Resistance of the body to infection: Inflammation

Resistance of the body to Resistance of the body to infection: Inflammation.infection: Inflammation.

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ObjectivesObjectives

Define Monocyte –Macrophage Cell Define Monocyte –Macrophage Cell System and describe how monocytes are System and describe how monocytes are converted into macrophages.converted into macrophages.

List the body tissues where this system is List the body tissues where this system is active.active.

Describe the functions of macrophagesDescribe the functions of macrophages Define InflammationDefine Inflammation Describe the stages of inflammationDescribe the stages of inflammation

Recommended reading: Tortora & Derrickson. . Recommended reading: Tortora & Derrickson. . Principles of Anatomy and Physiology.12th edn. Principles of Anatomy and Physiology.12th edn. 20092009

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The MPS (Mononucleur The MPS (Mononucleur phagocytic system) (RE phagocytic system) (RE System)System)

Monocytes leave circulation Monocytes leave circulation to enter tissueto enter tissue

Enlarge in size as they Enlarge in size as they move towards site of move towards site of inflammation/infection inflammation/infection (WANDERING (WANDERING MACROPHAGES)MACROPHAGES)

Some collect at specific Some collect at specific sites in body tissuessites in body tissues

(FIXED MACROPHAGES)(FIXED MACROPHAGES)

Secrete Interleukins which Secrete Interleukins which stimulate bone marrowstimulate bone marrow

NO macrophages in the CNS: NO macrophages in the CNS: job done by MICROGLIAjob done by MICROGLIA 3

Phagocytosis by macrophagesPhagocytosis by macrophages

1. Chemotaxis1. Chemotaxis 2. Adherence2. Adherence 3. Ingestion3. Ingestion 4. Digestion4. Digestion 5. Killing5. Killing

1 MicrobeCHEMOTAXIS

Lysosome

Digestiveenzymes

Pseudopod

Phagocyte

ADHERENCE INGESTION

Plasmamembrane

DIGESTION

KILLINGResidual body(indigestiblematerial)

Digested microbein phagolysosome

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Phases of phagocytosis

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InflammationInflammation: nonspecific response : nonspecific response of the body to tissue damage.of the body to tissue damage.

Caused byCaused by bacterial infection, trauma, chemicals, bacterial infection, trauma, chemicals,

heat, hypoxiaheat, hypoxia

Cardinal signsCardinal signs 1. Redness1. Redness 2. Pain2. Pain 3. Heat3. Heat 4. Swelling4. Swelling 5

Redness; Swelling; HeatRedness; Swelling; Heat vasodilatationvasodilatation increased capillary permeability to increased capillary permeability to

allow leakage of fluid into interstitial allow leakage of fluid into interstitial spaces along withy WBCsspaces along withy WBCs

(Emigration of WBCs)(Emigration of WBCs)

As result of release of As result of release of HistamineHistamine from mast cells, basophils from mast cells, basophilsKininsKinins (bradykinin) peptides : chemotaxis (bradykinin) peptides : chemotaxisProstaglandin E Prostaglandin E from damaged tissues from damaged tissues LeukotriensLeukotriens from basophils and mast cells from basophils and mast cells - increase adherence of phagocytes- increase adherence of phagocytes - increase permeability- increase permeability - act as chemotactic agents- act as chemotactic agents

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PainPain Kinins & PGs Kinins & PGs stimulate free nerve stimulate free nerve endingsendings

Local edema produces pressure and Local edema produces pressure and painpain

Release of clotting factorsRelease of clotting factors to to localize the bacterialocalize the bacteria

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Response of WBcs during inflammationResponse of WBcs during inflammation::

1st line of defence1st line of defence:: Locally present Locally present macrophages reach the site of injury within a macrophages reach the site of injury within a few minutes and start phagocytosis. few minutes and start phagocytosis.

2nd line of defence2nd line of defence i. neutrophils are attractedi. neutrophils are attracted to the inflamed to the inflamed

area by area by CHEMOTAXIS.CHEMOTAXIS. ii. increase capillary permeabilityii. increase capillary permeability iii. neutrophils stick to capillary walls at the iii. neutrophils stick to capillary walls at the

site of site of inflammation inflammation (Margination)(Margination) iv. stored neutrophils are brought into iv. stored neutrophils are brought into

circulationcirculation

All this takes a few hours . The neutrophils which are now All this takes a few hours . The neutrophils which are now plenty at site of injury start their phagocytic action.plenty at site of injury start their phagocytic action.

