Transduction

DNA transferred with the help of a bacteriophage

Two types of phages

Lytic: : virulent, phage replication is independent of replication of bacterial

replication

Temperate: lysogenic

Phage genome integrates into bacterial genome forming prophage by the

process of lysogeny.

Thus the replication in both occur concurrently and the bacterium doesn't
die.

If the repressor protein quantity goes down, this phage follows a Lytic
cycle. Thus repressor protein is the main factor.

Thus it can follow both cycle depending on the repressor protein.

Packaging error of the bacterial genome in the phage leads to the

genome transfer among the bacteria. The new bacteria will have new
properties of the first bacteria.

Conjugation

Discovered by lederburg and Tatum

In E. Coli

fertility or conjugative plasmids have the extra function of Conjugation

Horizontal gene transfer of F plasmid through the conjugation tube/ sex

pili

Whenever conjugation happens, F+ remains F+ but F- becomes F+

R plasmid
Resistance plasmid

When F plasmid transfers antibiotic resistance genes

Thus R plasmid is a specialized F plasmid

Resistance transfer factor is the F plasmid

Resistance determinant is R plasmid

Features of R plasmid drug resistance transfer

Multiple drug resistance gene transfer

Both horizontal and vertical transfer

Transferred both intra and inter species

Most common method of antibiotic resistance transfer between bacteria

Comparing by mutation

Always vertical

Single resistance

Within species

Less common

Less dangerous

Thus plasmid is the most common site of antibiotic resistance in bacteria

R plasmid were first discovered in Shigella

Lysogenic conversion

Chemically exotoxins are polypeptides

Therefore the genes would be lying with the chromosome or the plasmid

But sometimes the gene for exotoxin lies in the phage genome

Thus now the non pathogenic bacteria would produce exotoxin.

Eg. Corynebacterium diphtheriae

Makes diphtheriae toxin with the help of Beta phage

This is not a horizontal transfer

Both benefit as both multiply and grow

Transposition
Transposons
Jumping genes
Insertion sequence

Barbara Mc Lintok

the transposon, can move in and out of chromosome and plasmid

Exists in free and bound form

The basic information that they carry is genes for insertion. May carry
other functions.

Genetic change happens by loss of function in the existing genome by

insertion of the transposon

Therefore genetic change happens

This is not horizontal transfer

Immunology

Immunity is a resistance that a person develops against an infecting

organism or it's toxic product

Innate( born with it), relatively non specific, recognize conserved

important components called

Pathogen associated molecular patterns(PAMP's)

Pattern recognition receptors( on humans)

Eg. Toll like receptors(wow in Germany)

Only 13 TLR's have been recognized

Thus all are innate

Acquired/ adaptive(develop after birth), highly specific

They work separate and together as well

TLR2: teichoic acid, thus unique to gram positives

Also recognizes B- Glucan/Zymosan, recognize fungi

TLR3: recognize intermediate double stranded RNA, intermediates during

viral replication in host cell

TLR4: LPS, recognizes gram negative bacteria

TLR5: flagellin, motile bacteria

TLR9: CPG motifs

Classically in bacteria, C-G-C-G patterns are very common

P stands for phosphate backbone

Thus a marker for recognition of bacteria

Acquired immunity

High specificity

It goes along with high diversity

Memory

Not a feature of innate, coz the response by innate is always same

Acquired response becomes faster and higher in magnitude

That is why acquired is divided into primary and secondary

Vaccination depends upon the memory aspect of acquired

Self/ non self discrimination

But still Innate is more important as it works 24*7 since birth.

It is our first line of defense

Has a barrier function:

Skin

Acidity of stomach

Mediators of innate

Two categories

Cellular innate

Humoral innate

Cellular mediators are

Neutrophils

Eosinophils

Basophils

Monocytes

NK cells

Neutrophils are 60-70% of WBC's

By virtue of its numbers, it is mobilized first, representing acute

inflammation.

