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224 Cards in this Set

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Mechanical Epithelial Barriers Part of Innate Immunity:
-Tight Junctions
-"Cleansing" Mechanisms
Mucous Membranes
Skin
Cornea&Conjunctiva
These mechanical barriers are located between Epithelial Cells and are the First means for Exclusion of Pathogens:
Tight Junctions
These Mechanical Barriers are located at certain Epithelial surfaces to limit Colonization:
-Examples:
-"Cleansing" Mechanisms
Skin
Cornea & Conjunctiva
Tears&Lashes
Mucosa:
GIT
Respiratory Tract
Female Repro Tract
Function of the Skin as a "Cleansing" Mechanism at certain epithelial surfaces to limit Colonization:
Desquamation (Shedding of outer layers of the Skin)
Function of the Gastrointestinal Tract as a "Cleansing" Mechanism:
-Mucus traps incoming particles & facilitates their removal
-Peristalsis
Function of the Respiratory Tract as a "Cleansing" Mechanism:
-Mucus
-Ciliated Epithelium (Mucociliary Transport)
(Traps Large particles Before
they can reach the Lungs)
Antibodies are part of which Immunity?
Adaptive Immunity
Which class of Antibodies are most commonly found at Epithelial Surfaces?
IgA
Where are Phagocytic cells Located?
-May be present at some Epithelial Surfaces
(Ex: In the Lungs, Alveolar Macrophages are in Direct Contact with Air)
Where in the Epithelia are Macrophages present?
Lamina Propria
How do Normal Microbial Flora at certain Epithelial Surfaces Inhibit Establishment of new organisms?
-Competing for Nutrients & Space
-Releasing Antimicrobial Substances
5 Examples of Impaired Barrier Function:
-Breaks in Epidermis (Trauma)
-"Dry Eye" (Keratitis Sicca)
-Ileus (a loss of Peristalsis)
-Changes in Normal Microbial Flora of GIT
-Primary Viral Infection of the Trachea & Bronchi
3 Consequences of "Dry Eye" (Keratitis Sicca):
-Reduction of:
Tear Production
Mechanical Cleansing
Antimicrobial substances
bathing the Cornea
Causes and Consequences of "Ileus" (Loss of Peristalsis):
-Following Abdominal Surgery
-Overgrowth of Intestinal Microbial Flora
-Crossing of Intestinal Bacteria into the Bloodstream
Consequence of a Primary Viral Infection of the Trachea & Bronchi:
-May predispose to Secondary Bacterial Infection by Damaging MUCOCILIARY TRANSPORT
NEUTROPHIL:
-Classification?
-Aka?
-Normal Location?
-Recruited into Inflammed Tissues?
-Lifespan?
Functions?
-Professional Phagocyte
-Polymorphonuclear Phagocyte
-Blood
-Yes(EARLY)
-Short
FXNS:
PAMP/DAMP Recognition
Signaling Molecules (some)
Pathogen Destruction
MACROPHAGE:
-Classification?
-Aka?
-Normal Location?
-Recruited into Inflammed Tissues?
-Lifespan?
Functions?
-Professional Phagocyte
-Mononuclear Phagocyte (Many other names depending on tissue)
-ALL Body Tissues (Monocytes in Blood)
-Yes (LATE)
-Long
FXNS:
Sentinel
PAMP/DAMP Recognition
Signaling Molecules
Cell-Cell Communication
Pathogen Destruction
3 Phases of Phagocytosis & Killing:
1. Recognition & Attachment
2. Internalization
3. Killing/Destruction
What happens during 2nd Phase of Phagocytosis?
-Internalization
-Plasma Membrane envelopes the Pathogen
-Pathogen enclosed in a Membrane-Bound Vacuole called a "Phagosome"
3 Types of Killing/Destruction:
-Oxygen-Independent
-Oxygen-Dependent
-Nitric Oxide-Dependent
What substances are responsible for O2-Dependent Phagocytosis?
-Antimicrobial Constituents of Lysosomes
In what form are Lysosomes in within ALL cells?
In Professional Phagocytes, what are Lysosomes especially loaded with?
