit

(anemia, thrombocytopenia,


Disorder of digestion with the development of malabsorption syndrome.

secondary immunodeficiencies

Secondary immunodeficiencies

Secondary immunodeficiencies are determined by a lot of pathological states which lead to the involution of lymphoid tissue,lymphopenia,hipogammaglobulinemia.

They are the following:

pathologic states associatedwithlossof proteins:

nephrotic syndrome, combustions, exsudative enteropathy

dystrophias, avitaminoses

Viral(flu), bacterial (holera),

micotic (candidosis) infections, helminthiases

Massive surgical interventions and/or

postoperatoryyatrogeniccomplications (irradiation, imunosuppressives: GCS,CS)

Lymphoreticular tumors(lymphogranulomatosis,etc.)

semeiology of is affections3

Semeiology of IS affections

In childrenfirst 3 yrs of lifethe state of immunodeficiencycan be determined by

thymomegaly, which is induced by hypothalamo–hypophysar-suprarenalaxe affection.

In stress situations an rapid accidental involutionof thymus can be developing, inwhich a massivereleasing of T-lymphocytesin blood has place, their massive death inthymus with their phagocytosis by macrophages has place .

Transitory deficit of humoral immunityis characteristic forfirst year age children,

between 6 – 9 months.

semeiology of is affection

Semeiology of IS affection

Primary affection ofnonspecific factorsof protection includes

disorders in Complement System

disorder of phagocytosis.

semeiology of is affection1

Semeiology of IS affection

The genetic deficit can involve each component of Complement System, which shell alter their cascade activation.

It is clinically manifesting throughdecreased resistance at bacterial infections (C1, C2, C3, C5), increasedincidence of hipersensibilitydiseases (C1, C2, C4). Deficit of C1leads to developmentof angioneurotic recurrent edema.

semeiology of is affection2

Semeiology of IS affection

Patients with disorderedphagocytosis support frequent infections causedby microorganismsusuallynon pathogene.

In chronic granulomatosis (syndrome of paradoxes) the patients are resistant toinfectionswith high virulence microorganiss (streptococci, meningococci, pneumococci), but are sensibletoconditioned pathogene microorganisms (Escherihia coli, staphylococci).

semeiology of is affection3

Semeiology of IS affection

A global affection of all components ofImmune System

And of humoral nonspecific iactors

Is characteristic for


critical periods in the immune system development

Critical periods in the Immune System development

Tere are a periods, when the organism immunesystem in growing and development

Generates paradoxal orunadequate responsesto antigenic stimuli.

I-st critical period – first month of life.

II-ndcritical period – from 3 to 6 month of life.

III-rdcritical period – second year of life.

IV-thcritical period – from 4 to 6 yrs of life.

V-thcritical period – period of adolescence.

critical periods in the immune system development1

Critical periods in the Immune System development

First critical period–

first month of life.

A decreased activity of phagocytes

is observing.

Lymphocytesare capable toreact

at antigenic stimuli and mitogenic


Humoral immunity is ensured by

maternal IgG.

critical periods in the immune system development2

Critical periods in the Immune System development

The second critical period–

from 3 to 6 months of life.

Maternal antibodies disappear fromchild’s plasma,

the proper IgM is synthesizing as a response to antigenic stimuli.

Deficit of IgA predisposesto frequent

infectionsof respiratory pathways (viral).

Immunocompetent cellshave a diminished activity.

In this period the primary immunodeficiences are manifesting.

critical periods in the immune system development3

Critical periods in the Immune System development

The third critical period–

the second year of life.

Immune system is completely functional.

The capacityof IgG synthesis increases,

but the mechanisms of local protection

remain insufficient developed.

Thismaintainsa high receptivity of the

child’s organism to different

pathogene agents.

critical periods in the immune system development4

Critical periods in the Immune System development

The fourth critical period–

from 4 to 6 years of life.

The antibodies synthesis, excepting IgA,

achieves the level of adult.

Concomitantlythe titre of IgE increases.

The activityof local protection factors

remains diminished.

In this age the tardive congenital immune defficiencies are clinically manifesting.

critical periods in the immune system development5

Critical periods in the Immune System development

The fifth critical period–

the period of adolescence.

The gonadian hormones secreted in this

period inhibate the immune reactions.

As a result the autoimmune andlymphoproliferativepathologies can develop.

The increased receptivity

to diverse micobial agents is observing.