Works against extra cellular bacteria

Has TLR on its surface

Makes a phagosome, which fuses with lysosomes and forms

phagolysosome

Can cause oxidative( main) and non oxidative damage by toxic peptide
called defensins

Oxidative burst

Reactive oxygen intermediates

By the help of NADPH oxidase

Oxygen converted into super oxide which further forms peroxide which
further forms hydroxyl ion( most potent, most toxic ion)

Chronic Granulomatous Disease

Gene for NADPH oxidase present on X chromosome absent or defective

It's a XR

Male child

Repetitive infections of S. Aureus, nocardia, candida, aspergillus

Chronic granulomas are formed

Usually in intestinal mucosa, can cause obstruction

Nitro blue tetrazolium test

Dye in oxidized form is colorless and purple in reduced forms

Neutrophils is mixed with oxidized dye( less electrons)

If NADPH oxidase present, ROI formed, dye turns purple

Test positive in normal and negative in diseased

Back to neutrophils

Life span of 3-5 days

Dead bacteria with dead neutrophils forms pus

Importance of pus depends on its position, dangerous if cannot be

drained

Eosinophils

1-3% of circulating WBC's

Broadly Anti helminthic

Recognizes PAMP's on helminths

Produces major basic protein

Basophils

Less than one percent

Least abundant

Important role in disease manifestation

Type 1 HS

Monocytes

5-6%

Macrophages in tissue and monocytes in blood

Dynamic

Can change into each other

CD: cluster of dierentiation

CD 14

Kupfer, microglial( gittre) , dust, mesangial, langerhans, Osteoclast

Langhans cell: many macrophages fuse to form

Horse shoe shaped arrangement

Second cells to reach the site of attack

Indicate chronic inflammation

Work mainly against Intracellular pathogens

Kill by oxidative and non oxidative mechanism

Form granulomas

Have long life span, thus no formation of pus

Thus aka granulomatous inflammation

Back to Chronic Granulomatous disease

Macrophages can't kill the bacteria as their oxidative mechanism is

defective, thus large granuloma formed

Macrophages also act as antigen presenting cells

MHC2 is used to present the Ag to T helper cells

Thus here integration happening with acquired

NK cells
Natural killer cells
Aka Large granular lymphocyte
CD 16,56

It is a part of innate immunity

Anti viral

Anti tumor

It recognizes the human cells infected with virus or converted into tumor
cells( altered self cell)

Senses for a surface protein: MHC1

All cells express MHC1 except RBCs

All NK cells are MHC unrestricted

It senses the down regulation of MHC1 and kills it.

It produces two chemicals

Perforins: creates a hole in the cell

Granzyme: triggers cell for apoptosis

Called natural coz finds the altered self cell itself and kills itself

ADCC: antibody dependent cell cytotoxicity

When virus infect a cell or the cell turns into tumor cells, they present
some surface proteins

Here the NK cell takes the help of an Ab to kill the cell which was coated
by the Ab.

Thus both innate and acquired working here

FcR is CD16 which is on the NK cells

Thus ADCC is not a natural killer process.

Humoral innate immunity

Lysozyme

CRP

Interferons

Complement system

Lysozyme

Discovered by Alexander Fleming

It's a type of PRR

Attaches to bacterial cell wall PARP

Found in all secretions except CSF, sweat and urine

CRP

Carbohydrate is for C

First PRP to be discovered

Recognizes carbohydrate on pathogens

Acute phase reactants, levels increase in few hours of inflammation

It is a B- globulin, thus not an Ab, produced in hepatocytes

Detected in blood by

Precipitation tests

Agglutination tests

Systemic autoimmune diseases: done serially and indicates the stages of

the diseases

Interferons
Glycoproteins

Alpha: leukocytic interferons, produced by leukocyte

Beta: Fibroblastic interferons, produced by fibroblasts

Gamma: immune interferons, produced by T cells

Alpha and B are broadly antiviral

Although they are species specific

Only work in similar vertebrate species

Action

Paracrine fashion

Alert other uninflected cells

The cells start producing RNAase and go into an antiviral state

The viral mRNA is destroyed by this enzyme, thus translation is

inhibited( not transcription as mRNA is already formed)

Therefore interferon does not act directly on the virus

The TLR3 which senses double stranded RNA intermediates is the reason
that interferon is able to identify the infected cell

TLR3 and 9 are Intracellular , all other on surface

Acquired immunity
Cellular and humoral

Cellular
T lymphocyte

CD 3

All immune cells arise from bone marrow

Thymus imparts it's function

Further divided into helper and cytotoxic T cells

Helper: CD3,4

Cytotoxic: CD3,8

Both are mature but Naive( no fight against non self cell as yet)