-Vacuoles
-Antimicrobial Substances
Defensins
Lysozyme
Proteases
many more
What molecules are responsible for O2-Independent Phagocytosis?
Reactive Oxygen Intermediates (ROI)
When are ROI Generated?
During the Respiratory Burst
What is a Respiratory Burst?
A NEW Metabolic Pathway in which molecular O2 is converted to Reactive forms that can damage Microorganisms (and the animal's own tissues)
What are the Most Lethal ROI?
-Superoxide Radical (O2-*)
-Hypochlorite (HOCl*)
-Hydroxyl Radical (OH*)
What molecules are responsible for NO-Dependent Phagocytosis?
Nitric Oxide Radicals (NO*)
Where are NO Radicals generated?
In Macrophages that have been activated by INF-y
EOSINOPHILS:
-Phagocytic Capacity?
-Most Commonly Associate with?
-Types of Receptors?
-Functions?
-Yes
-Defense against Helminth Larvae migrating thru Tissues & with some Protozoa
-Fc Receptors for IgE & IgG
FXNS:
-Antibody-Dependent Cellular
Cytotoxicity (ADCC)
-Generate Oxygen
Intermediates
Regarding Eosinophils, describe the process of ADCC:
-Bind to Parasites coated with IgE & IgG (Abs)
-Release their Lysosomal contents onto the Surface of the Parasite
The ONLY Class of Lymphocytes that are a part of the Innate Immune System?
Natural Killer (NK) Cells
NK CELLS:
-Aka?
-Normal Location?
-Recruitment?
-Large Granular Lymphocytes (LGLs) (b/c of Appearance)
-Tissues
-Recruited to Inflammed tissues from the Blood
NK Cell Recognition System:
-Receptors that Activate NK cells recognize?
-Receptors that Inhibit NK cells recognize?
ACTIVATE NK:
-Stressed Cells
-IgG
INHIBIT NK:
-Normal Proteins on ALL
cells (a form of MHC Class I
Molecules)
Disposal Functions of NK cells:
Kill Cells:
-Infected w/ INTRAcellular
Parasites (Not allowing
them to Replicate)
-That have been Genetically
Transformed (Cancer)
-Secrete INF-y (Activates Macrophages)
4 Fates of NK cells:
1) NO MHC Class I & NO Activating Ligands = NO Response
2)MHC Class I binds Inhibitory Receptor & NO Activating Ligands = NO Response
3)NO MHC Class I & Activating Ligands bind Activating Receptor = NK Attacks Target Cell
4)MHC Class I Binds Inhibitory Receptor & Activating Ligands Bind Activating Receptor = Outcome determined by Balance of Signals
3 Locations of Complement Proteins:
-Plasma
-Interstitial Fluids
-Most Secretions
3 Pathways for Complement Activation:
1) Alternative
2) Lectin
3) Classical
The Alternative Pathway for Complement Activation is Activated by:
-Microbial Cell Walls
-Basement Membranes
The Lectin Pathway for Complement Activation is Activated by:
-Collectins (C-Reactive Proteins, Mannan-Binding Lectin)
The Classical Pathway for Complement Activation is Activated by:
IgG or IgM Abs Bound to Antigens
5 Essential Complement Functions:
1) Mast Cell Activation
2) Chemotaxis
3) Opsonization
4) Microbial Killing (Pore Formation)
5) Enhance Antibody Production
Effect & Mediator of Mast Cell Activation:
-Initiates Inflammation
-C3a, C5a
Effect & Mediator of Chemotaxis:
-Recruits Neutrophils
-C5a
Effect & Mediator of Opsonization:
-Facilitates Phagocytosis
-C3b
Effect & Mediator of Microbial Killing (Pore Formation):
-Membrane Attack Complex
-C5b678(9)n
Effect & Mediator of Enhancing Antibody Production:
-Further Activates B Cells
-C3b
4 Kinds of Cell Signaling:
-Juxtacrine Signaling
-Autocrine Signaling
-Paracrine Signaling
-Endocrine Signaling
Type of Cell signaling where signaling molecules are located in the plasma membrane of a cell & require direct contact for signaling?
Juxtacrine Signaling
Type of Cell Signaling where Signaling Molecules are released by a cell and act on the SAME cell?
