overview of the immune system dr. gamal badr phd in immunology (paris sud university, france)...
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Overview of the Immune system
Dr. Gamal BadrPhD in Immunology (Paris Sud University, France)
Associate Professor of ImmunologyAssiut University, EgyptTel: +2 01110900710Fax: +2 0882344642
E-mails: [email protected] or [email protected] Websites:
http://www.aun.edu.eg/membercv.php?M_ID=393 https://www.researchgate.net/profil/Gamal_Badr/
http://scholar.google.com.eg/citations?hl=en&user=dz13dkQAAAAJ
Topics
Microbes: why they are formidable foes.
Gross anatomy of the immune system
Cells of the immune system
how the immune system protects
Immune recognition of pathogens: innate versus adaptive immunity
Cytokines and the inflammatory response
Pathogen: microbe that causes diseaseAntigen (Ag): material (from a pathogen) that induces an immune response
Immunogen: material that induces an immune response
Innate (natural) immunity: rapid, non specific immune response
Adaptive (acquired) immunity: slower, specific immune responseLeukocytes: WBCs
Lymphocytes: specialized blood cells that mediate adaptive immunity (e.g. T and B cells)
Immunity: Body defense against exogenous(microbes) and endogenous(tumor cells) agents.
Reaction of the body against any foreign Ag.
Immune response
Non specific
Specific
by B- cells
The cells of the immune system are developed in the primary lymphoid organs (bone marrow & Thymus), and they interact with antigens in secondary lymphoid organs (lymph nodes, spleen, addendix, Peyer’s patch etc.).
Lymph nodes: collect antigens from tissues
Spleen: collects antigens from blood stream
Lymphocytes arise in the stem cells in the bone marrow and then differentiate in the bone marrow (B cells) or thymus (T cells).
Organs of the immune system
T and B lymphocytes migrate via the peripheral blood to the peripheral/secondary lymphoid organs: lymph nodes, spleen, addendix, Peyer’s patch etc.
Naïve lymphocytes circulate between the blood and these organs until they encounter antigen. They become activated when they recognized an Ag in the secondary lymphoid organs.
The afferent lymphatic vessels carry APC cells from infected tissues to the lymph nodes where they activate T cells
Activated T cells (after they have undergone proliferation and differentiation) leave via the efferent lymphatic vessels
The cells of the immune system circulate through the body via lymph and blood. Pathogens and their antigens are transported from tissues via lymphatic vessels to the lymph nodes where they encounter immune cells.
QuickTime™ and aTIFF (LZW) decompressorare needed to see this picture.Most blood cells act to fight infection.
Adaptive immunityInnate
immunity
Dentritic cell(DC)
Cells of the immune system
Blood cells lineages
QuickTime™ and aTIFF (LZW) decompressorare needed to see this picture.Lymphocytes of the adaptive immune
systemT helper cells: regulate other immune cellsT cytotoxic (killer) cells: kill infected cells
B cells: produce antibodies (immunoglobulin)DC and macrophage (APC): directly kill microbes by phagocytosis and
other mechanisms. They also help to activate T cells (connection between innate and adaptive immunity)
NK cells are lymphocytes that have characteristics of innate and adaptive immunity.
