Immune system - Specifics of children's immunity

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Immune system - Specifics of children's immunity




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Presentations text content in Immune system - Specifics of children's immunity

Slide1

Immune system - Specifics of children's immunity

Oral immunity and

immunopathological

processes in the mouth

Slide2

 Immunity

Microorganisms are in the air we breathe and in/on the food we eat;

Thus our epithelial surfaces are continuously exposed to microorganisms;

Disease occurs when microorganisms invade epithelial surfaces;

However, we have a long infection-free periods and that infections are the exception rather than the rule;

This resistance (immunity) of epithelial surfaces to invasion, is a characteristic which is present from birth, and is therefore called

innate (natural) immunity

.

Slide3

Immunity

A complex of physiological processes whose function is to store the constancy of the internal environment of the body;

Protects the body from all foreign endogenous and exogenous factors.

Slide4

Innate Immunity

This prevents entry of microorganisms into tissues or, once they have gained entry, eliminates them prior to the occurrence of disease.

Slide5

Characteristics

Present from birth;

Non-specific - acts on many organisms and does not show specificity;

Does not become more efficient on subsequent exposure to same organisms.

Slide6

Prevention of entry of organisms

Mechanical barriers at body surfaces, skin, mucous membranes - disruption leads to infection;

Antibacterial substances in secretions,

lysozyme

,

lactoferrin

, low pH of stomach contents.

Slide7

The immune system is composed of two main categories:

Nonspecific immunity - provides general protection;

First line of defense;

Second line of defense;

Specific immunity - the body recognizes specific pathogens;

Third line of defense.

Slide8

Nonspecific immunity

First line of defense:

mechanical barriers;

Skin;

Mucosa;

Chemical barriers:

Saliva:

Enzymes;

Secretory

immunity.

Slide9

Second line of defense

Nonspecific inflammation;

Phagocytosis

:

Neutrophils

;

Macrophages;

Histiocytes

;

Natural "killer" cells:

Kill tumor cells;

Kill infected cells.

Slide10

Nonspecific protective factors

Tissue factors;

Cellular factors;

Humoral

– mediators.

Slide11

Tissue factors

Skin;

Mucosa;

In the mouth - continuous oral mucosa.

Slide12

Cellular factors

Act after overcoming tissue barrier;

Vascular cell phenomenon – inflammation;

Sensitized cells;

From the stem cells of the bone marrow;

Hematopoietic -

neoplastic

cells;

Cells of specific immunity.

Slide13

Protection`s cells

Macrophages;Microphages;PMNs;Three cell populations;Mature cells:Neutrophils;Eosinophils;Basophils;Mast cells;Platelets;Killer cells.

The light micrograph

shows the

multilobed

nucleus, because of which these cells are also called

polymorphonuclear

leukocytes, and the faint

cytoplasmic

granules. 

Slide14

Macrophages

Mononuclear phagocytes;

Derived from

monocytes

;

They are:

Histiocytes

;

Fixed macrophages (in the lymph nodes and spleen);

Osteoclasts

;

Kupffer

cells;

Microglial

cells;

Langerhans

cells.

Slide15

Characteristics of the macrophages

They have receptors for:

Immunoglobulins

;

Complement;

Antigens;

Lymphokines

;

Cause "oxidative burst“:

Released superoxide anion;

It turns into H

2

O

2;

Kill pathogenic factor;

Digest it

intracellularly

.

Slide16

The next steps are:

They transfer antigens to lymphocytes;

lymphocytes are sensitized;

Induce a specific immune response;

Separate bioactive substances;

Regulate the immune response.

Slide17

Microphages (granulocyte) - PMNs

Neutrophils:Involved in inflammation;Separate membrane oxidases;Include object within the cell;Forming phagosomes;Eosinophils:Regulate allergic reactions:Interleukins;Interferons;Cytokines;Growth factors.

Basophils

Anaphylactic

degranulation

;

Mediated by

IgE

antibodies;

Receptors binding;

Exocytosis

.

Slide18

Mast cells

Involved in non-specific inflammation;

In allergic reactions of immediate-type;

In

degranulation

;

Released histamine:

Serotonin;

Heparin;

Bradykinin

;

Hyaluronic

acid.