Autocrine Signaling
Type of Cell Signaling where Signaling Molecules are released by a cell and act on NEARBY cells?
Paracrine Signaling
Type of Cell Signaling where Signaling Molecules are released by a cell and act on cells in other parts of the body?
Endocrine Signaling
Intercellular signaling molecules:
-Regulation?
-Half-Life?
-Fate?
-Highly regulated to ensure that they are only active when needed
-Short (Most)
FATE:
-Removed after acting on another cell
-Degradation by Enzymes
Protein Signaling Molecules:
-CYTOKINES
-Chemokines
-Hematopoietic Cytokines
-Inflammatory Cytokines
-Antiviral Cytokines
-Immunologic Cytokines
Term that describes Cytokines as having multiple actions on multiple cell types?
Pleiotropic
Characteristic of Cytokine actions?
-Highly Redundant (More than one Cytokine may have the SAME function)
Hematopoietic Cytokines:
-Function?
-Subtypes?
-Promote Growth & Maturation of Blood Cells
-G-CSF & others
Inflammatory Cytokines:
-Function?
-Subtypes?
-Regulate Inflammation
-IL-1
-IL-6
-TNF-a
-IFN-y & others
Antiviral Cytokines:
-Function?
-Subtypes?
-Increase the Resistance of Cells to Viral Infection
-The Interferons
Immunologic Cytokines:
-Function?
-Subtypes?
-Regulate ADAPTIVE Immune Responses
-IL-2
-IL-4 & others
A group of Cytokines characterized by their capacity to Form Colonies of Cells in Culture dishes?
Colony-Stimulating Factors (CSF)
Where do CSF arise from?
-Leukocyte Stem Cells found in Bone Marrow
Subtypes of CSF:
-G-CSF (Granulocytes)
-M-CSF (Macrophages)
-GM-CSF (Combination of Both)
What cells do CSFs Activate & Generate?
-Neutrophils
-Macrophages
2 Things that limit Therapeutic use of Cytokines or Cytokine Inhibitors?
-Toxic at High Doses
-Limited Availability of Animal Cytokines
CYTOKINE:
G-CSF:
-Type?
-Souce?
-Action?
-Hematopoietic
-Macrophages+
-Promotes Neutrophil Production from Bone Marrow
CYTOKINE:
IL-1, IL-6, TNF-a:
-Type?
-Souce?
-Action?
-Inflammatory
-Macrophages ++
-Pro-Inflammatory Cytokines
-Induce Acute-Phase Responses
CYTOKINE:
IFN-a, IFN-B, IFN-w:
-Type?
-Souce?
-Action?
-Antiviral
-Most Cells
-Antiviral
-Promote Adaptive Immunity
CYTOKINE:
IFN-y:
-Type?
-Souce?
-Action?
-Inflammatory, Antiviral, Immunologic
-T Cells & NK Cells
-Activates Macrophages
CYTOKINE:
IL-2:
-Type?
-Souce?
-Action?
-Immunologic
-T Cells
-Promotes Proliferation of T Lymphocytes
CYTOKINE:
IL-4:
-Type?
-Souce?
-Action?
-Immunologic
-Th2 Cells
-Promotes IgE secretion by B Lymphocytes
CYTOKINE:
IL-5:
-Type?
-Souce?
-Action?
-Immunologic
-Th2 Cells
-Recruits & Activates Eosinophils
CYTOKINE:
IL-10, TGF-B:
-Type?
-Souce?
-Action?
-Immunologic
-Many Cells including Treg
-Inhibit Inflammatory & Adaptive Immune Responses
Which Cytokine is used to increase Neutrophil counts in dogs treated with certain Anti-Cancer agents?
G-CSF
In Europe & Japan, Which Cytokine is labeled for treatment of some Viral Infections in cats?
IFN-w
Which Cytokine is occasionally used in the US for to treat Human Viral Infections?
IFN-a
(Evidence for a beneficial effect is very weak)
Which Cytokine has WEAK Antiviral Activity?
IFN-y
Which Cytokines are important for Allergic Reactions & Defenses against Helminths & Arthropod Larva?
IL-4
IL-5
Inflammation is considered part of which Immunity?
