21. Immune mechanisms of inflammation (local and systemic PowerPoint Presentation, PPT - DocSlides

21. Immune mechanisms of inflammation (local and systemic PowerPoint Presentation, PPT - DocSlides

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22. Physiological mechanisms of regulation of the immune system. Cytokines (classification according to the function).. 23. Defence against extracellular pathogens .. 24. Defence against intracellular .. ID: 312824

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Presentations text content in 21. Immune mechanisms of inflammation (local and systemic

Slide1

21. Immune mechanisms of inflammation (local and systemic reaction).

22. Physiological mechanisms of regulation of the immune system. Cytokines (classification according to the function).

23. Defence against extracellular pathogens .

24. Defence against intracellular .

25. Anti-viral defence.

26. Defence against multicellular parasites.

27. Tumour immunology - tumour antigens, mechanisms of defence.

28. Alloimmune reaction. Types of transplantations and immunological examination before transplantation. Immunologically privileged tissues.

29. Types of graft rejection and their mechanisms. GvH. Principle of materno-foetal tolerance. Rh incompatibility

Slide2

Inflammation

Slide3

Inflammation

Is

a

physiological

response

to

breach

integrity

of

the

organism

,

leading

to

localization

of

damage

,

protection

against

infection

of

damaged

sites

and

healing

.

Slide4

Causes of inflammation

Physical

injury

Infection

by

pathogens

Damage

caused

by

chemicals

Cancer

Alergic

disease

Autoimmune

disease

Slide5

Inflammation

Inflammation acute (physiological reactions, damaged tissue heals completely) chronic (usually pathological reactions, destruction of tissue and compensation with fibrous tissue) Response of the organism local systemic

Slide6

Local body's response to inflammation Signs - pain (dolor), heat (calor), redness (rubor), swelling (tumor)

Slide7

Local inflammation

The first signals for the development of inflammatory reactions originate from activated

phagocytes

,

mast cells

,

complement

a

nd substances released from

damaged cells

and extracellular matrix components.

Slide8

Local inflammation

vasodilation

and

increased vascular permeability

(histamine, serotonin, bradykinin, complement components C3a, C5a, leukotrienes, prostaglandins) =>

redness

and

swelling

increased expression of adhesion molecules

on endothelial cells (TNF, IL-1) => capture leukocytes and phagocytes

influence nociceptors

(prostaglandins, ...) =>

pain

Increase temperature

(IL- 1, IL-6, TNF, prostaglandins)

Slide9

Local inflammation

Slide10

Systemic inflammation

leukocytosis

fever

(TNF

a

, IL-1, IL-6, IFN

)

↑ tissue metabolism

↑ mobility of leukocytes

↑ IFN, cytokines and Ig production

↑ expression of Hsp

acute phase proteins

(IL-6, TNF, IL-1)

Slide11

Acute phase proteins

produced by hepatocytes:

CRP

- opsonization, complement activation

SAP

- opsonization, complement activation

SAA

- attracting leukocytes

C3

,

C4

protease inhibitors - protection against secondary tissue damage

serum transport proteins

Slide12

Septic shock - the massive penetration of microorganisms into the bloodstream (  TNF) Anaphylactic shock - basophil degranulation after contact with allergen (histamin)

Systemic inflammation

Slide13

Repair of damaged tissue

after the elimination of pathogens and damaged cells by phagocytes

activation of angiogenesis

regeneration and tissue remodeling (

fibroblasts, smooth muscle cells, keratinocytes, epithelial cells

)

regulated by cytokines: PDGF, TGF

b

(

platelets, macrophages ...

)

Slide14

Physiological regulation

of the immune system

Slide15

Physiological regulation of the immune system

Regulation by antigen

Regulation by antibodies

Regulation by cytokines and cellular contact

Suppression mediated by T cells

Other factors influencing the outcome of the immune response

Regulation by cytokines

Slide16

Regulation by antigen

Immune responses induction and extinction

Affinity maturation of B lymphocytes

Maintaining immunological memory

Antigenic competition

Threshold density of the complex MHC II-gp Ag on APC

Slide17

Regulation by antibodies

Antibodies competes with the BCR for antigen (negative regulator of B lymphocyte stimulating)

IgG immune complexes bind to the BCR and Fc

g

R on

B cells, resulting in blocking of B cell activation

Regulation via idiotypic network

Slide18

Regulation by cytokines and cellular contact

Interaction APC - T lymphocyte

Interaction T

H

1 – macrophages

Interaction T

H

2 - B lymphocytes

Mutual regulation of activity T

H

1 versus T

H

2

Development of leukocyte subpopulations

Negative regulation of effector cells:

CTLA-4 - T cell inhibitory receptor, binds ligands CD80 and CD86

Inhibitory receptors of NK cells

Self-destruction interaction of the apoptotic receptor Fas with ligand FasL on the surface of activated T lymphocytes

Slide19

Suppression mediated by T cells

Mutual negative interactions mediated by Th1 and Th2 cytokines (

Th2 cells produce IL-4 and IL-10 which suppress the immune response, based on TH1 cells

)

Clonal elimination or anergi

tion of

T cells after

a

ntigen recognition on the surface of other cells than APC (

lacking co-stimulatory signals

)

Regulatory T cells

maintain tolerance

t

o autoantigens (Treg, Tr1)

Slide20

Factors influencing the outcome of the immune response

The

same

antigen

can

induce

an

active

immune

response

or

an

active

state

of

tolerance,

the

result

of

response

depends

on many

factors

:

State

of

the

immune

system

Properties

of

antigen

Dose

of

antigen

Route

of

antigen

administration

Slide21

Cytokines

(Tissue hormones)

Slide22

Cytokines

Regulatory proteins and glycoproteins produced by leukocytes and other cells

Essential regulators of the immune system

Apply outside the immune system (angiogenesis, tissue regeneration, carcinogenesis, treatment of many brain functions, embryonic development ...)

Cytokines - secreted

     - membrane (CD 80, CD86, CD40L, FasL ..)

Slide23

Pleiotropic effectOperates in a cascadeCytokine Network Cytokine system is redundant Effects of cytokines - autocrine - paracrine - endocrine Are known as interleukins (exception: TNF, lymphotoxin, TGF, interferons, CSF and growth factors)

Cytokines

Slide24

Distribution of cytokines by function

Proinflammatory cytokines (IL-1, IL-6,IL- 8,IL- 12,IL- 18, TNF)Antiinflammatory cytokines (IL-4, IL-10, TGF)Cytokines with the activity of hematopoietic cells growth factor (IL-2, 3, 4, 5, 6, 7, 9, 11, 14, 15, CSF, SCF, LIF, EPO) Cytokines applying in TH2 humoral immunity (IL-4, 5, 9, 13) Cytokines applying in the cell-mediated immunity TH1 (IL-2, 12, IFN, GM-CSF, lymphotoxin) Cytokines with antiviral effect (IFN-, IFN-, IFN- )

Slide25

Overview of the most important cytokines

CytokineProducedFunctionIL-1MF, NT cell costimulation, induction of TNF and IL-8, pyrogenIL-2Th1Growth factor for T cellsIL-4Th2, basophilsTh2 differentiation, B cell stimulation, isotype switching to IgE and IgG4, Th1 inhibitionIL-5Th2, eosinophilsB cell stimulation, growth factor for eosinophilsIL-6Th2, MF, NT and B cell stimulation, stimulation of Ig production, induction of acute phase proteins synthesis, pyrogenIL-8MF, other cellsGranulocyte activation and chemotaxis (primarily neutrophils)IL-10Th2,M, TregTh1 and MF inhibition, B cell differentiation to plasma cellIL-12MF, DC, BTh1 differentiation, NK stimulationTNFM, MF, NKInduction of local inflammation, endothelium activation, induction of apoptosisTGFbT, MF, plateletsThe anti-inflammatory effect (control of lymphocyte proliferation, control of Ig production, control MF activity), stimulation of fibroblasts and osteoblasts, gain production of extracellular matrixIFNaL, M, MFInhibition of viral replicationIFNbFibroblasts, epithelial cellsInhibition of viral replicationIFNgTh1, NKMF activation, stimulation of MHC gp. expression, Th2 inhibition

MF – macrophages; M – monocytes; N – neutrophils; DC – dendritic cells; NK – natural killers; L – lymphocytes; B – B cell; T – T cell

Slide26

Cytokine receptors

Consisting of 2 or 3 subunits One subunit binds cytokine, other are associated with cytoplasmic signaling molecules (protein kinases) Signaling subunit is shared by several different cytokine receptors - called receptor family Signaling through these receptors may lead to proliferation, differentiation, activation of effector mechanisms or blocking the cell cycle and induction of apoptosis

Slide27

Defense against extracellular pathogens

Slide28

Defence against extracellular pathogens

bacteria

(

gram-negative, gram-positive

cocci

,

bacilli

),

unicellular

parasites

pathogens

induce

inflammation

removed

by

phagocytosis

-

neutrophil

granulocytes

opsonization

(

IgG

and

IgA

antibodies

, C3b,

lectins

, CRP...)

