immunity by dr p r choudhary

7/25/2019 Immunity by Dr P R CHOUDHARY

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Immunity Body is protected against

invading micro-organism byvarious physical barriers likeskin &epithelial lining of lungs,eye, ear & GIT called as rst lineof defense.

If the rst line of defense fail tocontrol the invading pathogenthen the second line of defense

immune system is activated.


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Immune system

Immune system

"atural#"on-specic$

%cuired#specic$

B-'ymphocyte &%ntibodies

T- 'ymphocyte"eutrophil, mono,(acrophages

)ellular *esponsesmoral *esponses

luble factor in serumd body uid. comp. system

-Interferon-)*- "/

+umoral *esponses)ellular *espons

is available since birth.

t specic to a particular

roorganism.

- It is acuired after birth, e!pos(icro-organism.

- pecic for each species of

micro organism


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"atural immune system

+umoral responses0 1ue tosoluble factor in the serum &

body uid via-2. complement system

3.)-reactive protein

4.Interferon5s

6."atural killer cells


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system

The complement system includes 22

en7ymatic proteins 8hich are identied bythe number )2to )9,B & 1.

%ll these are present in blood.

%ctivation of this system then start aseuence of :)%)%1; *;%)TI


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)omplement system

)lassical path8ay-this is activated

by antigen-antibody reaction. >henantibody bind 8ith antigen then aspecic reactive site on the constant

portion of the antibody becomeuncovered 8here the protein )2bind

&thus gets activated .

The activates the othercomplement in a series of cascadereaction.


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)lassical path8ay

%g-Ig-)2

%g-Ig-)2)6b

%g-Ig-)2)6b-

)3a

%g-Ig-)2)6b-)3a-)4b

%g-Ig-)2)6b-)3a-)4b

)?b-)@ )A ) )9

)6

)6a

C)6b

)3

)3a

C)3b)4

)4a

C)4b)?

)?a

C)?b

auses 'ysis of the cellembrane of Bacteria

)auses-activation & 1egranulation


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%lternative ath8ay

%lternative or roperdinath8ay is initiated by bindingof the factor I#properdin$8ith

polysaccharide present in thecell 8all of invadingmicroorganism #bacterial

endoto!in$ & yeast cell8all#7ymogen$.

This binding start chain of

reaction that activate )4 &)?


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;Fect of activation ofcomplement system


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)omplement system


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)omplement system


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)- *eactive roteins

;ntry of foreign invaders thenactivate )-* 8hich coats the

invading antigen.

)-* coated organisms

activate the complementsystem 8hich in turnphagocytosis.


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Interferon5s

Dirally infected cells releaseinterferon5s 8hich help in

2. Eorms a protective ring onuninfectable cells thus decreasespread of infection.

3. Inhibits proteins synthesis bydegradation of m*"% so inhibitsreplication of viruses.


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"atural killer cells

2.They kill cell 8ithoutsensiti7ation & involvement ofmaor +isto compatibility

%ntigen.3.They 1estroy malignant cells

4.They kill antibody coated viruses.

6.+elp in rst line of defenceagainst viruses.


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)ellular *esponses

By help of )irculatinghagocytes-

2."eutrophil act as 2st

line ofdefence .

3.(onocyte - act as 3ndline of

defence .. *; of 'iver ,spleen, lymph

nodes kill invading organism.


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)ellular *esponses

By help of )irculatinghagocytes-

2."eutrophil act as 2st

line ofdefence .

3.(onocyte - act as 3ndline of

defence .. *; of 'iver ,spleen, lymphnodes kill invading organism.


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The %cuired immuneystem

If natural immune system failagainst invading pathogen thenthe acuired immune systemactivated.

%cuired immunity is mainly t8otypes.

2.+umoral immunity due tocirculating antibodies

- it maor defence against

bacterial infection.

Th % i d i


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The %cuired immuneystem

2. )ellular immunity Dia T 'ymphocytes

- it maor defence against

- viruses,

- fungi

- intracellular bacteria.It also responsible for

- 1elayed allergic reaction.

- reection of transplant of foreigntissue.

- 'ysis of tumor cells.

- %utoimmune disease.


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f ll l i


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tages of cellular immune*esponse

2. %ntigen rocessing & resentation . >henever antigen #bact. & virus$

enter host body then rst

phagocytosis by the (acrophages/Ha %ntigen presenting cell#%)s$.

%ntigen

%)s

1egradation

%ntigen olypeptide Eragm


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igen olypeptide Eragments #%E$

%E#Bact$

%EDiruse

C

C

(+)-I

(+)-II (ove on the surface of %

(ove on the surface of %


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3. *ecognition of antigen by T-'ymphocyte

%ntigen recognitionreceptors present on T-

'ymphocyte kHa T- cell-*eceptors #T)*s$.

"o8 %E bind 8ith T)*son T-'ymphocytes %nd T-

'ymphocyte can bediFerentiated in to )16

HT6& )1 'ymphocyte.

)1cell *ecogni7ed &

combine 8ith (+)-I%ntigen.

)16cells *ecogni7ed &

combine 8ith (+)-II

%ntigen.