May also be triggered by?
Innate
Adaptive Immune Responses
What 2 things help initiate Adaptive Immune Responses?
-Inflammatory Stimuli
-Cytokines
3 Microvascular Processes in Acute Inflammation:
-Vasodilation
-Increased Vascular Permeability
-Leukocyte Emigration
VASODILATION:
-Description?
-Functional Role?
-Mechanism?
-Chemical Mediators?
-Small Blood vessels Dilate
-Increases blood flow to the site of infection
-Relaxation of pre-capillary Sphincter in Arterioles
CHEMICAL MEDIATORS:
-Histamine
-Serotonin
-PGE2
INCREASED VASCULAR PERMEABILITY:
-Description?
-Functional Role?
-Mechanism?
-Chemical Mediators?
-Small Blood vessels allow fluid&proteins to escape into Interstitial Fluids
-Recruitment of Antimicrobial Plasma Proteins (Complement, Abs, etc.) to site of infection
-Gaps between Endothelial Cells
-Histamine
Leukocyte Emigration from small blood vessels into interstitium?
Diapedesis
In Diapedesis, what is the order of specific Leukocytes Emigrating?
-Neutrophils migrate EARLY
-Monocytes & Lymphocytes migrate LATER
What is the Functional Role of Leukocyte Emigration?
Recruitment of Phagocytes to site of infection
3 Steps involved in Leukocyte Emigration:
1. Adhesion to Endothelium
2. Diapedesis
3. Chemotaxis
What Chemical Mediators are involved in Leukocyte Adhesion to Endothelium?
-Histamine
-Serotonin
-IL-1
-TNF-a
What Chemical Mediators are involved in Chemotaxis during Leukocyte Emigration?
-Chemokines
-C5a
-Leukotriene B4
-Bacterial Peptides
Pattern Recognition Receptors (PRRs):
-Recognize?
-Normal Location?
-PAMPs of microbial agents
-DAMPs released from stressed or dead Host Cells
LOCATION:
-Plasma Membrane
-Cytoplasm
-Free molecules in Plasma
or Tissue
2 Soluble Recognition Molecules:
-Certain Complement Proteins (of the Alternative Pathway)
-Collectins (that activate the Lectin Pathway)
3 Classes of PAMPs:
-Viruses
-Bacteria
-Fungi
In Viruses, what are the 3 specific PAMPs?
-cytoplasmic RNA (esp. dsRNA)
-Certain sequences of Viral DNA
-Certain Viral Proteins
In Bacteria, what are 5 specific PAMPs?
-Lipopolysaccharide (LPS)
-Peptidoglycan
-certain sequences of Bacterial DNA
-Surface Mannose&other sugar
-Flagella
In Fungi, what are 2 specific PAMPs?
-Surface Mannose&other sugar
-Chitin
2 Features of Infection the Host Recognizes:
-Presence of Strangers (PAMPs)
-Presence of Danger (DAMPs)
What Cells detect PAMPs & DAMPs & release Mediators to initiate Inflammation & Recruit Phagocytes & Plasma-borne Substances?
Sentinel Cells
4 Types of Sentinel Cells:
-Epithelial Cells
-Macrophages
-Dendritic Cells
-Mast Cells
A specialized Tissue cell that has long, slender branching cytoplasmic processes specialized to capture Antigens & Initiate the Adaptive Immune Response?
Dendritic Cells
What tissue cells contain specialized Granules that store some of the key Mediators of Inflammation?
Mast Cells
9 Inflammatory Mediators:
-Histamine
-Serotonin
-PGE2
-IL-1
-TNF-a
-Chemokines
-Leukotriene B4
-Bacterial Peptides
HISTAMINE:
-Function?
-Source?
-Inhibitors?
-Vasodilation
-Mast Cells
-Antihistamines
SEROTONIN:
-Function?
-Source?
-Inhibitors?
-Increase Vascular Permeability
-Mast Cells
-Glucocorticoids
PGE2:
-Function?
-Source?
-Inhibitors?
-Enhances Vasodilation
-Mast Cells & Macrophages+
-NSAIDs & Glucocorticoids
IL-1:
-Function?
-Source?
-Inhibitors?