First detect CD4 to confirm that T cell, then 4 or 8 to sub classify

Helper T cells when starts functioning, divides into

Th1

Th2

Th17( secretes large amount of IL-17, found in MALT, recruit neutrophils,

over activity is asso with autoimmune reactions

Treg

Newer name

Earlier called Th3

Also has CD25

Also produces transcription factor called Fox-P

It has a function of suppressing the immune system

Under activity will cause autoimmune diseases

Ratio of Treg/ Th17 is being used to assess autoimmune diseases

Respective Ag is called Cognate Ag

Mature naive cytotoxic cell is denoted by Tc

Activated by cognate Ag, represented as CTL

Memory T cells are produced on activation

CD 45 RO is it's marker

Long life span

Humoral Acquired
Antibodies

Immunoglobulins

Secreted by plasma cells

Plasma cells are dierentiated B cells

B cell: CD19,20,21

Membrane distal domain(variable)

Membrane proximal domains(constant)

Alba variable and B variable

Both bind to an Ag

Thus only one Ag is bound to one TCR

Hence the valency of one TCR is one

TCR complex
Every TCR is asso with a transmembrane

Protein called CD3

Thus this combination is called

TCR complex

CD3 passes the signal inside the cell

While TCR interacts with Ag

Monoclonal / mono specific

All TCR's on the T cell have the same

structure

The diversity is maintained by

Dierent TCR on dierent T cell

Variability is because of the alpha and

B variables

Clonal proliferation
All the TCR are created in fetal life

Are created randomly and have

Nothing to do with Ag exposure

Repertoire: sum total of all the clones of

T cells created during fetal life

Thus clonal proliferation happens

Before Ag exposure

Clonal selection theory

The cognate Ag selects the T cell

Then the T cell proliferates monoclonally

Given by Paul Ehrlich

BCR
B cell receptor
It is an Ab

Fab part binds with Ag

Fc part sticks on the surface of the B cell

These are called membrane Ig: mIg

Normally Ab are soluble, not these

The Fab part interacts with 2 Ag

Thus valency of single BCR is 2

This B cell is monoclonal as all the BCR are identical and bind to the
same Ag

Thus dierent B cells have dierent BCR accounting for diversity

Therefore, just like TCR, BCR are also created in fetal life

Same mechanism for clonal proliferation

But the dierence arises when

B cell matures in plasma cells, it secretes the BCR( now known as soluble
Ab) in solution form

Thus TCR is always stuck while BCR can occur in both forms

Thymic education

Precursor T cell arise from bone marrow

Go to thymus for education

The cell that enters the Thymus is called double negative(CD4,8 negative)

And it gets converted into double positives

Then it converts into single positive

4 into helper Th and 8 into Tc

Therefore there is positive selection

T lymphocyte is educated to learn to recognize the MHC molecule.

If it learns to recognize, stimulus to select.

If fails, stimulus to kill

Stromal cells in the thymus express MHC 1 and 2

If a double positive cell is not able to recognize any MHC

It is killed

If it recognizes MHC 2, CD8 is repressed and converted to Th cell

If it recognizes MHC 1, CD4 is repressed and converted to Tc cell

Thus Th is restricted to MHC 2 and Tc to MHC 2

Then these T cells are presented to this scenario of negative selection or

clonal deletion

Negative selection

The repertoire has to be freed of self Ag

Thymus presents the self Ag

Thus the TCR which recognizes the self Ag is destroyed. These cells are
killed. This is negative selection.

Thus autoimmunity happens due to ABSENCE of clonal deletion/

negative selection

Sequestered Ag: lens protein, spermatozoa protein

B cell education
Only negative selection happens here

All the self Ag are exposed in the stromal cells of Bone marrow

Central/ primary

Thymus

Bone marrow

Peripheral/ secondary

Spleen( blood borne infections)

Lymph nodes( infection of tissues)

MALT( mucosal infection)

Spleen
Main T cell area: periarteriolar sheath

Outer to the periarteriolar sheath are the germinal centers: rich in B cell

lymph Node
Aerent lymphatics

Eerent lymphatic exits from the central part

Helpful in tissue based infections

Cortical is the B cell area

Paracortical is the T cell area

Dierent varieties of Acquired Immunity

Active and passive

Active

Expose the person with Ag

Ab forms in response to that

Immune system gets activated

Thus memory is a feature of active

Thus longer lasting

Lag phase seen

Passive

Preformed Ab is given

Own immune system doesn't get stimulated

Temporary eect

No memory

Helpful in immunocompromised pt.

No lag phase

Thus better in emergency situation

Primary active

First time exposure to Ag

IgM formed

Takes 2-3 weeks

When subsequent exposure occurs

IgM falls as these binds with Ag

This is Negative phase

Then the IgG is formed in 3-5 days

Anity/ avidity

As the response matures, anity increases

Thus seen more in secondary

???