Dentritic cell(DC)
Antigen presenting cells
(APC)
Antigen (Ag)
Cells of the Immune system (WBCs)
1- Granulocytes Neutrophils Eosinophils Basophils
2- Agranulocytes Lymphocytes
B cells T cells (many types) NK cells
Monocytes/Macrophages Dendritic cells
Divisions of leukocytes
Granulocytes Neutrophils
Band cells (immature neutrophils)
Eosinophils Basophils
AGranulocytes (Mononuclear cells)
Lymphocytes (many types)
Monocytes Dendritic cells
Neutrophils Granulocyte Phagocytes Short life span
(hours) Very important at
“clearing” bacterial infections
Cytoplasmic granules
Eosinophils A granulocyte A cell-killing cells
Orange granules contain toxic compounds
Important in parasitic infections
Basophils A granulocyte A cell-killing cells
Blue granules contain toxic and inflammatory compounds
Important in allergic reactions
Lymphocytes Many types;
important in both humoral and cell-mediated immunity
B-cells produce antibodies
T- cells Cytotoxic T cells Helper T cells
Memory cells NK cells
Benign WBCs Disorders
Leukopenia (Leukocytopenia) - Leukopenia: is a decrease in the number of WBCs Neutropenia is most common cause
Absolute neutrophil count (ANC) < 1.5 x 109 cells/L Many causes
Benign racial neutropenia common African Americans and Yemenite Jews may have ANC as low as 1.0
Viral infections Epstein-Barr, Hepatitis B, HIV
Drugs Careful review of medications ; be suspicious of any medication
recently started in patient with acute onset neutropenia Splenomegaly Autoimmune disorders
SLE (lupus), Rheumatoid Arthritis, etc. Bone marrow disorders
Leukocytosis Leukocytosis: is an increase in the number of WBCs WBC count > 11,000 Determine which type of WBC is leading to the
leukocytosis Neutrophilia = most common
Causes: Infection Connective tissue disorders Medications (especially steroids, growth factors) Cancer Myeloproliferative disorders Cigarette smoking Stress (physiologic)
Pain, trauma Idiopathic (unknown cause)
Leukocytosis Patients with acute bacterial infection often present
with neutrophilia and band formation Bands = young neutrophils
Viral infections are usually associated with low WBCs ; leukocytosis may suggest complications Ex: bacterial pneumonia with underlying
influenza infection
Leukocytosis Lymphocytosis: is an increase in the number or
proportion of lymphocytes in the blood Causes:
Viral infections: HBV, HCV, EBV, CMV Tuberculosis Pertussis Drug Reaction Stress (physiologic): Trauma, cardiac arrest,
etc Malignancy: ALL, CLL, lymphoma
Malignant WBCs Disorders
Types of Hematopoietic Malignancies
Leukemias • Acute leukemias • Acute myeloid leukemia • Acute lymphoblastic leukemia • Chronic leukemias • Chronic myeloproliferative disorders • Chronic lymphoproliferative disorders
Lymphomas • Non-Hodgkin's lymphoma • Hodgkin's disease
Plasma cell disorders • Myeloma
Myeloid vs. Lymphoid Myeloid malignancies
Acute myeloid leukemia Chronic myeloproliferative disorders
Lymphoid malignanciesB-cell malignancies• Acute lymphoblastic leukemia, B-cell type• Non-Hodgkin’s lymphoma, B-cell types• MyelomaT-cell malignancies• Acute lymphoblastic leukemia, T-cell type• Non-Hodgkin’s lymphoma, T-cell typesHodgkin’s disease
Leukemia Leukemia is a type of cancer of the blood or bone
marrow characterized by an abnormal increase of immature WBCs called “blasts".
Leukemia is a broad term covering a spectrum of diseases. In turn, it is part of the even broader
group of diseases affecting the blood, bone marrow, and lymphoid system.
Chronic Leukemia Chronic myelogenous leukemia (CML)
Translocation between long arms of chromosomes
9 and 22 ; “Philadelphia Chromosome” ; bcr/abl
protein
Chronic lymphocytic leukemia (CLL) Clonal malignancy of B-lymphocytes Course is usually indolent ; affects older patients, average age at
diagnosis is 70 years
Acute Leukemia Acute Myelogenous Leukemia (AML)
Most common in adults Usually no apparent cause
Exposure to radiation, benzene, and certain chemotherapy drugs (alkylators) associated with leukemia
Underlying myelodysplastic syndrome (MDS) is risk factor Symptoms and signs
Related to replacement of marrow space by malignant WBCs Patients often very ill for period of just days or weeks Skeletal pain Bleeding Gingival hyperplasia Infection Pancytopenia with circulating blasts is hallmark ; bone marrow
biopsy required Auer rods on peripheral smear are pathognomonic
Lymphoma Hodgkin’s disease
Malignancy of B-lymphocytes Reed-Sternberg cells Various subtypes ; “nodular
sclerosing” is most common Non-Hodgkin’s Lymphoma (NHL)
Heterogeneous group of cancers affecting lymphocytes
Myeloma Malignancy of plasma cells
Abnormal paraproteins are created leading to systemic problems
IgG – 60% IgM – 20%
Primarily disease of elderly (median age 65 years)
Most common hematologic malignancy among African Americans ; #2 among Caucasians
Production of antibodies
TH1
MHC II
B cell
B cell
Pathogen (virus or bacteria)
B cell binds pathogen
Pathogen is internalized
and degraded
Peptides from the pathogen are presented (MHC II) to the T cell resulting in the