-Induce Endothelial Adhesion Molecules
-Mast Cells
-Glucocorticoids
TNF-a:
-Function?
-Source?
-Inhibitors?
-Induce Endothelial Adhesion Molecules
-Macrophages+
-Glucocorticoids
CHEMOKINES:
-Function?
-Source?
-Inhibitors?
-Chemotaxis
-Many Cells
-Glucocorticoids
C5a:
-Function?
-Source?
-Inhibitors?
-Chemotaxis
-Complement Activation
-Glucocorticoids
LEUKOTRIENE B4:
-Function?
-Source?
-Inhibitors?
-Chemotaxis
-Mast Cells & Macrophages+
-NSAIDs (some) & Glucocorticoids
BACTERIAL PEPTIDES:
-Function?
-Source?
-Inhibitors?
-Chemotaxis
-Bacteria
What Inflammatory Mediators are Inhibited by Glucocorticoids?
-ALL (SANS Histamine & bacterial peptides)
2 Disposal Mechanisms in Inflammation:
-Phagocytosis & Killing by Professional Phagocytes
-Complement-Mediated Lysis
Order in which Professional Phagocytes act at site of Infection:
-Tissue Macrophages (Immediately)
-Recruited Neutrophils (later)
-Recruited Macrophages (even later)
During Acute-Phase Response to Inflammation:
Inflammatory Cytokines:
-Which ones?
-Released from?
-Act Where?
IL-1
IL-6
TNF-a
-From Macrophages +
ACT:
-Locally & at Distant Sites:
CNS
Liver
Bone Marrow
Which cells Synthesize Acute-Phase Proteins?
Hepatocytes
5 Functions of Acute-Phase Proteins:
-Amplify Host Defenses
-Recognition of PAMPs
-Microbial Killinig
-Regulate Host Defenses
-Assist in Tissue Repair
2 APPs associated with Recognition of PAMPs:
-Mannan-Binding Lectin (A Collectin)
-C-Reactive Protein (CRP)
2 APPs responsible for Microbial Killing:
-C3
-C4
How do APPs Regulate Host Defenses?
Limit inflammation to site of infection
APP that assists in Tissue Repair:
Fibrinogen
(Measured in Horses when an inflammatory condition is suspected)
Biomarkers of Infection & Acute Inflammation in veterinary medicine?
Acute-Phase Proteins
(APPs)
4 Major APPs:
-Serum Amyloid A (SAA)
-C-Reactive Protein (CRP)
-Haptoglobin (Hp)
-Major Acute Phase Protein (MAP)
Major APPs in:
-Cat?
-Dog?
-Horse?
-Cow?
-Pig?
Major APPs:
-SAA
-SAA, CRP
-SAA, Hp
-SAA, CRP, MAP
Term for Elevated White Blood Cell Count?
Leukocytosis
Leukocytosis is most commonly due to elevation of which Leukocyte Count?
-Neutrophil
-Term for Elevated Neutrophil Count?
Neutrophilia
Mechanism responsible for Leukocytosis?
Macrophage Synthesis of Hematopoietic Cytokines that Stimulate Production & Release of Neutrophils from Bone Marrow
As a Negative Feedback Mechanism, Inflammatory Cytokines also do what?
Trigger release of Cortisol from the Adrenal Cortex
-Most common components of Antigens:
-Proteins
-Polysaccharides
(Lipids & Nucleic acid do but arent good Antigens)
2 Features of a "Good" Antigen:
1. Large Size
2. Molecular Complexity
2 Important Determinants of the ability of an Antigen to induce an Adaptive Immune Response:
-Dose
-Route of Administration
What are comprised of many Antigens?
Infectious agents
Which Antigens have more than one Epitope?
Protein Antigens (Especially)
In an Infection, Which Immune response sees many Epitopes?
Adaptive Immune Response
What is the Action of an Individual Epitope?
Each Epitope may Activate one or more Lymphocyte
4 Key Features of Lymphocytes that distinguish them from other Leukocytes:
-Circulation from Blood to Lymphoid Tissues&Back
-Individual, Specific Antigen Receptors in Plasma Membrane
-Clonal Proliferation
-Confer Memory to Adaptive Immune System
What happens to a Lymphocyte when it is activated by contact with an Antigen?