Slide19

Platelets

They are nuclear-free

cytoplasmic

fragments;

They are derived from bone marrow

megakaryocytes

;

They have haemostatic function;

Involved in coagulation.

Slide20

Killer cells

They represent a third population lymphocytes;

They are located in the circulating blood;

They have a

cytotoxic

effect;

Participate in the second line of defense.

Slide21

Mediators of inflammatory response

Bioactive substances:

From the plasma;

From different cells;

Their production is stimulated by:

Microorganisms;

Own proteins;

Slide22

Mediators effect of the inflammatory response

By binding to the receptors;

By target cells;

Direct enzyme activity;

Or oxidative degradation;

Slide23

The mediators of the the inflammatory response are:

Vasoactive

amines;

Plasma proteins;

Interferons

.

Slide24

Vasoactive amines

Histamine:

Released from mast cells;

Influences:

Smooth muscle fibers;

Small blood vessels;

Inflammatory action:

Inhibits

lysosomal

enzyme;

Inhibits

chemotaxis

.

Slide25

Serotonin

Synthesized in nerve endings;

Shortens the smooth muscle fibers;

Dilates blood vessels;

Increased permeability.

Slide26

Plasma proteins

Complement system;

It consists of 20 serum proteins;

They react with the cascade of reactions;

The enzyme catalyzes the reaction of a following:

They are involved in specific

and nonspecific protection.

Slide27

Kinin system

Plasma proteins of the beginning of the reaction;

Bradykinin

:

Increases vascular permeability;

Causes contraction of smooth muscle fibers;

Follows vascular dilatation;

Causes a pain.

Slide28

Coagulation system

Activated by various substances in the tissue destruction;

Stops the movement of microorganisms;

Makes them available for

phagocytosis

;

Stops bleeding;

Decreased

neutrophil

chemotaxis

;

Reduces permeability.

Slide29

Other mediators - interferons

They are low molecular weight proteins:

Leukocytes -

α-

interferon;

Fibroblasts -

β-

interferon;

Lymphocytes - immune interferon;

Their action is to block:

Replication of the viral RNA;

The reproduction of the tumor cells;

Regulate the immune system.

Slide30

Arachidonic acid

lipid mediator;

Formed quickly;

Acts locally;

It produces:

Prostaglandins;

Leukotrienes

;

Hypoxines

.

Slide31

Nonspecific defense mechanisms

Inflammation

Slide32

Inflammatory reaction

Major defense mechanism;

Is a sequence of vascular and cellular reactions;

They provide counteraction of the pathogens;

The basic phenomenon of the inflammation is

phagocytosis

.

Slide33

Types of inflammation

Nonspecific inflammatory response:

Before the formation of antibody;

Specific inflammatory reaction:

At the second meeting with the pathogen antigens;

Or at a later stage of the initial meeting;

Sensitization occurs of the

immunocompetent

cells;

It include specific immune responses.

Slide34

The process of the inflammation

Starting with local hypoxia;

Starting release of the

vasoactive

substances;

Separated the histamine, serotonin, prostaglandins,

kinins

;

They cause

vasodilation

;

This leads to congestive hyperemia;

Follows hypoxia;

The next result is acidosis;

Began massive migration of the microphages and macrophages;

Performed

phagocytosis

.

Slide35

Phagocytosis is mediated by macrophages and polymorphonuclear leucocytes

Phagocytosis

involves the ingestion and digestion of the following:

Microorganisms;

Insoluble particles;

Damaged or dead host cells;

Cell debris;

Activated clotting factors.

Slide36

1.Phagocytosis - ingestion and killing of microorganisms by specialised cells (phagocytes)

Phagocytes -

polymorphonuclear

leukocytes (

neutrophils

);

Mononuclear phagocytes (

monocytes

, macrophages);

2.

Opsonisation

- the process of coating micro-organisms with some of the proteins found in plasma, to make them more easily

phagocytosable

.

Slide37

INFLAMMATORY RESPONSE -INFLAMMATION

Complement and phagocytes exist mainly in blood so a mechanism is required to recruit these elements to the site of tissue invasion.

Slide38

Inflammation involves:

a) opening up of junctions between endothelial cells in post-capillary

venule

to allow plasma proteins to escape;

b) adhesion of leukocytes to endothelial cells of post-capillary

venule

, followed by emigration of phagocytes into tissues.