Slide29

Defence against extracellular pathogensOpsonisation and phagocytosis

Slide30

Defence against extracellular pathogens

Phagocytes

are

attracted

to

the

site

of

infection

by

chemotactic

substances

(C5a, C3a

and

chemotactic

products

of

bacteria

…)

ingested

bacteria

are

destroyed

by

the

microbicidal

systems

(

products

of

NADP-H

oxidase

,

hydrolytic

enzymes

and

bactericidal

substances

in

lysosomes

)

phagocytes

produce

proinflammatory

cytokines

(IL-1, IL-6, TNF)

Slide31

Defence against extracellular pathogens

IgM

- complement activation

IgG

- activation of complement, opsonization

IgA

- opsonization

sIgA prevents against infection by intestinal and respiratory bacteria

in the defense against bacterial toxins apply

neutralizing antibodies

(Clostridium tetani and botulinum …)

Slide32

Defence against extracellular pathogens

"indirect toxins - bacterial Lipopolysaccharide (LPS) stimulates big number of monocytes to release TNF, which can cause septic shock

individuals with immunodeficiency of phagocytes, complement and antibodies production are especially

at risk of infections with extracellular bacterial

Slide33

Defense against

intracellular pathogens

Slide34

Defense against intracellular pathogens

bacteria, fungi and unicellular parasites

intracellular parasites are resistant to the microbicidal mechanisms of phagocytes

macrophages

, which absorbed them, produce IL-12 →

T

H

1

differentiation, production of

IFN

g

and membrane TNF → activation of macrophages and production of

NO

Slide35

Defense

against

intracellular

pathogens

Slide36

TC lymphocytes apply in the defense against intracelular parasites, which escape from phagolysosomesindividuals with certain disorders of phagocytes and defects of T lymphocytes are at risk of infections with intracellular microorganisms

Defense against intracellular pathogens

Slide37

Defense against intracellular pathogens

Slide38

Anti-viral defense

Slide39

Anti-viral defence

interferons

-

production

of

IFN

a

and

IFN

b

is

induced

in

infected

cells

;

IFN

g

activates

macrophages

(

iNOS

)

IFN

a

and

IFN

b

-

prevents

viral

replication

-

induce

proliferation

of

NK

cells

-

increase the expression of HLA-I

Slide40

Anti-viral defence - interferons

Slide41

Anti-viral defence

NK cells

- ADCC

(Antibody-dependent cell-mediated cytotoxicity); NK cell bind with CD16 (Fc

g

receptor) to IgG

which has bound to the surface of

infected cell and then NK cell release perforins and granzymes (degranulation)

infected macrophages produce

IL-12

(a strong activator of NK cells)

Slide42

Anti-viral defence - NK cell activation

ADCC

Slide43

Anti-viral defence

in

the

defense

against

cytopathic

viruses

applied

antibodies

:

sIgA

inhibit

mucosal

adhesion

of

viruses

(defense

against

respiratory

viruses

and

enteroviruses

)

neutralizing

IgG

and

IgM

antibodies

activate

the

classical

pathway

of

complement

,

that

is

able

to lyse

certain

viruses

opsonized

viral

particles

are

phagocytosed

IgA

and

IgG

have

preventive

effect

in

secondary

viral

infection

Slide44

Anti-viral defence - antibodies

Slide45

Anti-viral defence

effector

T

C

lymphocytes

destroy infected cells in direct contact (granzym/perforin; FasL) and by produced cytokines (lymfotoxin)

some viruses after infection integrate into the host genome, where persist for years (varicella zoster, EBV, papillomavirus)

individuals with T lymphocyte immunodeficiency and with combined immune disorders are at risk by viral infections

increased susceptibility to herpes infections in individuals with dysfunction of NK cells

Slide46

Anti-viral defence – NK cells and Tc lymphocytes

Slide47

Defense against multicellular parasites

Slide48

Defense against multicellular parasites

IgE, mast cells, basophils and eosinophils

T

H

2

stimulation under the influence of IL-4 (mast cells and other APC stimulated by parasite)