Passive

Primary and secondary

Primary passive better than secondary

As with consequent exposure

Higher dose is needed

As the Ab was from an animal

We devlop a primary active response against primary passive

Low titre IgM formed

Thus it will remove some of the Ab given again

Then the secondary active will form IgG against secondary passive

This is called immune clearance

Acquired
Active
Passive

Further divided into

Natural. Artificial. Natural. Artificial

Natural infection. Vaccine. Transplacental ATS, ATS,ARS,ASV

Clinical/ sub clinical. Transfer, breast

Feeding(IgA)

???

Antigen

Ab generating substance

Stimulates the acquired immune response

Both Ab and cell mediated

Immunogenicity: ability of the Ag to stimulate the immune response and

cause the production of Ab

Antigenecity: The ability of the Ag to bind to the cognate Ab

Epitope is the small part of an Ag which has both the properties of

immunogenicity and antigenecity

Epitope of Ag binds with paratope of Ab

Failure of specifity

When epitopes are similar

Called as cross reactive epitopes

The Ab are called cross reactive Ab

Haptens/ Incomplete Ag

Low molecular wt molecule which has no immunogenicity but only

antigenecity

It can be converted into an Ag by combining with a carrier protein.

Landsteiner

The hapten does not start an Ab response

If given with a carrier, Ab response occurs, IgM formed

Now again the hapten is given, no secondary response

????

Determinants of a strong Ag
It depends on the titre of Ag

1. Chemicals

Protein>CHO> lipids

2. Degree of foreignness

More foreign, more strong

3. Size: ideal size is 100 kilodaltons

4. Susceptibility to tissue enzymes

If the tissue enzymes break the molecule into mid size molecules, it
becomes strong. Will dier from person to person

Dierent varieties of Agic specificities

1. Species specificity

Act as barriers to xenotransplant

2. Organ specific Ag

Mammalian brain

Rabies virus vaccine

Some sheep brain Ag also come along

Thus Ab formed against sheep brain as well

Which react with human brain

Heteophile Ag
Sharing of Ag across species not related to a particular organ

Eg. Weil Felix reaction

3 Ag of proteus

OX19

OX2

OX16

Similar to rickettsia

Which was very dicult to diagnose

Thus proteus is used to diagnose rickettsia

Isospecificity

These are the variations of the Ag distributed in the members of the

species

Eg. Blood group

Rh blood group

These are barriers to blood transfusion

Individual specific Ag
Specific to a particular individual

Hence a barrier to allograft( between same species aka homografts)

MHC / HLA Ag( 6p)

Antibodies

Immunoglobulins
Glycoproteins and not pure proteins

Protein more than CHO, sux always is more

Most of the Ab belong to Y globulin fraction

Monomeric structure of Ab

4 polypeptide chains

2 longer/ heavy chains

2 smaller/ light chains

Longer/ heavy bent at hinge, all mobility here

The light chains flanks the long chain

Both heavy chains bonded by inter heavy chain disulfide bonds below the
hinge

Two more disulfide bonds between the heavy and light chain

The amino terminal is always at the top

Carboxy group at the bottom

All arranged parallel

1st rule in Ab

The heavy chains are identical

All light chains are identical

Kappa light chains and lambda light chains

If kappa, both kappa

Kappa: lambda=2/3:1/3=2:1

All kappa light chains: gene is on chromosome 2

Lambda: 22

Heavy: 14

Variable heavy chain is the amino part

Constant is the remaining part

Similarily

Variable light is the amino part

Constant light is the carboxyl part

This 2 each

Vh associates with Vl to bind with Ag and is the response is specific

Thus the valency is 2 of a monomeric Ab

hypervariable region are seen in the variable region

HVR is the region which forms the exact bond with the Ag

HVR is a better response than paratope

HVR is aka Complementarity determining region CDR

Papain cuts the Ab just above the inter heavy chain disulfide bonds

Thus cutting towards amino terminal

Fragment no. 1 and 2 could bind with Ag

Fragment 3 can not bind

pepsin cuts below the inter heavy chain di sulfide bond

1 molecule having a valency

of 2

Fc portion further broken down

by pepsin

Concept of isospecificity

Isospecifity are the variations of the Ab and all variations are present
in all members of the species
It has nothing to do with specifity

It is also called Class or isotype

Ch region can have 5 variations

Alpha

Meu

Delta

Epsilon

Gamma

Cl has two variations: kappa and lambda

VH and Vl can have infinite variations

Ig class

Further sub class

A: A1 and A2

G: 1,2,3,4

Biological function depends on the class and the subclass

While binding depends on Vh and Vl

Thus when IgM changes to IgG by the same plasma cell( always
monoclonal), only the constant region changes, meu to gamma.