Inflammation is

localised

to area of infection or tissue injury by release of substances from micro-organisms or chemicals (chemical mediators) released from cells in tissues, e.g. histamine from 

MAST CELLS

. Once organisms destroyed inflammation settles down (

RESOLVES

).

Slide39

There are several stages of phagocytosis:

1.

Chemotaxis

;

2. Adherence;

3. Pseudopodium formation;

4.

Phagosome

formation;

5.

Phago-lysosome

formation.

Slide40

1. Chemotaxis

This is the movement of cells up a gradient of

chemotactic

factors;

It may be directly induced by a substance, produced as a result of complement activation;

It can also be indirectly induced as a consequence of release of preformed mediators within mast cells by the action of

eosinophil

chemotactic

factor, or

neutrophil

chemotactic

factor;

Leukotrienes

, produced by the metabolism of mast cell

arachidonic

acid, are also

chemotactic

.

Slide41

2. Adherence

This works reasonably well for whole bacteria or viruses, but less so for proteins or encapsulated bacteria;

In order to deal more effectively with encapsulated bacteria, antibodies directed against the capsule enable the

phagocytic

cells to ingest the organisms, using their

Fc

receptors.

Slide42

Adhesion

Performed by serum

opsonins

;

Some objects have receptors for antibodies and complement;

Their presence facilitates adhesion.

Slide43

3. Pseudopodium formation

This is the protrusion of membranes to flow round the "prey".

Slide44

4. Phagosome formation

Fusion of the 

pseudopodium

 with a membrane enclosing the "prey" leads to the formation of a structure termed a 

phagosome

.

Slide45

5. Phago-lysosome formation

The

phagosome

moves deeper into the cell, and fuses with a 

lysosome

, forming a

phago

-

lysosome

;

These contain hydrogen peroxide, active oxygen species (free radicals),

peroxidase

,

lysozyme

and hydrolytic enzymes;

This is known as the 

oxidative burst

, and leads to digestion of the

phagolysosomal

contents, after which they are eliminated by

exocytosis

;

Some peptides however, undergo a very important separate process at this stage;

Instead of being eliminated, they attach to a host molecule and end up being expressed on the surface of the cell within a groove on the molecule (antigen presentation).

Slide46

The speed of phagocytosis can be increased markedly by bringing into action two attachment devices present on the surface of phagocytic cells:

Fc

receptor:

 which binds the

Fc

portion of antibody molecules, chiefly

IgG

. The

IgG

will have attached the organism via its

Fab

site.

Complement receptor:

 the third component of complement (C3) also binds to organisms and then attaches to the complement receptor.

This coating of the organisms by molecules that speed up

phagocytosis

, is termed 

'

opsonization

'

, and the

Fc

portion of antibody, and C3 are termed 

'

opsonins

'

.

Slide47

Absorption

Invagination

of the cell wall;

Coverage of the site;

Formation of

phagosomes

;

Fusion with the

lysosome

;

Phagolysosome

formation;

Follows

hexose-monophosphate

cycle;

Release of superoxide anion;

Superoxide explosion;

Acidosis.

Slide48

Digestion - enzymatic digestion

Phagocytosis

graduated with digestion;

At incomplete

phagocytosis

part of the pathogenic properties of the particles are retaining;

Microphages digest them completely;

Macrophages digest them partially.

Slide49

Specific immunity - the third line of defense

Specific immune responses after primary inflammation - acquired immunity

Slide50

Acquired Immunity (adaptive Immunity/specific Immunity)

This type of immunity occurs in response to infection called 

ADAPTIVE

 as the immune system must adapt itself to previously unseen molecules;

Following recovery from certain infections with a particular microorganism, individuals will never again develop infection with the same organism, but can become infected with other microorganisms;

This form of protection is called 

IMMUNITY

 and an individual is said to be 

IMMUNISED

 against that organism;

The induction of immunity by infection or with a vaccine is called 

ACTIVE IMMUNITY

.

Slide51

PASSIVE IMMUNITY

Historically it has been shown that a non-immune individual can be made immune by transferring serum or lymphocytes from an immune individual - 

PASSIVE IMMUNITY

 ;

In passive immunity are involved:

Serum constituents (antibodies);

Lymphocytes.

