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Immunology > Immuno Test 1 (Part 1) > Flashcards

Immuno Test 1 (Part 1) Flashcards

1
Q

Primary Lymphoid Organs

A
  • Bone Marrow
  • Thymus
  • Produce the cellular components of the Immune System
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2
Q

Secondary Lymphoid Organs

A
  • Tonsils/ Adenoids
  • Lymph Nodes
  • Spleen
  • Locations where the immune responses occur
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3
Q

Non-encapsulated Lymphoid Tissue

A
  • Diffuse scattering of Lymphoid cells deep to the epithelium in the connective tissue
  • Located in Gastrointestinal tract, Genitourinary tract, and Respiratory passages
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4
Q

Single Nodular Tissue

A
  • Primary Nodule: infrequent

- Secondary Nodule: more frequent

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5
Q

Primary Nodule

A
  • More infrequent compared to secondary nodules
  • Consists of small lymphocytes
  • Not organized, so look like a small cluster of lymphocytes (No Germinal Center)
  • PRENATAL
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6
Q

Secondary Nodule

A
  • More frequent than Primary Nodule
  • Possesses a germinal center which stains lighter than the outer portion
  • Germinal center possesses a cluster of lymphocytes (maturing lymphocytes)
  • Possesses OUTER RING (cap), or MANTLE zone with smaller lymphocytes
  • MEMORY CELLS and MATURE LYMPHOCYTES collect in outer ring
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7
Q

Aggregate Nodular Tissue

A
  • TONSILS:
    1) Pharyngeal Tonsil (Adenoids): Nasopharynx
    2) Palatine Tonsils: Oral cavity
    3) Lingual Tonsils: Oropharynx
  • Lymphocytes infiltrate the epithelium
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8
Q

Pharyngeal Tonsil

A
  • ONLY ONE of these Tonsils
  • Pseudostratified columnar ciliated epithelium
  • Does possess Germinal Center
  • DOES NOT POSSESS CRYPTS!!!!!
  • Cilia are usually located in the airways
  • Located posterior nasopharynx
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9
Q

Palatine Tonsil

A
  • 2 of these Tonils
  • NON-KERATINIZED Stratified squamous epithelium
  • Possess THICK partial connective tissue capsule (PARTIAL CAPSULE)
  • Has Germinal Centers
  • Has 10 to 20 epithelial invaginations called CRYPTS per Tonsil
  • Located lateral wall of oral cavity
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10
Q

Lingual Tonsil

A
  • Small and Numerous Number of these Tonsils
  • Stratified squamous epithelium
  • No well defined capsule
  • Has Germinal Centers
  • Has ONE Crypt per Tonsil
  • Located posterior third of tongue
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11
Q

Mucosa-Assocaited Lymphoid Tissue (MALT)

A
  • Single or clusters of lymphoid nodules
  • Typically found in Gastrointestinal tract, Respiratory passageways, and Urinary tract
  • GALT are a form of MALT
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12
Q

Gut-Associated Lymphoid Tissue (GALT): Small Intestine

A
  • In Ileum called “PEYERS PATCHES”
  • Characterized by abundance of villi (increase surface area)
  • Single or clusters of lymphoid nodules
  • Characterized by Simple Columnar Epithelium with GOBLET CELLS (While looking balls, produce mucus and associated with GI tract
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13
Q

Gut-Associated Lymphoid Tissue (GALT): Vermiform Appendix

A
  • NO VILLI (only in small intestine)
  • Characterized by Crypts
  • Have Simple Columnar Epithelium with GOBLET CELLS
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14
Q

Capsulated Lymphoid Tissue

A
  • Have Lobules (Thymus)

- Doesn’t have Lobules (Spleen and Lymph Nodes)

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15
Q

Thymus

A
  • Produce only T lymphocytes
  • Decrease in size with age
  • Is largely replaced by FAT and CONNECTIVE TISSUE
  • Continues to produce T lymphocytes in adults
  • Pre-puberty (can see lobes) vs post-puberty (all Fat and CT)
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16
Q

Thymus Structure

A
  • Possess TWO LOBES
  • Posses connective tissue CAPSULE
  • Capsule associated with connective tissue SEPTA or SEPTUM(reaches deep into cortex) that penetrates to the medulla (inner portion)
  • Septa divides the Thymus into incomplete lobules
  • Lobules possess:
    1) Dark Outer CORTEX
    - Site of T-Lymphocyte MATURATION
    2) Light Inner MEDULLA
    - Medulla contains HASSAL’S CORPUSCLE
  • MACROPHAGES present in BOTH Cortex and Medulla
  • No lymphoid Nodules
  • No Germinal Centers
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17
Q