This is class switching

Rules regarding Ab

Single B cell is monoclonal

Both heavy and light chains are identical

Single plasma cell secretes only one class of Ab at one time

Class can change

Biological functions

IgM

Acute infection / recent infection / primary immune response

Present during fetal life, appear around 20 weeks of POG

Pentamer

Held by J chains at the Fc region

10 heavy chains and 10 light chains

10 Vh and 10 Vl

Thus valency is 10

Millionaire molecule

10^6 dalton

Thus it resides in intravascular compartment(80%)

It also acts as BCR, will be a monomer

Pentameter is always in circulation

Activates the Classical Complement system, strongest activator of it

Aka Agglutinating Ab or Lytic Ab

IgG

Secondary immune response

Past infection

Chronic infection

Monomer

2 heavy 2 light

Valency is 2

Highest concentration in serum

Longest serum half life

Four sub classes

In that order of concentration

Crosses placenta but G2 least capable

Maximum action against polysaccharide Ag: G2

G4 does not activate classical pathway, infact activates alternate

pathway

Aka precipitating Ab or Opsonizing Ab

Equally distributed in intravascular and extra vascular compartment

IgA
Local Ab

Mucosal Ab

Secretory Ab

Most abundant in breast milk

Two subclasses

A1>A2

Activates alternate pathway

Serum IgA ( monomeric) and secretory IgA ( dimeric)

J chain in dimeric is associated with secretory component

This component acts as a magnet for J chain produced by mucosal cell

Pulls it from sub mucosa to the lumen

J chain is formed by plasma cell

IgA is most abundant in humans

Total is more than all other combined

Thus if asked in blood, answer G

If asked in human, answer A

IgD


Monomer

Act as BCR(M also)

Thus marker of mature naive cell are IgM and IgD

Alternate pathway

Second highest CHO content

IgE

Lowest concentration

Shortest serum half life

Highest CHO content

Most heat labile

Reaginic Ab and homocytotropic Ab( it attaches to mast cells of any

human being as it has Fc epsilon receptor)

Monomer

Type 1 HS/ immediate type of HS reaction

Protein Ag

Exogenous.
Endogenous
Only two

Viral Ag

Tumor Ag

Exogenous

Theses are presented by APC

Most important are dendritic cells

Others are monocytes, macrophages and B lymphocytes

Exogenous peptides are broken down into small pieces

MHC 2 is utilized in the presentation of the exogenous Ag

All APC use MHC 2

MHC 2 presents the Ag to helper T cell

TCR on the Th cell will attach to the Ag

The outer part of alpha variable and beta variable bind to MHC 2

Inner part bind to the Ag

Thus it's a trivalent molecule

It is Ag dependent

Th needs another stimulus which is Ag independent

Costimulatory interaction

CD 80/86 on APC??

CD 28 on Th

Now the Th0 cell gets activated into

Th1 and Th2

Th1 cytokines

IL2, IL12 and Y interferon

Th2 cytokines

IL 4,5,6,9,10,13

Th1 pathway

Activated Th1 recruits the macrophages

Converting them into activated macrophages

Thus macrophage does the killing

Th1 helps the macrophage in concentrating around the Ag

This is Cell Mediated Immunity( physiological Th1 reaction)

Very important in fighting Intracellular pathogens like TB

If macrophages activated excessively

It becomes type 4 HS reaction( pathological Th1 reaction)

Th2 pathway

Th0 turns into Th2 cell

It activates B lymphocyte

Plasma cell formed

Ab formed

Humoral reaction

Good for extra cellular pathogens

T dependent pathway of B cell activation

Super Ag

It binds to outer aspect of B variable of TCR and outer aspect of

MHC2
Inner part of B variable is not aected

This activates as much as 20-30% of all T cell

Polyclonal activation as inner aspect has variability and outer aspect

might be similar

Massive cytokines release

Toxic shock syndrome

Fever

Shock

Generalized rash

Multiple organ failure

Death

B cell activation

T cell independent
Polysaccharide Ag
No memory
Limited switching( IgM to IgG2)

Child less than 2 years can not respond

T cell dependent
Protein Ag
Memory cell formed
Full range of class switching
Better
Even a child can respond below 2 years