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3rd line of defence3rd line of defence

More macrophages are recruited to come to the inflamed More macrophages are recruited to come to the inflamed area. Takes about 8 hours before the newly formed area. Takes about 8 hours before the newly formed monocytes and granulocytes come into the area.monocytes and granulocytes come into the area.

44thth line of defence line of defence Formation of these cells by bone marrow : stimulation by Formation of these cells by bone marrow : stimulation by

Interleukins, Tumour Necrosis Factor, GM and M Colony Interleukins, Tumour Necrosis Factor, GM and M Colony Stimulating Factors secreted by activated macrophages. Stimulating Factors secreted by activated macrophages. Takes 3-4 daysTakes 3-4 days

Macrophages also initiate immune process such as Macrophages also initiate immune process such as activation of T and B lymphocytesactivation of T and B lymphocytes

Collection of all these cells with the necrotic tissue forms Collection of all these cells with the necrotic tissue forms PUSPUS

Throbbing pulsating pain: presence of PUSThrobbing pulsating pain: presence of PUS9

Recap:Recap: Monocyte –Macrophage Cell System: Monocyte –Macrophage Cell System:

The Wandering & the Fixed The Wandering & the Fixed macrophages.macrophages.

Body tissues where this system is Body tissues where this system is active.active.

Phagocytosis by macrophagesPhagocytosis by macrophages InflammationInflammation Stages of inflammationStages of inflammation Pus formation Pus formation

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Innate and acquired Innate and acquired immunity immunity

Innate ImmunityInnate Immunity

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Objectives:Objectives:Define and classify Immunity into the two types:- Define and classify Immunity into the two types:- innate and acquired.innate and acquired. Describe the process of innate immunityDescribe the process of innate immunity Define the term antigenDefine the term antigen Describe the two types of acquired immunity: Describe the two types of acquired immunity: cell cell mediated and humoral. mediated and humoral. Understand that two types of lymphocytes, T Understand that two types of lymphocytes, T and B, and B, are responsible for acquired immunityare responsible for acquired immunity Appreciate that B lymphocytes produce Appreciate that B lymphocytes produce antibodiesantibodies List the types of antibodies.List the types of antibodies. Describe the principal of vaccination Describe the principal of vaccination List commonly used vaccinationsList commonly used vaccinations Define allergy and describe the role of IgE in Define allergy and describe the role of IgE in allergy allergy List common allergic conditionsList common allergic conditions

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Immunity is the body’s ability to resist Immunity is the body’s ability to resist organisms and toxins which may cause damage organisms and toxins which may cause damage

INNATE : INNATE : external physical, and chemical barriers external physical, and chemical barriers present in the body at birthpresent in the body at birth

ADAPTIVE /ACQUIRED: ADAPTIVE /ACQUIRED: immunity is the ability to immunity is the ability to defend against specific bacteria, toxins, viruses, toxins – defend against specific bacteria, toxins, viruses, toxins – substances called ANTIGENssubstances called ANTIGENs

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IMMUNITY

Innate Acquired

-Salivary lysozomes-Tears with lysozomes-Acid in stomach-Macrophages/-Neutrophils-Skin as a barrier-NK Cells

Antibodies : B lymphocytesIg G commonestIgMIgE allergyIgG A milkIg D rare: unknown function

Humoral

Cell mediated

T lymphocytes:1. Helper T cells2. Killer: Cytotoxic)3. Memory4. Suppressor

NATURAL KILLER CELLSResemble early large T cellsFound in blood and lymphoid tissueRecognize and destroy virally infected cells & cancer cells

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ANTIGENS ANTIGENS are proteins/ are proteins/ polysaccharides which polysaccharides which excite immune excite immune mechanisms. mechanisms.