Thymus Cortex

A
  • Dark
  • T-lymphocyte maturation
  • Cells:
    1) Subscapular Thymic Epithelial Cells (line cortex)
    2) Thymic Cortical Epithelial Cell (induces new T cells, grown downward towards medulla)
    3) Maturing T cells (Developing Thymocytes)
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18
Q

Thymus Medulla

A
  • Lighter
  • Site of mature Lymphocytes
  • Cells:
    1) HASSAL’S CORPUSCLE
    2) Thymic Medullary Epithelial Cells
    3) Dendritic Cells
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19
Q

Hassal’s Corpuscle

A
  • Only present in MEDULLA
  • Closely packed Epithelial Cells
  • Release factor that STIMULATES Thymic Dendritic Cells to complete maturation of T-Cells
  • Look like PINK globs in the Medulla
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20
Q

Thymus Blood Barrier

A
  • Only exists in the Cortex
  • Prevents most circulating antigens from reaching developing T cells
  • EPITHELIAL- RETICULAR CELLS are bound to the capillaries
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21
Q

Spleen

A
  • Left Superior Quadrant
  • Macrophages present to destroy old RBC
  • Spleen traps Antigens
  • Reservoir for 1/3 of PLATELETS
  • HEMATOPOIESIS takes place there
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22
Q

Spleen General Organization

A
  • Surrounded by connective tissue CAPSULE
  • Capsule components:
    1) Collagen
    2) Elastic Fibers
    3) Smooth Muscle
  • TRABECULAE extend from the capsule and divide the spleen into incomplete compartments
    - Not very organized
  • NO Cortex/ Medulla
  • PARENCHYMA is made up of reticular fibers supporting two main components of the Spleen: RED and WHITE Pulp
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23
Q

White Pulp

A
  • Rich in Lymphoid Tissue

- Purple color

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24
Q

Red Pulp

A
  • Rich in RBC

- Pink Color

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25
Q

White Pulp Organization

A

1) Germinal Center
2) Corona aka crown (B cells and Antigen presenting cells)
3) Marginal Zone (Red pulp and White pulp interact)
4) Central Artery
5) Periarteriolar Lymphoid Sheaths (surround the central artery and comprised of T CELLS)

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26
Q

Red Pulp Organization

A
  • Splenic Cord formed by RETICULAR CELLS (solid cord)
  • Splenic Sinusoid (space for blood)
  • Pennicillar Arteries
  • Macrophage sheathed capillaries
  • Circulating blood cells
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27
Q

Spleen Blood Flow

A

1) Splenic Artery from Celiac Trunk
2) Splenic artery divides into Trabecular Arteries which follow the Trabeculae into the parenchyma of the Spleen
3) Trabecular arteries divide into Central Arteries which PENETRATE the White Pulp and are surrounded by Periarteriolar Lymphoid Sheaths
4) Central Arteries produce Radial Arteries while in the White Pulp that deep into the Marginal Zone sinuses (blood pools here)
5) Central Arteries leave the White Pulp and enter the Red Pulp as Penicillar Arteries, which either end in the Splenic Sinusoids (closed circulation) or into the Red Pulp (open circulation)
6) The Penicillar Arteries and the small capillaries that they produce are sheathed by Macrophages, that are responsible for REMOVING damaged RBCs and particles from the blood

  • White Pulp= Radial Arteries
  • Red Pulp= Penicilliar Arterioles
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28
Q

Lymph Nodes

A
  • Smallest, most numerous encapsulated Lymphoid Organs
  • In line filters of Lymph
    • Remove antigens and cellular debris
    • Produce Lymphocytes
    • Add antibodies
  • Lymph gets duped into the veins
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29
Q

Lymph Node General Organization

A
  • Surrounded by connective tissue CAPSULE
  • TRABECULAE extend into the parenchyma between the cortical nodules
  • Outer Cortex
  • Inner Medulla
  • HILUM: blood enters via arteries, leaves via veins and lymph leaves via EFFERENT lymph vessels
  • Surrounded by connective tissue CAPSULE
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30
Q

Lymph Node Cortex

A
  • Outer Cortex (B cell RICH)
    • Lymphatic Nodule
      • Germinal Center
      • Mantle
    • Subcapsular/ Cortical Sinus
  • Inner Cortex (T cell RICH)
    • Lymphatic Nodules
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31
Q