T

H

2 stimulate B cells with BCR-specific parasite antigens

isotype switching under the influence of IL-4 to IgE

IgE

bind to Fc

e

RI on mast cells and basophils

Slide49

Defense against multicellular parasites

multicellular

parasite

binds

to

IgE

on mast

cell

cross

-

linking

of

several

molecules

Fc

RI

initiate

mast cell

degranulation

(

release

of

histamin

,

tryptase

, serotonin…)

activation

of

arachidonic

acid

metabolism

(

leukotriene

C4, prostaglandin PGD2) -

amplification

of

inflammatory

responses

cytokine

production

by mast cell (TNF, TGF

, IL-4, 5, 6)

Slide50

Defense against multicellular parasites

Histamine

vasodilatation, increase vascular permeability (erythema, edema, itching)

bronchoconstriction (cough)

increases intestinal peristalsis (diarrhea)

increased mucus secretion

This helps eliminate the parasite.

Slide51

Mast cell activation

Slide52

Defense against multicellular parasites

eosinophils

fagocyte

complexes

of

parasitic

particles

with

IgE

via

their

receptors

for

IgE

eosinophils

use

against

parasites

extracellular

bactericidal

substances

released

from

granules

(ECP-

eosinophil

cationic

protein, MBP-major basic protein…)

Slide53

Defense against multicellular parasites - eosinophils

Slide54

Tumour immunology

Slide55

Tumor antigens

Tumor – specific antigens (TSA)

complexes

of MHC

gp

I with abnormal fragments of cellular proteins

(chemically induced tumors, leukemia with chromosomal translocation)

complexes of MHC

gp

with fragments of oncogenic viruses proteins

(tumors caused by viruses: EBV, SV40, polyomavirus…)

abnormal forms of glycoproteins

(sialylation of surface proteins of tumor cells)

idiotypes of myeloma and lymphoma

(clonotyping TCR and BCR)

Slide56

Tumor antigens

b) Tumor -

associated

antigens

(TAA)

present

also

on

normal

cells

differences

in

quantity

,

time

and

local

expression

auxiliary

diagnostic

markers

Slide57

Tumor - associated antigens

onkofetal antigens -

on normal embryonic cells and some tumor cells

-fetoprotein

(AFP) - hepatom

carcinoembryonic

antigen

(CEA) - colon cancer

melanoma antigens -

MAGE-1, Melan-A

antigen HER2/neu -

receptor for epithelial growth factor, mammary carcinoma

EPCAM –

epithelial cell adhesion molecule, metastases

differentiation antigens of leukemic cells -

present on normal cells of

leukocytes

linage

CALLA

-acute lymphoblastic leukemia (CD10 pre-B cells)

Slide58

Anti-tumor immune mechanisms

Immune controltumor cells normally arise in tissues and are eliminated by T cells Anti – tumor immune responsetumor cells are weakly immunogenicoccurs when tumor antigens are presented to T lymphocytes by dendritic cells activated in the inflammatory environment

Slide59

Anti-tumor immune mechanisms

If

tumor

cells

are

detected

, in defense

may

be

involved

non-

specific

mechanisms

(

neutrophilic

granulocytes

,

macrophages

, NK

cells

,

complement

)

and

antigen-

specific

mechanisms

(T

H

1

and

T

C

cells

,

antibodies

).

Slide60

DC are necessary for activation of antigen specific mechanismspredominance of TH1 (IFN g, TNFa)specific cell-mediated cytotoxic reactivity – TCactivation of TH2 → stimulation of B cells→ tumor specific antibodies production (involved in the ADCC)tumor cells are destroyed by cytotoxic NK cells (ADCC)interferons - antiproliferative, cytotoxic effect on tumor cells - INFg - DC maturation

Anti-tumor immune mechanisms

Slide61

Regulatory T cells prevents removal of cancer cells and thus contribute to the development of the tumor.

Slide62

Mechanisms of tumor resistance to the immune system

high

variability

of

tumor

cells

low

expression

of

tumor

antigens

sialylation

some

anticancer

substances

have

a

stimulating

effect

production

of

factors

inactivating

T

lymphocytes

expression

of

FasL

→ T

lymphocyte

apoptosis

inhibition

of

the

function

or

durability

dendritic

cells

(NO, IL-10, TGF-

b

)

Slide63

Transplantation

Slide64

Transplantation= transfer of tissue or organ autologous - donor = recipient syngeneic - genetically identical donor and recipient (identical twins) allogeneic - genetically nonidentical donor of the same species xenogenic - the donor of another species implant - artificial tissue compensation