Haptens small molecules Haptens small molecules which must combine with which must combine with proteins to excite proteins to excite antigenicityantigenicity

Characteristics of antigens:Characteristics of antigens:

i. Immunogenicity: i. Immunogenicity: provoke formation of provoke formation of specific antibodiesspecific antibodies

ii. Reactivity ii. Reactivity The antigen The antigen reacts with the antibody it reacts with the antibody it generatesgenerates

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Innate ImmunityInnate Immunity Present at birthPresent at birth

Involves external physical, and chemical Involves external physical, and chemical barriersbarriers

Helps humans resist diseases such as Helps humans resist diseases such as

- Distemper - Distemper ( ( الكالب الكالب سل (( سل - Cattle plague - Cattle plague ( ( الماشية الماشية طاعون (( طاعون - Viral infections of animals- Viral infections of animals

(Lower animals do not get many human (Lower animals do not get many human diseases:diseases:

Polio, Mumps, Cholera, Syphilis, Polio, Mumps, Cholera, Syphilis, Measles)Measles)

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InterferonsInterferons: : ((αα, , ββ, , γγ)) : :

proteins produced by viral proteins produced by viral infectedinfected

-- lymphocytes lymphocytes

- macrophages- macrophages

- fibroblasts- fibroblasts

Mechanism of actionMechanism of action: :

-enter non-infected cells-enter non-infected cells

-induce production of anti--induce production of anti-viral proteinsviral proteins

- stop viral multiplication- stop viral multiplication

CANNOT STOP VIRUSES FROM ENTERING CANNOT STOP VIRUSES FROM ENTERING CELLSCELLS

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Complement systemComplement system C1-C9C1-C9:: - - proteins which are normally lying inactive in proteins which are normally lying inactive in bloodblood ActionAction: when activated by antibodies- increase : when activated by antibodies- increase phagocytosis, promote inflammationphagocytosis, promote inflammation

Iron binding proteinsIron binding proteins Action: Action: deprive bacteria of iron by binding to itdeprive bacteria of iron by binding to it

Antimicrobial proteinsAntimicrobial proteins

- i. i. Defensins & Cathelicidins by Neutrophils and Defensins & Cathelicidins by Neutrophils and macrophages, macrophages,

epitheila:epitheila:- ii. Dermicidin by sweat glandsii. Dermicidin by sweat glands- iii. Thrombocidin by plateletsiii. Thrombocidin by platelets

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Natural Killer cells (NK Cells)Natural Killer cells (NK Cells)

LymphocytesLymphocytes Effective against tumour cells, Effective against tumour cells, viral viral

infected cells, any cells which infected cells, any cells which have have

abnormal proteinsabnormal proteins

Action byAction by: :

i. i. Release of proteins called PERFORINS_ dig Release of proteins called PERFORINS_ dig holes in to the cell membrane- cell gets flooded holes in to the cell membrane- cell gets flooded with H2O) from ECF and cell burstswith H2O) from ECF and cell bursts CYTOLYSISCYTOLYSIS

ii. ii. Release of Release of GRANYZYMEGRANYZYME which promote cell which promote cell

apoptosisapoptosis InflammationInflammation PhagocytosisPhagocytosis by Macrophages and Neutrophilsby Macrophages and Neutrophils

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ACQUIRED IMMUNITYACQUIRED IMMUNITY

(Adaptive immunity)(Adaptive immunity)

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Objectives: Innate and acquired immunity 2 & Objectives: Innate and acquired immunity 2 & 33Define Acquired immunity as CELL Define Acquired immunity as CELL MEDIATED & HUMORAL MEDIATED & HUMORAL Describe the role of the thymus in Describe the role of the thymus in processing of T processing of T lymphocyteslymphocytes List the 4 types of T lymphocytes List the 4 types of T lymphocytes involved, involved, appreciate that AIDS is a disease caused appreciate that AIDS is a disease caused by ineffectiveby ineffective T lymphocyte functions .T lymphocyte functions .Recognition of selfRecognition of self Recognize that transplanted organs are Recognize that transplanted organs are likely to be likely to be destroyed by cell mediated immune destroyed by cell mediated immune mechanisms.mechanisms. Define auto-immune diseaseDefine auto-immune disease Name important autoimmune disorders.Name important autoimmune disorders. Appreciate that stress and aging affect Appreciate that stress and aging affect immune immune mechanisms adverselymechanisms adversely

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Acquired (Adaptive) immunityAcquired (Adaptive) immunity is the ability is the ability to defend against specific bacteria, toxins, to defend against specific bacteria, toxins, viruses, toxins – substances called viruses, toxins – substances called ANTIGENsANTIGENs

i. Cell mediated immunity:i. Cell mediated immunity:

-by -by activatedactivated T Lymphocytes in the lymph T Lymphocytes in the lymph nodes:nodes:

-active in tissues-active in tissues

ii. Humoral ii. Humoral

-by -by activatedactivated B lymphocytes which B lymphocytes which develop develop

circulating antibodies.circulating antibodies.