Slide52

Immune system responds to microorganisms but not to its own cells and that the system knows that the body has been infected previously with a particular organism

This implies:

IMMUNOLOGICAL RECOGNITION;

SELF/NON-SELF DISCRIMINATION;

IMMUNOLOGICAL SPECIFICITY;

IMMUNOLOGICAL MEMORY.

Slide53

Immunity is mediated by the IMMUNE SYSTEM, which responds to infection by mounting an IMMUNE RESPONSE

An immune response must:

RECOGNISE a microorganism as foreign (non-self) as distinct from self (

AFFERENT LIMB

);

RESPOND to a micro-organism by production of specific antibodies and specific lymphocytes;

MEDIATE the elimination of micro-organisms (

EFFERENT LIMB

).

Slide54

IMMUNOGEN and ANTIGEN

An agent which evokes an immune response is called an 

IMMUNOGEN

.

The term 

ANTIGEN

 is applied to a substance which reacts with antibody.

Slide55

Cellular Basis Of Immune Response

Key cells are lymphocytes - have capacity to

recognise

microorganisms;

There are two types which develop in bone marrow from a common precursor:

T-cells

 - mature in thymus;

B-cells

 - mature in bone marrow;

These two types of lymphocyte are used in 3 ways to fight infection.

Slide56

Strategy One: elimination of extracellular microorganisms

In response to infection B-cells mature into PLASMA cells which secrete soluble recognition molecules (ANTIBODIES);

B-cells

recognise

microbes because they express membrane bound antibody which acts as an antigen receptor;

At time of first infection there is no antibody in blood and level does not begin to increase until between 7-10 days afterwards;

The level of antibody rises slowly to a low peak and then gradually declines towards baseline - 

PRIMARY RESPONSE

.

Slide57

SECONDARY RESPONSE

On subsequent exposure to same micro-organisms the level of antibody begins to increase within 24 hours and reaches a high level which is sustained.

Slide58

 Epitope or Antigenic determinant

Antibody

recognises

structures on surface of bacteria - proteins, carbohydrates, lipids;

When we have an infection we produce antibodies which

recognise

many different types of structure on bacterial surface;

Thus serum from an immune individual contains many different types of antibodies each of which

recognise

different structures on surface of membrane;

Each of these structures is called an 

epitope

or 

antigenic determinant.

Slide59

 Effector  mechanisms

Antibody is soluble and diffuses through tissues to target extracellular microorganisms;

Binding of antibody to microorganisms activate two 

effector

 mechanisms to eliminate micro-organisms;

Activation of complement system - bacterial

lysis

or

opsonisation

;

Phagocytosis

 by

neutrophils

and macrophages with intracellular killing.

Slide60

Strategy Two: Elimination of micro-organisms which normally survive for long periods in macrophages

Even when antibody and complement

opsonise

certain bacteria and

phagocytosis

occurs, they are not killed but survive and multiply in macrophages (e.g. Mycobacterium tuberculosis);

Elimination occurs by use of a subpopulation of cells called 

Helper T-cells;

These cells

recognise

macrophages containing intracellular bacteria by means of T-cells antigen receptor, which is not an antibody;

They help macrophages to kill bacteria by

synthesising

soluble molecules (

cytokines)

which stimulate bacterial killing mechanisms of macrophages.

Slide61

Strategy Three - Elimination of microorganisms which infect cells without an endogenous antimicrobial defence system

Viruses are obligate intracellular pathogens, can infect any type of cells, and most cells do not possess antimicrobial mechanisms;

During intracellular replication virus proteins appear on the surface of the infected cell;

A second subset of T-cells -

cytotoxic

T-cells

-

recognises

these viruses (foreign) antigens and secretes

cytotoxic

molecules which kill the infected cells.

Slide62

Acquired immunity is characterized by:

Specificity:

Immune responses are specific to each agent acting as an antigen;

Memory:

At repeated meeting with antigen the body recognizes it;

It acts to store their information.

Slide63

Specific immune responses

Humoral immune

responses

:

Cellular immune

responses

.

Slide64

Specific protective factors

Antigens;

Antibodies;

Immune cells:

T-lymphocytes;

B-lymphocytes;

Mediators.