activation of the B cell
B cell proliferationB cells differentiate into
antibody-secreting plasma cells
Produce antibodies against pathogen
Plasma cells
Antigen recognition by T-cells
Cytotoxic T cells recognize antigen presented by MHC I and kills the cell
Kills
Cytotoxic T cell
MHC I
TH1 cells recognize antigen presented
by MHC II and activates
macrophages
TH2 cells recognize antigen presented
by MHC II and activates B cells
Activates
TH1
MHC II
Macrophage
Virus-infected
cell
Apoptotic cell
Dead intracellular
bacteria
Activates
TH2
MHC II
B cell
Anti-toxin antibodies
Th1 and Th2 response
To
Th1 Th2
NKMØ
B cell
TcPMN
IFN- IL-4
IL-10
IL-5
IL-6
IL-13
IL-2
TNF-IL-8
Monocytes/Macrophage Monocyte is a
young macrophage There are tissue-
specific macrophages
MØ process antigen, are phagocytes and produce cytokines (esp., IL1 & IL6)
Dendritic cells Found mainly in
lymphoid tissue Function as
antigen presenting cells (APC)
Most potent stimulator of T-cell response
Mechanism of the Immune response
• Physiological barriers at the portal of entry (The Skin & Mucous Membranes)
• Alternative pathway of complement
Mechanisms of Innate Immunity
A. Epithelial Surfaces1. Skin & mucous membrane - protect against
invasion by microbes. Healthy skin - high salt conc. in sweat - sebaceous secretions - long chain fatty acids & soaps Respiratory tract - nose architecture - cough reflex - mucosal secretions - phagocytes in alveoliIntestinal mucosa - mucus , peristalsis
A.Epithelial Surfaces
2. Saliva - inhibits many micro-organisms.3. Gastric acidity - destroys many microbes.4. Conjunctiva - flushing action of lachrymal
secretions. antibacterial substance - present in tissue fluid & all secretions except cerebrospinal fluid (CSF), urine & sweat - also present in phagocytes
A.Epithelial Surfaces
5. Flushing action of urine6. Acidic pH of adult vagina
7. Spermine & zinc in semen is antibacterial.
B. Antibacterial substances in blood & tissues1. Complement system - Alternative pathway of complement leads to opsonization of microbes2. Basic polypeptides – like leukins derived from leucocytes & platelets 3. Lactic acid in muscle & inflammatory zone 4. Lactoperoxidase in milk. 5. Interferons - antiviral
C. Microbial antagonism
- resident flora on skin & mucosa prevent colonization by pathogens.
- altered flora following oral antibiotics may lead to enterocolitis (inflammation of the digestive tract).
D. Cellular factors
1. Phagocytic cells are 2 types - polymorphonuclear (PMN) leukocytes - mononuclear phagocytes: in blood & tissues
monocytes macrophages
Imp. link between innate & acquired immunity
Chemotaxis - phagocytes are attracted to the site of infection by chemotactic factors.
Phagocytosis
This process involves - recognition & binding
- ingestion
- digestion
Requires opsonins - molecules on the surface of certain bacteria which bind to the receptor on phagocytes - Opsonization.
Killing by granulocytes through phagocytosis
Macrophages and neutrophils recognize pathogen by means of cell-surface receptors Example: mannose receptor, CD14 receptor, scavenger receptors,
glucan receptor etc. Binding of macrophage (MØ) or neutrophils with pathogen leads to
phagocytosis Bound pathogen is surrounded by phagocyte membrane Internalized (phagosome) Killing of pathogen (Phagolysosome)
Oxidative burst (synthesis of hydrogen peroxide (H2O2)or free oxygen radicals)
Acidification Antimicrobial peptides (e.g. defensins)
* Phagolysosome = lysosome +phagosome
Phagocytosis
The macrophage expresses receptors for
many bacterial
constituents
Mannose
receptor
LPS receptor (CD14)
Scavenger
receptor
Bacteria binding to macrophage receptors initiate the release of cytokines and small lipid mediators of
inflammation
Lipid mediators
Cytokines
Lysosome
Phagolysosome
Phagosome
Macrophages engulf and digest bacteria to
which they bind
Bacteria
B cell: CD19+T helper cell: CD3+, CD4+ & CD8-T cytotoxic cell: CD3+, CD8+Macrophages/ monocyte: CD14+NK cell: CD3neg, CD16+ & CD56+
CD Structurally defined leukocyte surface molecule that is expressed on cells of a particular lineage (“differentiation”) and recognized by a group (“cluster”) of cell-specific antibodies is called a member of a cluster of differentiation (CD)
Cytokines Cytokines are soluble proteins that are produced in response to an
antigen and function as chemical messengers for regulating the innate and adaptive immunity
Innate immune system Macrophages and Dendritic cells produce:
Tumor necrosis factor-alpha (TNF-) Interleukin-1 (IL-1) Interleukin-12 (IL-12)
Adaptive immune system T-lymphocytes produce:
Interleukin-2 (IL-2) Interleukin-4 (IL-4)
02.10.07 Dr Ekta, Microbiology, GMCA
InvaginationInvagination
phagosome phagosome formationformation
fusion with lysosomefusion with lysosome
phagolysosomephagolysosome
release of lysosomal contentsrelease of lysosomal contents
Process of Phagocytosis
D. Cellular factors
2. Natural killer cells:
Class of lymphocytes important in non- specific defense against viral infections & tumor cells.