-active in blood-active in blood 24

IMMUNITY

innate acquired

Salivary lysozomesTearsAcid in stomachNeutrophilsSkin as a barrier

Antibodies :Ig G commonestIgMIgE allergyIgG A milkIg D rare: unknown function

humoral

Cell mediated

T lymphocytes:1. Helper T cells2. Killer: Cytotoxic)3. Memory4. Suppressor

Antigen: foreign substance: protein, which excites immune reaction

B lymphocytesBecome plasma cells Produce antibodies

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The activation of LymphocytesThe activation of Lymphocytes

Origin of lymphocytes:Pluripotent stem cells in the embryoBone marrow

Reach Immunocompetence by developing antigen receptors on their surface

Develop in marrow: as - B lymphos& Pre T lymphos

mature in the Thymus- T lymphos.

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Activation of lymphocytes so that they Activation of lymphocytes so that they develop IMMUNOCOMPETENCEdevelop IMMUNOCOMPETENCE

T lymphocytes migrate to thymus before birth, T lymphocytes migrate to thymus before birth, and continue until a few months post birth and B and continue until a few months post birth and B lymphocytes s go to the bone marrow (& liver ?)lymphocytes s go to the bone marrow (& liver ?)

Rapid division Specific reactivity to antigens and development of

antigen receptors Non-reactive to “self” T cells released from Thymus go to different T cells released from Thymus go to different

lymphoid tissues as Helper T cells (CD4 cells) lymphoid tissues as Helper T cells (CD4 cells) and Cytotoxic T cells ( CD8 cells)and Cytotoxic T cells ( CD8 cells)

B lymphocytes: develop antibodies against the B lymphocytes: develop antibodies against the antigens and become PLASMA cellsantigens and become PLASMA cells

The Helper T cells, Cytotoxic T cells and B cells The Helper T cells, Cytotoxic T cells and B cells are EFFECTOR cells: die after taking part in are EFFECTOR cells: die after taking part in immune activityimmune activity

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Clone Clone ( ( النسيلة وطبيا النسيلة إستنساخ وطبيا formation by formation by (( إستنساخlymphocyteslymphocytes

Both B and T cells are involvedBoth B and T cells are involved Exposure to a particular antigen excites “cloning” of Exposure to a particular antigen excites “cloning” of

that type of cell or make that type of cell or make IDENTICAL cells by CLONAL IDENTICAL cells by CLONAL SELECTION (proliferation & differentiation)SELECTION (proliferation & differentiation)

Any time this antigen re-enters the body, these clones Any time this antigen re-enters the body, these clones are formed to destroy itare formed to destroy it

Role of MEMORY cells, both T and BRole of MEMORY cells, both T and B Are not associated with the initial response to Are not associated with the initial response to

antigenantigen They “REMEMBER” when an antigen enters body They “REMEMBER” when an antigen enters body

again, again,

and act by initiating formation of more clones of and act by initiating formation of more clones of that type that type

of lymphocyte of lymphocyte They do not die: they have a long life.They do not die: they have a long life. Types of Memory cells: Helper, Killer, B Types of Memory cells: Helper, Killer, B

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T lymphocytes

i. Helper T cells ii. Cytotoxic T cellsiii. Memory T cells iv. Suppressor T cellsI & ii = Regulatory T cells?)

B lymphocytes

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Maturation and function of B Maturation and function of B lymphocyteslymphocytes

B lymphocyts are activated by B lymphocyts are activated by HELPER T & B cellsHELPER T & B cells

Formation of plasma cells: Formation of plasma cells: manufacture manufacture

ANTIBODIESANTIBODIES against specific against specific antigenantigen

Antibodies

Ig G- commonestIgMIgE - allergyIgA - milkIg D rare: unknown function

Antigen-Antibody reactions

1. Agglutination ( متراصة )2. Enhance phagocytosis3. Neutralizes antigen4. Demobilizes bacteria5. Activation of complement system6. Precipitation of soluble antigens

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Physiological Physiological principles of principles of immunizationimmunization

Small dose of non Small dose of non virulent antigen virulent antigen (bacteria/virus) is (bacteria/virus) is givengiven

Antibodies are formed Antibodies are formed against this (type against this (type IgM). This is the IgM). This is the PRIMAY responsePRIMAY response

Few weeks later same Few weeks later same antigen dose is antigen dose is repeated: much bigger repeated: much bigger antibody response: antibody response: Secondary response- Secondary response- IgGIgG ) )