Slide65

Antigens

All substances carrying foreign genetic information and which are inducing a specific immune response.

Slide66

Types of antigens

According to the effect:

Strong;

Weak;

Haptens

– They do not form antibodies, but is connected to them;

According to its specificity:

Heteroantigens

- of a different kind;

Antigens of the same type but of another individual;

Autoantigens

- These antigens should, under normal conditions, not be the target of the immune system, but, due to mainly genetic and environmental factors, the normal immunological tolerance for such an antigen has been lost in autoimmune disease.

Slide67

Characteristics of the antigens

Extrinsic

- other than those of the host;

Antigenicity

- develop antibodies;

Immunogenicity - create immunity;

Specificity - sets of sites in a protein chain called antigenic determinants;

High molecular weight proteins;

Soluble and absorbable colloidal

Slide68

Antigen-Antibody Interaction

The specific association of antigens and antibodies is dependent on hydrogen bonds, hydrophobic interactions, electrostatic forces, and van der Waals forces

Slide69

Slide70

Adjuvants

Substances that enhance the immunogenicity;

They are in a dental plaque.

Slide71

Antibodies

Proteins to different

immunoglobulins

;

Are formed at the entry of the antigen;

They are constructed from a sensitized plasma cells;

Types:

IgM

;

IgA

;

IgG

;

IgD

;

IgE

;

IgA

-S

Slide72

Slide73

Antibodies according to the type of reaction

Precipitins;

Agglutinins;

Antitoxins;

Lysines

;

Autoantibodies

;

Blocking

monovalent

antibodies.

Slide74

immunoglobulins

Proteins with a common structure and activity of antibodies.

Slide75

Construction of the immunoglobulin molecule

1 – light chains; 2 – heavy chains; 3 – constant region; 4 – changing area -Binding antigen.

2

1

1

3

4

Slide76

Immunoglobulin G - dimmer

Represents 75-80% of all

Immunoglobulins

;

Synthesized in

utero

;

Cross the placental barrier;

Activates complement;

Causes:

Agglutination;

Precipitation;

Neutralization;

Opsonization

.

Slide77

Immunoglobulin A - monomer

10-15% of the total immunoglobulin;

Do not synthesized in

utero

;

Do not cross the placenta;

 Activates complement by alternative pathway;

  There are anti-adhesive and

opsonized

effect;

  Increases in chronic inflammation.

Slide78

Immunoglobulin A - S (secretory)

Dimer

possessing a fragment of

secretory

component and connecting chain;

In the mouth is secreted from the salivary glands;

Participated in the first line of defense of the enamel and lining mucosa;

The main factor of local immunity.

Slide79

immunoglobulin M

Represents 6-9% of the total

immunoglobulins

;

Represents a

pentamer

with ten active centers;

When sensitization it occurs a first;

Its synthesis begins in early childhood or first meeting with antigens.

Slide80

immunoglobulin D

Receptor

immunoglobulins

of the mature beta-lymphocytes.

Slide81

immunoglobulin E

Antibodies of the allergic reactions;

In the blood they are in low concentrations;

Adsorbed to the surface of:

mast cells

basophil

leukocytes

Platelets

Cause hypersensitivity

Slide82

Action of the antibodies

Adsorption to microbial surface;

Prevent its adhesion;

Opsonized

bacterial cells;

Receptor binding between

phagocytic

cell and the particular antibody fragment;

Agglutinate microorganisms;

Precipitate molecular antigens;

Defense and neutralize cell;

Make them available to complement;

Neutralize viruses;

Cause hypersensitivity;

Protective or pathological inflammation.

Slide83

Cytokines - common name of a group of proteins

Small protein molecules;

Mediators and regulators of:

Immunity;

Inflammation;

Hematopoiesis

;

They are produced in at immune stimulus.

Slide84

Types of cytokines

Lymphokines

- by lymphocytes;

Monokines

- from the

monocytes

;

Chemokines

– with

chemotaxis

activity;

Interleukins - from one leukocyte and acting on other;

Interferons

.