Clonal Proliferation
2 Major Classes of Lymphocytes in Adaptive Immunity:
B&T
2 Subdivision of T Lymphocytes based on the exact nature of their Antigen Receptor:
-Tαβ
-Tγδ
Tαβ Lymphocytes are further subdivided based on their:
1. Function
2. Expression of Functional Surface Molecules
2 Subdivisions of Tαβ Lymphocytes Based on their Function and Expression of Functional Surface Molecules:
-CD4
-CD8
B LYMPHOCYTES:
-Function?
-Antigen Receptor?
-Identifying Surface Molecules?
-Microanatomic Location in Secondary Lymphoid Tissues?
-Secrete Abs (Immunoglobulins)
-Membrane form of Immunoglubulin (mIg or BCR)
-CD79a and CD79b (aka Igα & Igβ)
-Follicles (Nodules)
3 Subdivisions of T Lymphocytes based on their Action:
1. Helper T Lymphocytes (Th)
2. Cytotoxic T Lymphocytes (Tc or CTL)
3. Regulatory T Lymphocytes (Treg)
4 Major Types of Th Lymphocytes based on which cells they Activate:
1. Type 1 (Th1)
2. Type 2 (Th2)
3. Type 17 (Th17)
4. Follicular Helper (Tfh)
Action of Th Lymphocytes:
-Help, or augment, Adaptive Immune Responses by Activating other Leukocytes.
Th1 activates:
Macrophages
Th2 Activates:
Eosinophils
Th17 Activates:
Neutrophils
Tfh Activates:
B Lymphocytes
Function of Tc Lymphocytes:
Kill cells that express Antigens of INTRAcellular Pathogens
2 Functions of Treg Lymphocytes:
-Inhibit Adaptive Immune Responses
-Help to avoid Immune Responses to "Self Antigens"
Antigen Receptor on all T Lymphocytes:
T-Cell Receptor (TCR)
Identifying Surface Molecules on all T Lymphocytes:
CD3
Identifying Surface Molecules on all Th Lymphocytes:
CD4
Identifying Surface Molecule on Tc Lymphocytes:
CD8
Microanatomic Location of all T Lymphocytes in Secondary Lymphoid Tissue:
Diffuse Tissue
What are used to classify Leukemias and Lymphomas in People & Dogs?
Surface Markers:
Immunoglobulin
CD3
CD4
CD8
CD79 ++
In Dogs, Which Lymphomas have a Poorer Prognosis?
T Cell Lymphomas (CD3)

as opposed to B Cell Lymphomas (CD79)
Term for Lymphocytes that have not previously been recognized & antigens been activated:
Naive Lymphocytes
Which Lymphocytes have different Circulation Patterns?
Effector Lymphocytes
Which Lymphocytes tend to return to the type of Lymphoid Tissue in which they were First Activated?
Memory Lymphocytes
2 Methods of Administration of Vaccines:
-Mucosal Sites (Intranasal)
-Systemic
Which method of vaccine administration provides better Local Immunity?
-Given at Mucosal Sites (For Mucosal (Respiratory/GIT) Infections esp)
Which method of vaccine administration provides a longer duration of Immunity?
Systemic
The Immunoglobulin molecule in B Lymphocyte Antigen receptors (BCR) consist of:
2 Peptide Chains:
-Heavy Chain
-Light Chain
TCRαβ is comprised of:
2 Peptide Chains:
-α
-β
(Encoded on different
Chromosomes)
TCRγδ is comprised of:
2 Peptide Chains:
-γ
-δ
(Encoded on Different
Chromosomes)
How many Antigen Receptors does each Lymphocyte (Both T & B) express in its membrane?
ONE
Since each lymphocyte (Both T & B) expresses a SINGLE Antigen Receptor in its Membrane, How Many Antigens does each Lymphocyte Respond to?
ONE
(or Cross-Reacting Antigens)
2 Regions in Each Peptide Chain that are a Common feature of Immunoglobulins & TCRs:
-Constant Region
-Variable Region (Unique to each receptor)
Which Region of the Peptide Chain Recognizes (Binds to) Antigens?