IgG

IgM

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Common vaccinations:Common vaccinations:

BacterialBacterial DPTDPT TyphoidTyphoid CholeraCholera

ViralViral PolioPolio MeaslesMeasles InfluenzaInfluenza

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Use of immunity for protectionUse of immunity for protection

1. Active immunity:1. Active immunity:

vaccinationsvaccinations

2. 2. Passive immunityPassive immunity

a. Mother to fetus : IgG antibodies a. Mother to fetus : IgG antibodies via placentavia placenta

Ig A in milkIg A in milk

b. Injection of Immunoglobulinsb. Injection of Immunoglobulins

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Aging & ImmunityAging & Immunity - Old people get infections/cancers more - Old people get infections/cancers more

easilyeasily

- Response to vaccines is decreased- Response to vaccines is decreased

- They produce more auto-antibodies to - They produce more auto-antibodies to own tissuesown tissues

- T cells respond less to antigens- T cells respond less to antigens

Stress and ImmunityStress and Immunity -- Decreases in stressDecreases in stress: : effect of main effect of main

stress stress

hormone: corticosteroidshormone: corticosteroids

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MHCs Major Histocompatibility Complexes MHCs Major Histocompatibility Complexes (MHCs)(MHCs)

Human Leucocyte Antigen (HLA)Human Leucocyte Antigen (HLA)

MHC I : present on all body cells (NOT RBC)MHC I : present on all body cells (NOT RBC)

MHC II : on Antigen presenting cells MHC II : on Antigen presenting cells

(Macrophages, Dendritic cells, B (Macrophages, Dendritic cells, B cellscells))

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Process of antigen presentation: Process of antigen presentation: Exogenous Exogenous antigens: outside cells antigens: outside cells (bacteria, toxins, pollens, viruses)(bacteria, toxins, pollens, viruses)

1.1. Ingestion and digestion of antigen Ingestion and digestion of antigen to form peptide fragmentsto form peptide fragments

22. Synthesis of MHC II molecule . Synthesis of MHC II molecule in the ER and their packagingin the ER and their packaging

3. Peptide fragments + MHC II mols Vesicles fuse

4. Peptide s and MHC II then fuseTo form a complex

5. Complex inserted in to plasma membrane

6.APC then migrates to lymphoid tissueTo meet lymphocytes through receptors

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Phagocytosis orendocytosis ofantigen

APCs present exogenous antigens in association with MHC-II molecules

Antigen-presentingcell (APC)

MHC-IIself-antigen

Antigenpeptidefragments

Key:

Exogenousantigen

1 Phagocytosis orendocytosis ofantigen

Digestion ofantigen intopeptide fragments

Phagosomeor endosome



MHC-IIself-antigen


Key:

1

2

Exogenousantigen






Synthesis of MHC-II molecules

MHC-IIself-antigen


Key:

Endoplasmicreticulum

1

3

2

Exogenousantigen






Packaging of MHC-IImolecules into a vesicle


MHC-IIself-antigen


Key:


1

4

3

2

Exogenousantigen






Vesicles containing antigenpeptide fragments andMHC-II molecules fuse



MHC-IIself-antigen


Key:


1

5

4

3

2

Exogenousantigen



Antigen peptidefragments bind toMHC-II molecules







MHC-IIself-antigen


Key:


1

5

6

4

3

2

Exogenousantigen



Antigen peptidefragments bind toMHC-II molecules







MHC-IIself-antigen


Key:


Vesicle undergoesexocytosis andantigen–MHC-IIcomplexes are insertedinto plasma membrane

1

5

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4

3

2

Exogenousantigen

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Endogenous antigens : INSIDE body Endogenous antigens : INSIDE body cells cells (toxins, viral proteins, abnormal proteins by (toxins, viral proteins, abnormal proteins by

cancer cells)cancer cells)

Digestion of these proteins

Peptide s and MHC I then fuseTo form a complex

Formation of MHC I

Peptide fragments + MHC I mols Vesicles fuse

Complex inserted in to plasma membrane

APC then migrates to lymphoid tissueTo meet lymphocytes through receptors

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Endogenous AntigensEndogenous Antigens

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Recognition of SELFRecognition of SELFT cells must know own MHCT cells must know own MHC s : s :SELF RECOGINITIONSELF RECOGINITION

T cells must NOT react to own peptide fragmentsT cells must NOT react to own peptide fragments : TOLERANCE : TOLERANCE