Activated by interferons & selectively kills viral infected cells & tumor cells.
Cell killing – NK cells NK cells do not require prior immunization
or activation They attach to ‘target’ cells Produce cytotoxic proteins (perforin &
Granzymes ) onto the surface of tumor or viral infected cells.
Effector proteins penetrate cell membrane and induce programmed cell death (Apoptosis)
Apoptosis: Cellular Suicide
•Nuclear fragmentation•Proteolysis•Blebbing•Death
Remnantsundergo
phagocytosis
Number increases during parasitic infections & allergic conditions.
Not efficient phagocytes but their granules contain molecules that are toxic to parasites.
E. Temperature - Many micro- organisms are temperature dependent e.g. tubercle bacilli,
pathogenic to mammals, do not infect cold-blooded animals.
- destroys infecting pathogen : e.g. fever induction used to destroy Treponema pallidum before penicillin became available for treatment.
D. Cellular factors
2. Eosinophils:
F. Inflammation
“Inflame” – to set fire. Inflammation is “A dynamic response of vascularised tissue to injury.” It is a protective response. It serves to bring defense & healing mechanisms to the site of injury. A type of non specific defense mechanism. Tissue injury or irritation caused by the entry of pathogens or other irritants lead
to inflammation. Events: that occur are – vasoconstriction followed by vasodilatation
- Increased vascular permeability, stasis, hyperemia, accumulation of
leukocytes, exudation of fluid, and deposition of fibrin.
Changes are brought about by chemical mediators like histamine. Signs : redness, heat, swelling, pain and lose of function.
Cardinal Signs of Inflammation
Redness : Hyperaemia (increase of blood
flow to different tissues).
Warm : Hyperaemia
Pain : Nerve, Chemical mediators. Swelling : Exudation (escape of fluid,
cells, and cellular debris from blood vessels and their deposition in tissues)
Loss of Function
Process of Inflammation
Innate vs. adaptive immunity
Innate immunity First line of defense (present in all individuals at all
times) Immediate (0 – 4 hours) Non-specific Does not generate lasting protective immunity
Adaptive immune response (late: > 96 hours) Is initiated if innate immune response is not adequate
(> 4 days) Antigen-specific immunity Generates lasting protective immunity (e.g.
Antibodies, memory T-cells)
Adaptive, Acquired, Specific immunity
Acquired Immunity
Passive Active
Cell mediated immunity Humoral Immunity
By T cell activation By B cell activation& production of Abs
Adaptive immune system Initiated by ingestion of pathogen by an
immature dentritic cell Antigen-presenting cell (APC)
Dendritic cells, macrophages, and B cells Migrate through lymph to the regional lymph nodes Interact with naive T lymphocytes (present antigen to
activate T cells) Proliferation Differentiation
Active and passive immunity
Active immunity: long-lasting protection (memory), multiple effector mechanisms activated, lag time
Passive immunity: rapid protection, short duration
Active Immunity Resistance developed by an individual as a
result of an antigenic stimulus.
Also called Adaptive immunity.
Involves active functioning of the host’s immune system leading to the synthesis of antibodies and / or the production of immunologically active cells.
Passive Immunity Resistance transmitted to a recipient in a
readymade form.
Preformed antibodies are administered.
No antigenic stimulus.