Slide65

Allotransplantation

differences in donor-recipient MHC gp and secondary

histocompatibility Ag

alloreactivity of T lymphocytes

- the risk of rejection and

graft-versus-host disease

Slide66

ABO compatibility (matching blood group) -risk of hyperacute or accelerated rejection (= formation of Ab against A or B Ag on graft vascular endothelium) HLA typing (matching tissue type) - determining of HLA alelic forms by phenotyping or genotyping Cross-match - detection of preformed alloantibodies (after blood transfusions, transplantation, repeated childbirth) Mixed lymphocyte reaction - testing of T lymphocytes alloreactivity

Tests prior to transplantation

Slide67

Tests prior to transplantation HLA typing

1) Serotyping

(microlymfocytotoxic test)

Allospecific serums

(obtained from multiple natal to 6 weeks after birth, or commercially prepared sets of typing serums (monoclonal antibodies))

Principle

- the incubation of lymphocytes with typing serums in the

presence of rabbit complement, then is added the vital

dye which stained dead cells

- cells carrying specific HLA are killed by complement

Number of death cells is a measure of serum toxicity, positive reaction is considered more than 10% dead cells

Slide68

HLA - serotyping

Slide69

2) Molecular genetic methods 2a) PCR-SSP = Polymerase chain reaction with sequential specific primers Extracted DNA is used as a substrate in a set of PCR reactionsEach PCR reaction contains primers pair specific for a certain allele (or group of alleles) Positive and negative reactions are evaluated by electrophoresis, each combination of alleles has a specific electrophoretic pattern

Tests prior to transplantation

HLA typing

Slide70

2b) PCR-SSOPCR reaction with sequence-specific oligonucleotides Multiplication of hypervariable sections of genes coding HLA Hybridization with enzyme or radiolabeled DNA probes specific for individual alleles 2c) PCR-SBTSequencing based typingThe most accurate method of HLA typingWe get the exact sequence of nucleotides, which compares with a database of known sequences of HLA alleles

Tests prior to transplantation

HLA typing

Slide71

determination of preformed alloantibodies recipient serum + donor lymphocytes + rabbit complement → if cytotoxic Ab against donor HLA Ag are present in recipient serum , Ab activate complement → lysis of donor lymphocytes. Dye penetration into lysis cells. positive test = the presence of preformed Ab → risk of hyperacute rejection! → contraindication to transplantation

Tests prior to transplantation

Cross-match testing

Slide72

Slide73

Mixed lymphocyte reaction (MRL) determination of T lymphocytes alloreactivity mixed donor and recipient lymphocytes → T lymphocytes after recognition of allogeneic MHC gp activate and proliferateOne-way MRL determination of recipient T lymphocytes reactivity against donor cells donor cells treated with chemotherapy or irradiated lose the ability of proliferation

Tests

prior to

transplantation

Slide74

One-way MRL

Slide75

Immunologically privileged sites and tissues

Transplantation of some tissues don´t lead to the induction of allogeneic reactivity

Evolutionarily significant, protection of vital organs (brain, eye, gonads)

Factors protecting immunologically privileged structures

isolation from the immune system

(

minimal content of lecocytes)

preference of T

H

2 reactoin, supression of T

H

1 reaction

FasL expression

production of TGF

b

Slide76

Rejection

hyperacute

accelerated

acute

chronic

Slide77

Hyperacute rejection

minutes to hours after transplantation

humoral mediated immune response

mechanism:

if in recipients blood are present

preformed

or

natural Ab

(IgM anti-

carbohydrate Ag)

before transplantation

→ Ab + Ag of graft

(MHC gp

or endothelial Ag)

graft damage by activated complement

the graft endothelium: activation of coagulation factors and platelets, formation thrombi, accumulation of neutrophil granulocytes

prevention:

negative

cross match

before transplantation,

ABO

compatibility

Slide78

Accelerated

rejection

3 to 5

days

after

transplantation

caused

by

antibodies

that

don´t

activate

complement

cytotoxic

and

inflammatory

responses

triggered

by

binding

of

antibodies

to

Fc

-

receptors

on

phagocytes

and

NK

cells

prevention

:

negative

cross

match

before

transplantation

,

ABO

compatibility

Slide79

Acute rejection

days to weeks after the transplantation or after a lack of

immunosuppressive treatment

cell-mediated

immune response

mechanism:

reaction of recipient

T

H

1

and

T

C

cells

against Ag

of graft tissue

infiltration by lymphocytes, monocytes, granulocytes

around

small

vessels

→ destruction of tissue transplant

Slide80

Chronic rejection

from 2 months after transplantation

the most common cause of graft failure

mechanism is not fully understood:

non-immunological factors (tissue ischemia) and T

H

2 response

with production alloantibodies, pathogenetic role of cytokines

and growth factors (TGFβ)

fibrosis of the internal blood vessels of the transplanted tissue, endothelial damage →impaired perfusion of graft → gradual loss of its function

dominating findings: vascular damage

Slide81

Rejection

Factors

:

The

genetic

difference

between

donor

and

recipient,

especially

in

the

genes

coding

for

MHC

gp

(HLA)

Type

of

tissue

/ organ -

the

strongest

reactions

against

vascularized

tissues

containing

many APC (skin)

The

activity

of

the

recipient

immune

system

-

the

immunodeficiency

recipient has a

smaller

rejection

reaction

;

immunosuppressive

therapy

after

transplantation

suppression

of

rejection

Status

of

transplanted

organ -

the

length

of

ischemia

,

the

method

of

preservation

,

traumatization

of organ at collection

Slide82

Bone Marrow TransplantationRemoval of hematopoietic stem cellsMyeloablationTransplantationEngraftmentRejectionGraft-versus-host reaction

Slide83

Graft

-versus-host (

GvH

)

disease

after

bone

marrow

transplantation

GvH

also

after

blood

transfusion

to

immunodeficiency

recipients

T-

lymphocytes

in

the

graft

bone

marrow

recognize

recipient

tissue

Ag

as

foreign

(

alloreactivity

)

Slide84

Acute

GvH

disease

days

to

weeks

after

the

transplantation

of

stem

cells

damage

of

liver, skin

and

intestinal

mucosa

prevention

:

appropriate

donor

selection

,

the

removal

of

T

lymphocytes

from

the

graft

and

effective

immunosuppression

Slide85

Chonic GvH disease months to years after transplantation infiltration of tissues and organs by TH2 lymphocytes, production of alloantibodies and cytokines → fibrosis process like autoimmune disease: vasculitis, scleroderma, sicca-syndrome chronic inflammation of blood vessels, skin, internal organs and glands, which leads to fibrosis, blood circulation disorders and loss of function

Slide86

Graft versus leukemia effect (GvL)

donor T lymphocytes react against residual

leukemick cells of recipient (setpoint response)

mechanism is consistent with acute GvH

associated with a certain degree of GvH (adverse

reactions)

Slide87

Immunologic relationship between mother and allogenic fetus

Slide88

Immunologic relationship between mother and allogenic fetus fetal cells have on the surface alloantigens inherited from his fatherTolerance of fetus by mother allow the following mechanisms: the relative isolation of the fetus from maternal immune system (no mixing of blood circulation) trophoblast - immune barrier witch protects against mother alloreactive T lymphocytes (don´t express classical MHC gp, expresses non-classical HLA-E and HLA-G)suppressin of TH1 and preference of TH2 immune mechanisms in pregnancy

Slide89

transfer of small doses of fetal antigens in maternal circulation causes tolerance ...

Slide90

Rh incompatibility

Complications in pregnancy: production of

anti-RhD antibodies

by RhD- mother carrying an RhD+ fetus (hemolytic disease of newborns)

During childbirth or abortion

(after 8 weeks of gestation) fetal erythrocytes can penetrate into the bloodstream of mother →

immunization

, formation of anti-RhD antibodies

Slide91

Rh incompatibility

Slide92

Rh incompatibility

After childbirth, investigate Rh factor of born child, if is child Rh+, mother gets up to 72 hours after birth injection of anti-RhD antibodies (administered after abortion too)

Anti-Rh(D) antibodies bind to RhD Ag on baby´s red blood cells,

this Ag than can´t bind to BCR and can´t activate B lymphocytes, this immune comlexes also inhibit B lymphocytes

Slide93

Rh incompatibility

During

next

childbirths

,

if

fetus

is

Rh

+

and

mother

produce

anti

-

Rh

antibodies

,

this

Abb

destroy

red

blood

cells

of

fetus,

which

can

lead

to

fetal

death

,

or

in severe

postpartum

anemia

(

anemia

neonatorum

)

and

neonatal

jaundice

(

icterus

gravis

neonatorum

)

For

each

pregnant

woman

during

the

first

trimester

investigate

blod

Rh

factor

and

the

presence

of

antibodies

, in

Rh

-

women

performed

a test

for

antibodies

also

in II.

and

III.

trimester

Slide94

Thank you for your attention

Slide95

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