Variable Region
How many Gene Segments are encoded in the Variable Regions of All Receptor Peptide Chains?
2-3
In what cells are the 2-3 Gene Segements encoded in the Variable Regions of All Receptor Peptide Chains Rearranged in? What do they Form?
-Lymphocyte Precursors
-A Functional Exon
-How many copies of each Gene Segment are Present?
-Multiple
-How Many Copies of each Gene Segment is incorporated into a Functional Exon for the Variable Region?
ONE
What is responsible for generation of many different Variable Regions?
Combinatorial Selection of Gene Segments
3 Gene Segments of the Variable Region of the Ig Heavy Chain:
-V Gene Segments
-D Gene Segments
-J Gene Segments
During rearrangement of the chromosomes, at which Site within the Variable Region of the Ig Heavy Chain are additional bases Added&Others Removed?
Joining Sites
How Many Potential Immunoglobulin Antigen Binding Sites are there?
>10^13
What is the Total Diversity for Both TCRαβ and TCRγδ?
>10^15
Type of disease in Arabian foals due to an inability to splice chromosomes together following strand breaks such as those required to generate functional Variable Region Genes?
Inherited Immunodeficiency
Consequence of Inherited Immunodeficiency in Arabian Foals?
Can NOT Synthesize Antigen Receptors &
Completely LACK T & B Cells
Do Abs or TCRs bind Directly to Antigens?
Abs
How are Antigens Presented to TCRs?
Major Histocompatibility Complex (MHC) Molecules
Which Lymphocytes are specialized to recognize Antigens that are inside of other cells?
T Cells
Which molecules have a groove/Peptide-Binding Cleft at their Tip into which small antigenic peptides can fit?
MHC Molecules
MHC CLASS I:
-Structure?
-# Genes Per Species?
-Normally Expressed by?
-Present Antigens To?
-Antigens Presented?
- α2 - α1
α3 - β2 + Microglobulin Subunits
-2-3
-ALL Nucleated Cells
-CD8 T Lymphocytes
Synthesized INSIDE the cell:
-Viral Antigens
-Intracellular Parasites
MHC CLASS II:
-Structure?
-# Genes Per Species?
-Normally Expressed By?
-Present Antigens To?
-Antigens Presented?
-β1 - α1
β2 - α2
-2-3
EXPRESSED BY:
-Dendritic Cells
-Macrophages
-B Cells
-CD4 T Lymphocytes
-Synth. OUTSIDE Cell& Internalized:
-Extracellular Parasites
-Extracellular Phase of
Intracellular Parasites
Antigen Processing of Which MHC Class involves:
-Tumor Antigen Coding in Nucleus
-Proteasomes
-Peptides Entering ER thru TAP Channel
MHC Class I
Antigen Processing of Which MHC Class involves:
-Endosomes
MHC Class II
How Many different peptides can Each MHC Class I & II molecule bind?
MANY, but not INDISCRIMINATELY
Are the binding requirements more stringent for Ag:Ab binding or peptide:MHC binding?
Ag:Ab
Is peptide:MHC Binding Selective or Specific?
Selective
Is Ag:Ab binding Selective or Specific?
Specific
2 Functions of ALL Dendritic Cells (DCs):
Function as Sentinel Cells to:
-Capture Antigen
-Activate Innate Immune
Mechanisms
3 DC Subpopulations:
-Myeloid
-Follicular
-Plasmacytoid
DC: MYELOID:
-Originate from?
-State at which they enter tissues?
-Location?
-Function?
-Bone Marrow
-Immature State
-Most Tissues:
Lymph Nodes (diffuse cortex)
Spleen (periarteriolar sheath)
Thymus
FXN:
Capture & Process Ags
Present Ag + MHC to Tcells
3 Methods by which Immature Myeloid DCs that have entered tissues from Bone Marrow Capture Ags:
-Phagocytosis
-Pinocytosis
-Receptor-Mediated
Endocytosis
Method by which Myeloid DCs Capture Ags that involves Molecules binding to Membrane Receptors & Being Internalized by the Cell:
Receptor-Mediated Endocytosis
3 Molecules that Immature myeloid DCs (become activated) in response to:
-PAMPs
-DAMPs
-Inflammatory Cytokines
What do myeloid DC synthesized Activation Signals delivered to T Cells together with the Ag presented by the mature myeloid DC initiate?