Positive selectionPositive selection Immature T cells (before activation) form receptors that react Immature T cells (before activation) form receptors that react

with self MHCs & form a self antigen-MHC binding & recognize with self MHCs & form a self antigen-MHC binding & recognize the MHCthe MHC

T cells that don’t form and recognize this complex under go cell T cells that don’t form and recognize this complex under go cell deathdeath

Negative selectionNegative selection

i. Deletion: self reactive T cells undergo natural cell death i. Deletion: self reactive T cells undergo natural cell death (apoptosis)(apoptosis)

ii. Anergy : Unresponsive to antigen stimulationii. Anergy : Unresponsive to antigen stimulation Tolerance to SELF (own tissue) develops during embryonic Tolerance to SELF (own tissue) develops during embryonic

lifelife 42

Abnormal immune reactions:Abnormal immune reactions: Basically categorized as Basically categorized as

HYPERSENSITIVITY:HYPERSENSITIVITY:

AllergyAllergy:: Harmful effects of hypersensitivity Harmful effects of hypersensitivity to environmental (exogenous) antigento environmental (exogenous) antigen

Autoimmune diseaseAutoimmune disease: when the body : when the body defence mechanisms act against the self.defence mechanisms act against the self.

When immune mechanisms of one When immune mechanisms of one individual produces reactions in another individual produces reactions in another person, it is know as person, it is know as ALLO IMMUNITY.ALLO IMMUNITY.

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AUTOIMMUNE disordersAUTOIMMUNE disorders Non recognition of SELFNon recognition of SELF causes this reaction. causes this reaction. .. Sequestered antigensSequestered antigens: tissue not drained by : tissue not drained by

body lymphatics, have never been exposed to body lymphatics, have never been exposed to body immune mechanisms. Eg. Cornea of the eye. body immune mechanisms. Eg. Cornea of the eye. That is why anybodies cornea can be grafted on to anyone That is why anybodies cornea can be grafted on to anyone else’s eye. But if accidentally such tissue enters the body, it else’s eye. But if accidentally such tissue enters the body, it will excite a severe immune responsewill excite a severe immune response..

Neo(new) antigensNeo(new) antigens a chemical binds to a body a chemical binds to a body tissue, forms a new antigen which is now new to tissue, forms a new antigen which is now new to immune mechanisms of the host. immune mechanisms of the host.

Infectious diseaseInfectious disease may induce formation of a may induce formation of a substance which is similar to one of the host substance which is similar to one of the host tissues. This then excites a reaction. Egs. tissues. This then excites a reaction. Egs. Rheumatic heartdisease; glomerulonephritisRheumatic heartdisease; glomerulonephritis

Supressor cell dysfunction Supressor cell dysfunction the negative feed back the negative feed back control is not there.control is not there.

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ALLOIMMUNITY: Immune system of one ALLOIMMUNITY: Immune system of one individual reacts against antigens of another individual reacts against antigens of another individual: classically mismatched blood individual: classically mismatched blood transfusion reactions, and Hemolytic disease transfusion reactions, and Hemolytic disease of the new born (Rh factor deficiency)of the new born (Rh factor deficiency)

CONGENITAL immune deficiency: CONGENITAL immune deficiency: AgammaglobulinemiaAgammaglobulinemia

HIV as a immune disorder. This is an HIV as a immune disorder. This is an ACQUIRED immune deficiency syndromeACQUIRED immune deficiency syndrome

HIV is a RETRO virus. It carries a RNA which enters HIV is a RETRO virus. It carries a RNA which enters the host cell by combining with a cell surface receptor the host cell by combining with a cell surface receptor and then converts into a DNA. Once inside it may and then converts into a DNA. Once inside it may increase in number.increase in number.

CD4 lies on surface of Helper T cells. HIV attaches to CD4 lies on surface of Helper T cells. HIV attaches to it, enters Helper T cells, and then destroys them.it, enters Helper T cells, and then destroys them. 48

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Some autoimmune Some autoimmune diseasesdiseases

Hashimoto’s Thyroiditis Hashimoto’s Thyroiditis (Hypothyroid disease)(Hypothyroid disease)

Graves Disease (Hyperthryroidism)Graves Disease (Hyperthryroidism) Myasthenia GravisMyasthenia Gravis Multiple SclerosisMultiple Sclerosis Atrophic gastritis Atrophic gastritis

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Resistance of the body to infection: Inflammation