Host’s immune system is not actively involved.
Comparison of Active & Passive Immunity
Active immunity Produced actively by host’s
immune system Induced by infection or by
immunogen Durable effective protection Immunity effective only after
long period Immunological memory present
Booster effective Not applicable in the
immunodeficient
Passive immunity Received passively, no active
host participation Readymade antibody transferred
Transient, less effective Immediate immunity
No memory
Not effective Applicable in the immunodeficient
Active immunity Natural active immunity – results from an
infection by a parasite e.g. an attack of measles give lifelong immunity.
Artificial active immunity – resistance induced by vaccines.
Vaccines are preparations of live or killed micro- organisms or their products.
Passive immunity
Natural passive immunity – resistance passively transferred from mother to baby
Artificial passive immunity – resistance passively transferred by the administration of readymade antibodies. e.g. tetanus immunoglobulin
Lymphocytes (effector cells of the adaptive immune system)
Antigen receptors with single specificity (T and B cells) Gene re-arrangement
T and B cells have 2 distinct recognition systems for detecting pathogens
T cells - recognize intracellular pathogens (T cell receptors, TCR)
B cells – recognize extracellular pathogens (immunoglobins, BCR)
Clonal selection Interaction of antigen and lymphocyte receptor Activation of lymphocyte Differentiation (progeny with identical specificity)
Cell mediated immunity: Antigen recognition by T-cells
T cells detect presence of intracellular pathogens T cells receptors Peptide fragments Major histocompatibility complex (MHC)
MHC I (cytotoxic T cells /CD8) MHC II (T helper (1 and 2)/ CD4)
Cell death
Cell mediated immunity: Antigen recognition by T-cells
Cytotoxic T cells recognize antigen presented by MHC I and kills the cell
Kills
Cytotoxic T cell
MHC I
TH1 cells recognize antigen presented
by MHC II and activates
macrophages
TH2 cells recognize antigen presented
by MHC II and activates B cells
Activates
TH1
MHC II
Macrophage
Virus-infected
cell
Apoptotic cell
Dead intracellular
bacteria
Activates
TH2
MHC II
B cell
Anti-toxin antibodies
Antigen presenting cells (APC)
Dendritic cell
Macrophages
B cell
Antigen-presenting cells are distributed differentially in the lymph node
An antigen-presenting cell (APC) or accessory cell is a cell that displays foreign Ag complexe with major histocompatibility complexes (MHC) on their surfaces. T cells may recognize these complexes using their T cell receptor (TCR). These APC engulf and process antigens and present them on their surface to T-cells.
Lymph node Lymph node Lymph node
MMM
MMM
Listeria
Listeria
Where does antigen processing take place?
M
M
Incubate with CHLOROQUINE
TAdd Listeriaspecific T cells
T CELLS BIND
NO T CELLS BINDChloroquine inhibits lysosomal function (a lysosomotrophic drug)
Antigen processing involves the lysosomal system
Ag presentation to T cells
The T cell antigen receptor (TCR)
Carbohydrates
Hinge
Monovalent
Resembles an Ig Fab fragment
Fab
Fc
No alternative constant regions
Transmembrane region
Never secreted
Domain structure: Ig gene superfamily
Heterodimeric, chains are disuphide-bonded
Cytoplasmic tail
Very short intracytoplasmic tail++
+Positively charged amino acids in
the TM region
Antigencombining site
Antigen combining site made of juxtaposed V and V regions
T cell co-receptor (TCR) molecules
CD8
MHC Class I MHC Class II
CD4
CD4 and CD8 can increase the sensitivity of T cells to peptide antigen MHCcomplexes by ~100 fold
Ag
Th1 and Th2 response
To
Th1 Th2
NKMØ
B cell
TcPMN
IFN- IL-4
IL-10
IL-5
IL-6
IL-13
IL-2
TNF-IL-8
TCR and BCR (B cell Receptor)
Humoral Immunity
It is the production of proteins called “immunoglobulin's” or “antibodies”.
.
Memory (long-lived cells).
Humoral ImmunityHumoral ImmunityB Cell Receptors for AntigensB Cell Receptors for Antigens
B cell receptors Bind to specific, intact antigens Are often called membrane antibodies or membrane
immunoglobulin's (Ig)Antigen-binding
site
Antigen-binding site
Disulfidebridge
Lightchain
Heavy chains
Cytoplasm of B cell
VA B cell receptor consists of two identical heavy chains and two identical light chains linked by
several disulfide bridges.