Slide85

Cytokines, due to the action

Antiinflammatory

- activate macrophages and cellular immune response;

IL 1

IL 6

TNF

Antiinflammatory

- suppress cellular immune responses and stimulate antibody-dependent immunity

IL 4

IL 5

IL 10

IL 13

Slide86

Specific immunity cells - lymphocytes

Immunocompetent

cells;

Start development in:

Bone marrow;

Thymus;

lymph nodes;

Spleen.

Slide87

There are two classes lymphocytes

B-lymphocytes

Produce antibodies;

They attack the antigens;

Perform antibody-dependent immunity;

T-lymphocytes

Directly attack pathogens;

Mediate cell dependent immunity.

Slide88

B lymphocytes and humoral immunity

First stage of development

Precursors of the B-lymphocytes the first months after birth;

Second stage

After antigenic stimulation;

Development of sensitized B-lymphocytes in the spleen and lymph nodes;

They form

clonal

cell lines;

Produce antibodies;

Connect with antigens;

Antigen-antibody reaction.

Slide89

Humoral immune responses - with the participation of antibodies

Formed antigen-antibody complexes are more vulnerable to

phagocytosis

;

Nutralization

;

Precipitation;

Agglutination + complement;

Improving

imunoadhezion

;

Cytolysis;

Release of mediators;

Stimulation of immune responses.

Slide90

T-cell and cell-dependent immunity

T-lymphocytes

mediate

cell

immune

responses

Slide91

Development of T-lymphocytes

First stage:Development of precursor T- cells (thymocytes);Derived from the bone marrow;Differentiate in the thymus;

Second stage:

By the blood;

To T-dependent areas;

In lymph nodes and spleen;

Antigen by macrophages;

Activated surface receptors;

Repeated divisions of T-lymphocytes;

A branch of the T-lymphocytes to antibody;

Connect with them;

Release

lymphokines

.

Slide92

Types T-lymphocytes

Tk

- killer cells:

Released

lymphotoxins

;

Kill the target cell;

Th

- helper cells:

Regulate the function of B-lymphocytes;

Ts - suppressor cells:

Inhibit the differentiation of plasma cells to B-lymphocytes;

Tm - memory cells were performed immunological memory.

Slide93

Cellular immune responses

Direct cytolysis;

Release of mediators;

TM creates immunological memory;

This Immunity is against:

Bacteria;

Fungi;

Protozoa;

The invasion tissues;

Malignant cells.

Slide94

Immune tolerance

Tolerance to the resident

microflora

;

In the mouth - "adaptive immunity" or "immune tolerance“;

Regulatory system and integrated processes for maintaining immune homeostasis.

Slide95

Development of the immune system in childhood

Slide96

Intrauterine development

Passive immunity from mother

+

Developing own

immunoreactivity

=

Protection of the fetus from congenital infections

Slide97

Newborn

Rejected zero immunity;

Presence of the

phagocytic

activity of:

Complement;

Interferon;

Other factors of nonspecific immunity;

Congenital and acquired infections occur:

Undifferentiated clinic;

Tendency to generalization.

Slide98

Maternal antibodies

From the second month of the infant began to decline;

Within six months disappear;

When breast-fed infants are retained longer.

Slide99

Oral immunity of the newborn

Oral mucosa adapts as a barrier;

Supported by the emergence of

immunoregulatory

network;

Depend on microbial colonization;

Of food allergens;

Breastfeeding is the best way to shape the immune phenotype.

Slide100

Breastmilk

Contains immune cells;

Cytokines;

Growth factors;

Immunoglobulin A;

Provides early postnatal development of the

secretory

imunity

.

Slide101

Secretory IgA till 8 months is obtained from the mother - secretion begins thereafter

Modeling;

Inhibits:

Surface colonization of microorganisms;

Prevents penetration of harmful factors;

Neonatal period is critical for infections and allergies.

Slide102

Between the ages of 3 and 6 months

Immune reactions are more subdued;

More difficult recovery from infections;

Low productivity of lymphoid tissue;

Homeostasis is easily broken by:

Malnutrition;

Antibiotics.

Slide103

Between the ages of 6 and 12 months

The child is creeping;

He is started walking;

In contact with the environment;

First viral infections:

respiratory;

Retavirusi

;

bowel;

Herpes;

Measles;

Chickenpox;

Rubella;

Disease is more severe.