Polysaccharide vaccines
Pneumococcal
Meningococcal
H. Influenza

Thus all the polysaccharide vaccine have been turned into conjugate
vaccines by attaching a protein to the polysaccharide

This makes the reaction T dependent

Thus better class switching

Memory

Can be given below 2 years

Endogenous Ag: any protein Ag coming from our own cell

Viral Ag
Tumor Ag

All are presented in context to MHC 1

The Inner part of alpha and B variable of cytotoxic T cell bind to

Endogenous Ag

Outer aspect binds to MHC 1

MHC restriction

CD * MHC = 8

No co stimulation needed here

Perforins and granzyme used to kill the altered self cell

Cytotoxic T cell can get activated by Th1 cell and thus also a part of CMI

Th1 and Th2 are mutually exclusive

Complement system: classical cascade pathway

Coagulation pathway: also classical cascade pathway

Classical pathway

Activated by IgM> IgG when they are bound to their cognate Ag

The Fc region opens up when Ag binds with Fab

This helps C1q to bind to the Fc region

More Ch regions, more activation, this IgM more potent

C1q ,r, s are together called C1

C1s is an esterase

Both innate and acquired helping each other

Alternate pathway

Activated by IgA, IgG4, IgD

LPS

Snake venom

These Ab can directly activate without bounding to Cognate Ag.

Only requisite is to aggregate in large numbers

All the above provide a surface for C3 to attach

After formation of C5b , the pathway becomes common pathway

C1,2, 4 never figure in alternate

B, P, D never figure in classical

Biological functions
Most important Opsonizing agent: C3b

Chemotactic: C5a

Anaphylatoxin: c3a, c4a, c5a

MAC: C5,6,7,8,9

Hypersensitivity reactions

1 : immediate
2: cytotoxic
3: immune complex
4: delayed HS
5:

Type 1
Ag comes
IgE is formed which is homocytotropic

Acts on Mast cells through the FcER

Mast cells coated with IgE

Second exposure

Histamine released???

Local type 1

Hay fever( allergic rhinitis)

Allergic Asthma

Urticaria

Food allergy: peanuts, egg proteins, sea food

Atopy: genetic predisposition to develop type 1 local reaction

Systemic type 1

Anaphylaxis

Aka richets phenomena

Aka theobald smith phenomena

Penicillin allergy: massive circulatory collapse

Intradermal test is not fool proof, bolus dose can still cause

Type 2

Cytotoxic

IgM and IgG

Ag is on the cell

Classical complement pathway activated

MAC formed

Cell killed

Acute rheumatic fever

Good pasture syndrome

ABO incompatibility

Rh incompatibility

Hyper acute graft rejection

Idiopathic thrombocytopenic purpura

Drug induced hemolytic Anemia or thrombocytopenia

Drugs here act as Haptens

Sometimes the hapten binds to RBC receptor

Making it immunogenic

Ab formed

Classical Complent pathway activated

MAC formed

RBC lysed

Type 3
Immune complex type

IgM and IgG

Bind to a soluble Ag( if a cell, type 2)

Immune complex formed which is insoluble

Precipitates

Classical Complement activated

MAC formed

Local and systemic response

Local

Arthus reaction

Big immune complexes settle down locally

Hypersensitivity pneumonitis: inhaled Ag

Systemic

Serum sickness

Small immune complexes

Can circulate

Deposit in slow flowing sites

Glomerulonephritis

Skin rash

Arthritis

Raji cell assay to detect circulating immune complexes

Type 4

Delayed

Exogenous Ag

APC

Th

Th1

Macrophages

Which kill our own tissue

Contact dermatitis type

Ag comes on skin

Skin destroyed where contact happens

Poison ivy

Nickel/ chromium

Tuberculin type

Montoux test

Lepromin test

Fries test

Berylliosis

Type 5
Modifications of type 2

IgG and IgM

Cellular Ag

Complement is not activated

No MAC formed

Thus the cell does not die

No anatomical change

Functional loss

Could be stimulatory

Graves' disease

Ab against TSH receptor

Inhibitory

Myaesthenia gravis

Anti Ach Ab

Questions

IgG and IgM : 2,3,5

IgE:1

No Ab: type 4

Ag is free to start with, but Ab is cell bound: type 1

Ag is cell bound, Ab is free: 2, 5

Both are free: 3

Pathological Th1: type 4

Pathological Th2: all except type 4

Skin test

Type 4

Type 1: casoni's test

Type 3: shick test