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ymp ocy e


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. - ymp ocy e%ctivation

The )1type of T- lymphocyte after

combine 8ith (+)-I %ntigen, areactivated & diFerentiate into

- )ytoto!ic T-cell

- uppressor T- cell

- (emory T-cell

The )16type of T- lymphocyte after

combine 8ith (+)-II %ntigen, areactivated & diFerentiate into-

- +elper T-)ell

-


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.Immunity

2. *ole of cytoto!ic T-cell #Tc )ell$

Tc & "/ )ells are responsible for the attackphase of cellular response .

)ytoto!ic T- cell have some receptors on theirsurface & bind 8ith %ntigen Bearing cells #Target

cellHmacro$ & destroy them by follo8ingmechanism.

2.erforin killing Tc release hole forming proteincalled erforin

3.'ysisthrough cytoto!ic substance.4.Induction of %poptosis Tc secrete T(


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*ole of cytoto!ic T-cell #Tc )ell$


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%ttack hase of cell mediated Immunity

3. *ole of +elper T-cells-- +elper T cell are T8o types

T+2& T+3

2. +elper T+2cells- released 4 -cytokines

a$. Interleukin-3#I'-3$-activate )1cell to diF

in to )ytoto!ic & suppressor T- cells.

b$. J- interferon#IE"-J$- kill antigen bearing

cells.c$.Tumor necrosis factor-B#T"E-B$-induce

apoptosis in antigen bearing cells.

3. +elper T+3cells- secrete I'-6,?,@,2K &24

act on B-lymphocyte to produce antibodies.


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Eigure 43.A T-);'' *;


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Eigure 43.22 T-1;;"1;"T%"TIG;"

T*IGG;*I"G


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%ttack hase of cell mediatedImmunity

4. *ole of suppressor #Ts$ cells-2.Ts cells regulate the activity of

cytoto!ic T-cells.

3.Ts cells prevent cytoto!ic T-cellsdestroy o8n body tissue .

4.Ts cell also suppress theactivities of +elper T- cells.


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+umoral immunity

+umoral immunity is mediated byantibody.

It defense against most of;!tracellular bacterial pathogen&viruses.

It participates in immediate+ypersensitivity reaction type-I ,II ,&

III It is also associated 8ith certain

autoimmune disease5s

tage of +umoral immune


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tage of +umoral immune*esponse

Antigen processing & presentation.

Recognition of Antigen by Lymphocyte.

Activation of B- Lymphocyte

Production of Plasma & Memory cell by B-

Lymphocyte. Production of Antibodies by Plasma cell.

nactivation of Antigen by Antibodies by !"o "ays-

#. $irect attac% on the invading agents .Attac% on the Antigen !hrough 'omplement system.

B )ells and +umoral


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B )ells and +umoralimmunity

The humoral response is carried outby antibodies which are produced byPlasma cells.

Plasma cells are derived fromactivated B-cells that are produced in

the bone marrow


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The natural immune systemactivates Acquired immunity

Cells of the innate immune systemactivate the specic immune response.

A roup of cells called Antien presentin

cells !APC" activate the acquired immunesystem.

#acrophaes$ %endritic cells and B-cellsare e&amples of types of APCs.

APCs turn on the acquired immune systemby activatin T-'elper cells !T'-cells".

T'-cells in turn activate either the cell

mediated or the humoral immune system.


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%)

The #icrobial antien

is inested by an APCand partially diested.(raments frommicrobe bind with the

#'C )) to form a #'C)) *A comple& on thesurface of the APC


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%)

%)T+ % +elper T cell,specic for the

presented antigen,binds to the (+)IIH%g comple!


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%)

%)T+

%)T+

B

The helper Tcell thenactivates anappropriate B

cell by-


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The interactionbetween the T'-cell

and the B-cellcauses the B- cellto di+erentiate into

Plasma cells andmemory cells.

T'APC


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'umoral

immunity%)

%)

%)

T+

T+

B


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(emory cells

(emory cells do not react right a8ay but

are held in reserve for later infections. The secondary response that is carried out

by memory cells is diFerent in 4 8ays.((emory cells produce antibodies that bind

8ith greater aLnity to their antigens thanthe antibodies produced in the initialresponse.

(The response time is much vaster than theprimary response

(% greater number of antibodies areproduced.

Eunction of %ntibodies


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Eunction of %ntibodies

Antibodies function in ,ways to protect the body( %ggltination nhances

phaocytosis and reduces

number of infectious unitsto be dealt with

(


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(unction of Antibodies Cont000..

%ctivation of complement

Increases inammationthrouh the by products of thecomplement system !C1a andCa"

%ntibody dependant cellmediated cytoto!icityAntibodies attached to taretcell cause destruction by nonspecic immune system cells.


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%ntibodies %ntibodies or immunoglobulin5s are

J globulins, produce by plasmacells to %ntigenic stimulation.

%ll %ntibodies are immunoglobulin5sbut all immunoglobulin5s are notantibodies.

%ntibodies are ve types

IgG, Ig%,Ig(, Ig1 & Ig;

structure


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structure IgG type of

antibody Basicunit of all Igs.