Slide104

Aged 1 to 3 years

Close contact with adults;

Child is exposed to a variety of infections;

Cross-bacterial viral,

mycoplasma

, viral and infectious:

Immunological reactivity is better - organ development on immune

Serum reactions are weak

The antibody concentration is low

In the re-encounter with antigen antibody titer increases.

Slide105

After three years

Viral infections occur more easily;

Often subclinical and asymptomatic;

In school and adolescence incidence is close to that in adults.

Slide106

immunopathological reactions

Protection and adaptation of body

Slide107

Types of immunopathological reactions

Allergic;

Autoimmune;

Immunodeficiencies

.

Slide108

Allergic reactions

Upon re-entry of the antigen immune system responds in three ways:

A protective immune response;

With increased sensitivity - an allergic reaction;

No reaction –

anergy

.

Slide109

Allergic reactions can be four types

An antigen that causes an allergic

response is called

an

allergens

Slide110

First type - allergic immediate reactions

Hypersensitivity by

humoral

type;

Called anaphylactic or atopic;

Rapid immune response involving

IgE

;

It binds to mast cells;

Exempt mediators.

Slide111

The second type - the cytotoxic response

Humoral

-mediated;

Immediate-type;

Toxic effects on cells;

Cytolysis involving

IgM

,

IgD

and complement;

Target cells are erythrocytes, leukocytes and platelets.

Slide112

Third type - the antigen-antibody reaction

Immediate reactions;

Toxic effect of antigen-antibody complex.

Slide113

Fourth type - cell-mediated delayed reactions

Similar to cellular immune reactions;

Affects allergy;

Bacteria;

Viruses;

Fungi.

Slide114

Autoimmune reactions

The immune system is tolerant to its own tissues and antigens;

Breach of this tolerance;

Autoimmune reactions;

The body produces antibodies against its own cells and antigens.

Slide115

Adaptive immunity in the mouth may be impaired

Commensal

microorganisms have similar antigens;

They bind to the molecules of

macroorganism

;

Macroorganism

did

not perceive them now as foreign;

Or develop cross-immune response;

The body perceives its own cells as foreign.

Slide116

Common autoimmune diseases

Manifestation in the oral mucosa;

Dermato

Bullous

:

Pemphigus

;

lupus

erythematodes

;

Epidermolysis

bullosa

.

Slide117

Immunodeficiency states

Deficits in the

humoral

immunity or in the cellular immunity;

Susceptibility to infections.

Slide118

Congenital immunodeficiency conditions

Heritage, most often recessive;

Rare syndromes;

Appear in childhood;

Patients do not survive long;

Infections are fatal;

Affect the oral mucosa,

gingiva

and

periodontium

.

Slide119

Acquired immunodeficiency conditions

Malnutrition;

Viruses and bacteria;

Radiotherapy;

Prolonged

cytostatics

treatment ;

Corticosteroids and antibiotics.

Slide120

Oral immunity - defense mechanisms

A combination of local and systemic immune responses and mechanisms;

The basic function – protecting;

Preventing the entry of foreign antigens;

Tolerance to the resident

microflora

;

Food.

Slide121

Protective mechanisms of the oral mucosa - the first line of defense

Barrier;

Physiological exfoliation;

The degree of

keratinization

- nonspecific mechanism;

Protection, regardless of age;

Masticatory

act;

Washout effect of saliva;

Mucin

and

secretory

immunoglobulin A.

Slide122

Protective role of oral lymphoid tissue

Oral immune response is carried out by:

Intraoral lymphoid formations:

Palatal tonsils;

Lingual;

Pharyngeal;

Submucosal

lymphoid aggregations:

soft palate;

Floor of the mouth;

Tongue;

Cheeks;

Lips;

Extraoral

lymph nodes.

Slide123

Protective role of saliva

Mechanical action;

Salivary enzymes;

Leukocytes;

Buffer systems:

Bicarbonate;

Phosphate;

Protein;

Secretory

immunity.

Slide124

Protective role of gingival fluid

Transudate

of gingival capillary network

Dependent is:

The composition of the blood serum;

Permeability of the gingival epithelium;

Permanent presence of:

PMNL;

Phagocytic

cells;

Monocytes

.

Slide125

Slide126


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