Lymph Node Medulla

A
  • MEDULLARY CORDS: Primarily comprised of Macrophages and Plasma cells
  • MEDULLARY SINUSES: Spaces lined by Endothelial cells surrounded by Reticular Cells and Macrophages
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32
Q

Sinuses

A
  • Filter Lymph and direct flow
    • Mesh of Reticular Cells and fibers
    • Macrophages and follicular dendritic cells
    • Slows flow of lymph which facilitates antigen removal
  • Lymph is cleared of 90% of antigens and cellular debris (this is why the lymph passes slowly, to ensure antigens are cleared)
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33
Q

Neutrophils

A
  • Early phagocytosis and killing of microbes
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34
Q

Macrophages

A
  • Efficient phagocytosis and killing of microbes

- Secretin of cytokines that stimulate inflammation

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35
Q

NK Cells

A
  • Lysis of infected cells

- Activation of macrophages

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36
Q

Complement

A
  • Killing of microbes
  • Opsonization of microbes
  • Activation of Leukocytes
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37
Q

Mannose-binding lectin (collectin)

A
  • Opsinization of microbes

- Activation of complement cascade (lectin pathway)

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38
Q

C- reactive protein (pentraxin)

A
  • Opsonization of microbes
  • Activation of complement
  • Binds to PHOSPHOORYLCHOLINE on microbes and coats the microbes for phagocytosis by macrophages
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39
Q

TNF, IL-1, chemokines

A
  • Inflammation
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40
Q

IFN-alpha, beta

A
  • Resistance to viral infection
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41
Q

IFN- gamma

A
  • Macrophage activation
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42
Q

IL-12

A
  • IFN-gamma production of NK cells and T cells
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43
Q

IL-15

A
  • Proliferation of NK cells
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44
Q

IL-10, TGF-beta

A
  • Control of inflammation
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45
Q

Opsinization

A
  • The process by which a pathogen is marked for elimination
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46
Q

Recognition of Nonself by Innate Immune Response

A
  • Ability to discriminate between self and non self
  • Receptors recognize “pathogen-associated molecular patterns” (PAMPS)
  • PAMPS have no structural similarity with self Ags
  • Cells that recognize PAMPS are termed Patter Recognition Receptors (PRR)
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47
Q

Properties of PRR (Innate)

A
  • Have specificity for structures shared by classes of microbes (molecular patterns)
  • The receptors encoded in the germ line have LIMITED DIVERSITY
  • Distribution of receptors are NONCLONAL: identical receptors on all cells of the same lineage
  • Have a discrimination between self and non self antigens to prevent innate response
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48
Q

Toll-like Receptors (Innate)

A
  • Some TLRs are present on the cell surface, where they recognize products of extracellular microbes
  • Other TLRs are located in endosomes, into which microbes are ingested
  • Endosomal TLRs respond only to NUCLEIC ACIDS
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49
Q

TLRs Recognition Pathogens (Innate)

A
  • Gram pos bacteria = PGN —> TLR2

- Gram neg bacteria = LPS —> TLR4

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50
Q

TLRs Trigger Activation of Immune Cells (Innate)

A

1) Ligands bind to Toll-like receptors
2) Toll-like receptors activate signaling pathways
3) Pro-inflammatory cytokine secretion

  • NF-kappaB!!!!!!!
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51
Q

Toll Like Receptor 4

A

1) Complex of TLR4, MD2, CD14, and LPS is assembled on the macrophage surface
2) MyD88 binds TLR4 and activates IRAK4 to phosphorylate TRAF6, which leads to phosphorylation and activation of IKK
3) IKK phosphorylates IkappaB, leading to its degradation and the release of NFkappaB, which enters the nucleus
4) NFkappaB activates transcription of gene for inflammatory cytokines, which are synthesized in the cytoplasm and secreted via the ER

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52
Q

Innate Immunity: Complement

A
  • Complement system consists of serum protein which normally exist as soluble inactive precursors
    1) Upon activation, each precursor is cleaved into two or more fragments
    2) Large fragments have ENZYMATIC PROPERTIES and activate the downstream components resulting in formation of Membrane Attack Complexes, which disrupt the membrane of certain pathogens

3) Small fragments serve as:
- Opsonins
- Chemotactic factors
- Anaphylatoxins

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53
Q

Opsonins

A
  • Deposited on microbes and enhance their uptake by phagocytes bearing multiple complement receptors
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54
Q