Igs is M shaped

molecular itconsist of fourolypeptidechain.

- 3 +eavy #+$ & 3-'ight#'$ chain.

structure


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structure +eavy chain-

- +eavy chain have (olecular 8eight of ?K,KKK 1.

- +- chain are antigenically diFerent for each classof Ig and are named as-

- N in Ig%

- O in Ig1

- J in IgG

- P in Ig(

- Q in Ig;

;ach + chain consist of Dariable region #" Terminal$ & constant region #) Terminal$ Beco7variable seuence of amino acid & constantseuence of amino acid present.

;ach heavy chain consist of 66Kamino acid.

structure


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structure 'ight chain

- (olecular 8eight of light chain is3?,KKK 1.

- '- chain are of t8o type / #kappa$ &

R #'ambda$.- '- chain consist of variable region

to8ards #"+3$ Terminal & )onstant

region to8ards #)


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1iFerence in %ntibodies

Eeature IgG Ig% Ig(

Ig1 Ig;tructure monomer monomer panatamermonomer monomer

- + chain class y2,y3,y4,y6 N2,N3 PO Q

- ' chain class S & R S & R S & RS & R S & R -( > in /1 2?K 2@K-4? 9KK

2K 29K)arbohydrate content 4 2324 23

erum concn ngHdl 23 3 2.3K.K4 K.KKKK6

+alf life #days$ 32 @ ?4 3

lacental transfer yes "o "o"o "o

)omplement !ation classical %lternativeclassical "one "one

*ole in the body rotects the rotect the rotect

the *ole not type I body uid body surface blood


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%cuired immune deciency syndrome

The red ribbonis a symbol forsolidarity8ith+ID-positivepeople and

those living8ith %I1.

%cuired immune
http://en.wikipedia.org/wiki/Red_ribbonhttp://en.wikipedia.org/wiki/Social_solidarityhttp://en.wikipedia.org/wiki/Social_solidarityhttp://en.wikipedia.org/wiki/Red_ribbon


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%cuired immunedeciency syndrome

%cuired immune deciencysyndrome#%I1$ in 8hich decrease thenumber of +elper-T celldue to infection

of human immunodeciency virus #+ID$

%I1 8as rst detected in % in 292.

+ID is T8o types +ID-I %"1 +ID-II.

*;%1


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*;%1


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Transmission

There are mainly three routes ofTransmission.

2.arenteral route- is throuh blood

contact - 3nscreened blood Transfusion$

- Tattooin

- 3se of infected ra4ors $ syrinesand needles etc.

- oran transplants.


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Transmission

3. e!ual route 5 accounts for about617 of ')8 infection due to-

- multiple se& partners$

- se& wor/ers

- homose&ual

-articial insemination

T i i


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Transmission

. Trans-placentalroute-

infectioncan betransmitted

frominfectedmother to

her fetus.

tructure - +ID


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tructure - +ID ')8 is a retrovirus

havin roundedoutline and consistof-

)


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Dirus multiplication

Dirus multiplication 5 8hen virus

comes in contact 8ith the cellhaving receptors of T6 antigen#+elper-T cells , (onocyte ,

macrophages and some nervecells$ its sticks to the receptorssite and then passes into the

cell. Then free Genomic *"%synthesis a copy 1"% 8ith+elp of en7yme reverse

5

Incubation eriod


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Incubation eriod Daries from 3 to 2K years.

The rst 3 to @ month are called8indo8 period because in this

period test are negative. Thenon8ards +ID positivity isindicated by

2.resence of -36,3.%ntiviral antibodies

4.*eduction in number of T cell.

igns and symptoms


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igns and symptoms igns and symptoms are

mostly of secondary infection

due to decrease immunity. - *epeated episodes of

diarrhoea.

- ne!plained 8eightloss.

- rolonged cough.

- night s8eating

- continuous fever

- Tuberculosis

- Brain damage

- lcers

- /aposi sarcoma #)ancerof skin$.

ne!plained


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- ne!plained8eight loss

+ID Tests


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+ID - Tests 'ab test employed for diagnosis of

+ID infection may be classied into

three groups.2.creening tests are used to

screen %ntibodies against +ID.

- BM ;'I%

3. upplement tests.- These test alsodetect antibodies against +ID.

- BM >estern blot assay.

4. )onrmatory tests- these testconrm +ID infection in individual

8ho is sero positive. - virus isolation

- 1etection of 36 antigen

- 1etection of Diral nucleic acid by

olymerase )hain *eaction.

Treatment


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Treatment Triple drugs

treatment isemployed-

2.rotease inhibitor,

3.*eversetranscriptaseinhibitor

4.%UT#a7idothymidine$

6.Interleukins.

revention


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revention revention measures against +ID

infection include. - ;ducation.

- creening is carried out in case of

blood donors, organ donors , semendonors, Eoreigners and e! 8orker.

- Ban on rostitution.

- afer se! 8ith single artner , useof )ondoms and Barrier creams.

- se of disposable syringes, needle,

immunity by dr p r choudhary

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