(a)
Variableregions
Constantregions
Transmembraneregion
Plasmamembrane
B cell
V
V
C
C C
C
V
WHAT ARE ANTIBODIES?
Antigen specific proteins produced by plasma cells Belong to immunoglobulin (Ig) superfamily Located in blood and extravascular tissues, secretions and
excretions Bind pathogenic microorganism and their toxins in extracellular
compartments
Structural configuration of Antibody
Domains:Variable (V)
Single V domain in H and L chains
Constant (C)Single C domain in L chainsThree to four (C) domains in H chains
Chains:Light (L)Heavy (H)
CLASSES (ISOTYPES) OF IMMUNOGLOBULINS
Classes based on constant region of heavy chains Immunoglobulin A (IgA) alpha heavy chains
Immunoglobulin D (IgD) Delta heavy chains
Immunoglobulin E (IgE) Epsilon heavy chains
Immunoglobulin G (IgG) Gamma heavy chains
Immunoglobulin M (IgM) Mu heavy chains
Differentiation of heavy chains Length of C region, location of disulfide bonds, hinge region, distribution of
carbohydrate Classes have different effector functions
Different classes of Antibodies
Immunoglobulin ClassesImmunoglobulin Classes
IgG
Structure: Monomer Percentage serum antibodies: 80% Location: Blood, lymph, intestine Half-life in serum: 23 days Complement Fixation: Yes Placental Transfer: Yes (the only Ig) Known Functions: Enhances phagocytosis, neutralizes
toxins and viruses, protects fetus and newborn.
Immunoglobulin ClassesImmunoglobulin Classes
IgM
Structure: Pentamer Percentage serum antibodies: 5-10% Location: Blood, lymph, B cell surface (monomer) Half-life in serum: 5 days Complement Fixation: Yes Placental Transfer: No Known Functions: First antibodies produced during an
infection. Effective against microbes and agglutinating antigens.
Immunoglobulin ClassesImmunoglobulin Classes
IgAIgA
Structure: Dimer Percentage serum antibodies: 10-15% Location: Secretions (tears, saliva, intestine, milk), blood
and lymph. Half-life in serum: 6 days Complement Fixation: No Placental Transfer: No Known Functions: Localized protection of mucosal
surfaces. Provides immunity to infant digestive tract.
Immunoglobulin ClassesImmunoglobulin Classes
IgD
Structure: Monomer Percentage serum antibodies: 0.2% Location: B-cell surface, blood, and lymph Half-life in serum: 3 days Complement Fixation: No Placental Transfer: No Known Functions: In serum function is unknown.
On B cell surface, initiate immune response, discriminate between naïve (IgD+), memory (IgD neg) and plasma cells (IgD neg)
Immunoglobulin ClassesImmunoglobulin ClassesIgE
Structure: Monomer Percentage serum antibodies: 0.002% Location: Bound to mast cells and basophils throughout
body. Blood. Half-life in serum: 2 days Complement Fixation: No Placental Transfer: No Known Functions: Allergic reactions. Possibly lysis of
worms.
B
B
2. Binding and internalisation via Ig induces expression
of CD40
3. Antigen enters exogenous antigenprocessing pathway
4. Peptide fragments of antigen are loadedonto MHC molecules intracellularly.
MHC/peptide complexes areexpressed at the cell surface
B cells act as APC
1. Capture by antigenspecific Ig maximises
uptake of a single antigen
YYY
T cell help to B cells
B
Signal 1antigen & antigen
receptor
Th
1. T cell antigen receptor
2. Co-receptor (CD4)
3.CD40 Ligand
Th
Signal 2 - T cell help
MHC class II
Clonal SelectionClonal Selection
Only one type of Only one type of antibody—and one antibody—and one
type of B cell—type of B cell—responds to the responds to the
antigenic determinantantigenic determinant
That cell type That cell type then produces a then produces a large number of large number of
clonesclonesDr.T.V.Rao MD 93
Primary
Secondary
Benefits of Immunological MemoryBenefits of Immunological Memory
Latent periodGradual rise in Ab production taking days to weeks
Second exposure to same Ag.Memory cells are a beautiful thing.Recognition of Ag is immediate.Results in immediate production of protective antibody, mainly IgG but may see some IgM