Adaptive Immune Response
Which myeloid DCs lack Surface Molecules that Deliver Activation Signals to T Cells?
Immature myeloid DCs
When Immature myeloid DCs present Ag to a T Cell, What happens and What is this State Called?
-NO Adaptive Immune Response occurs
-T Cell is Inactivated
-Anergy
In Primary Lymphatic Tissues, Lymphocyte Precursors commit to become either:
-NK cells
-T Cells
-B Cells
3 Actions of T & B Lymphocyte Precursors:
1. Migrate to their unique Primary Lymphatic Tissue
2. Rearrange their TCR or Immunoglobulin Genes
3. Express their Antigen Receptor on their Plasma Membrane
4 Unique Primary Lymphatic Tissues that T & B Lymphocyte Precursors Migrate to:
-Thymus
-Cloacal Bursa
-Ileal Peyer's Patch
-Bone Marrow
After T & B Lymphocyte Precursors express their Antigen Receptor on their Plasma Membrane, they are considered:
Immature Lymphocytes
What accounts for the possibility of some Lymphocytes having receptors that would react with their own proteins or Polysaccharides?
Somewhat Random Rearrangement of Receptor Genes
Term for Lymphocytes having receptors that would react with their own Proteins or Polysaccharides:
Self-Antigens (Autoantigens)
Are Self-Antigens a good or bad thing?
BAD!
What happens to Immature Lymphocytes that recognize Self Antigens?
They Die via Apoptosis in Primary Lymphatic Tissues
In the Thymus, T Cells that rearrange the TCRα & TCRβ genes and become TCRαβ Lymphocytes also differentiate into:
-CD4 or
-CD8 Lymphocytes
What is the "rule" for Immature Lymphocytes in Primary Lymphatic Tissue?
If you can recognize antigen in this place, it is almost certainly a self antigen. You might be dangerous, so you must die.
2 Types of Selection for Tαβ Cells that interact with cells expressing MHC Class I & II molecules, with self peptides in their binding grooves:
-Positive Selection
-Negative Selection
Rules of Positive Selection:
-If you don't recognize self MHC molecules at all, you are useless. You die.
-If you recognized an MHC Class I molecule, you will become a mature CD8 T Cell.
-If you recognized an MHC Class II molecule, you will become a mature CD4 T Cell.
Rules of Negative Selection:
If you recognize SELF MHC molecules with HIGH Affinity (Strong Binding), you are dangerous.
-You Die
-CD4 T cells may =>nTreg
-But, if you recognize SELF MHC molecules with Moderate Affinity (Weak Binding), then you are not dangerous & potentially useful. You survive.
4 General Features of Lymphocyte Activation:
-Recognition = "Signal 1"
-Activation = "Signal 2"
-Proliferation
-Differentiation
What is responsible for the Recognition phase of Lymphocyte Activation?
Antigen Receptors in Cell Membrane
What is responsible for the Activation phase of Lymphocytes?
Costimulatory Signals Received from another Cell
Which phase of Lymphocyte activation involves many cycles of Cell Division?
Proliferation
2 Types of cells differentiated during Lymphocyte Activation & their Description:
-Effector Cells (Cells that perform a function/produce an effect)
-Memory Cells (Cells that persis for months to years)
Where are Adaptive Immune responses Initiated?
In Secondary Lymphoid Tissues:
-Lymph Nodes
-Spleen
-Jejunal Peyer's Patches
How are Adaptive Immune responses initiated in Secondary Lymphoid Tissues?
By Myeloid DCs presenting Antigens to & Activating CD4 Helper T Lymphocytes
Where & How are Antigens carried to?
-Lymph Nodes
-Afferent Lymphatic Vessels
2 Scenarios for Antigens carried to Lymph Nodes via Afferent Lymhpatic Vessels:
-Antigens may move FREELY in LV, enter LN & be captured by RESIDENT myeloid DCs or
-Ags may be captured by TISSUE myeloid DCs and Carried to LNs via LVs