Chemotactic factors

A
  • Attract immune cells
55
Q

Anaphylatoxins

A
  • Cause degradation of mast cells/ basophils and release vasoactive substances
56
Q

Innate Immunity Complement

A
  • Complement activation is based on an enzymatic AMPLIFYING CASCADE
  • Activation can be triggered by one of three pathways
    1) CLASSIC: Activated by antigen-antibody complexes
    2) ALTERNATIVE: Activated by microbial-cell walls
    3) LECTIN: Interaction of microbial carbohydrates with mannose-binding protein in plasma
57
Q

Cytokines

A
  • Cytokines produced by immune cells mediate Inflammation, Immunity, and Hematopoiesis
  • They can operate over a long range on distant cells (endocrine), over a short range of neighboring cells (paracrine), or on cell which produce those cytokines (autocrine)
  • Cytokines of Innate Immunite are divided into two classes:
    1) Pro-inflammatory: stimulate inflamamtion
    2) Anti-inflammatory: inhibit imflammation

*** In the INNATE IMMUNITY, only ONE Cytokine is Anti-inflammatory

58
Q

Chemokines

A
  • Small protein chemoattractants important fro trafficking of immune cells
59
Q

Cytokines of Innate Immunity

A
  • All of the Cytokines, except for one, are produced by Macrophages:
    1) TNF
    2) IL-1
    3) Chemokines
    4) IL-12
    5) IFN-alpha, IFN-beta
    6) IL-10
    7) IL-6
    8) IL-15
    9) IL-18

** IFN-gamma: produced by NK cells and T Lymphocytes, but its FUNCTION is to ACTIVATE MACROPHAGES

60
Q

Local vs Systemic Cytokine Effects

A
  • All of these are produced by Macrophages:
    1) IL-1 beta
    2) TNF-alpha
    3) IL-6
    4) IL-8
    5) IL-12
61
Q

IL-1 Beta

A
  • Activates endothelium
  • Activates lymphocytes
  • Local tissue destruction
  • **** CAUSES FEVER and produces IL-6
62
Q

TNF-alpha

A
  • Activates vascular endothelium and increases vascular permeability, which leads to increased entry of IgG, complement, and cells to tissues and increased fluid drainage to lymph Nodes
  • Has SYSTEMIC EFFECTS
    • Fever
    • Mobilization of metabolites
    • Shock
63
Q

IL-6

A
  • Has LOCAL EFFECTS
  • Lymphocyte activation and increased antibody production
  • Causes:
    • Fever
    • Induces acute-phase protein production by hepatocytes
64
Q

IL-8

A
  • Chemotactic factor recruits neutrophils, basophils, and T-cells to site of infection
65
Q

IL-12

A
  • Activates NK cells
  • Induces the differentiation of CD4 T cells into TH1 cells
  • This has an amplifying effect because T cells produce IFN-gamma
66
Q

IFN-gamma

A
  • Produced by NK cells and T cells, which ACTIVATES MACROPHAGES
67
Q

Hemopoiesis

A
  • Majority of immune cell types are produced from CD34+ Hemopoietic Stem Cells
  • HSC found in fetal liver, fetal spleen, neonate and adult bone marrow
  • HSC differentiate into mature cells of all blood lineages
  • Contact with stromal cells (epithelial, friboblast, macro) is required for differentiation
  • Adhesion molecules and cytokines are involved
  • Stromal cells produce cytokines like:
    1) Stem Cell Factor
    2) Monocyte Colony Stimulating Factor
    3) Granulocyte- Colony Stimulating Factor
  • Interaction of HSC with stromal and M-CSF results in monocytes
  • Interaction of HSC with stromal cells and GSF results in granulocytes
68
Q

Origin of Blood Cells

A
  • HSC (CD34+) can create Lymphoid Progenitor Cells (LPS) and Myeloid Progenitor Cells
  • Lymphoid PC lead to B and T cell formation
  • Myeloid PC lead to:
    1) Monocytes (macro and some dendritic cells)
    2) Granulocytes (Baso, Neutro, Eosino)
    3) NK cells
    4) Erythrocytes
    5) Megakaryocytic (platelets)
  • 3/4 of the nucleated cells in the bone marrow are committed to the production of Leukocytes
  • 90% of WBC remain in storage (Bone Marrow)
  • 2-3% of WBC circulating
  • 7-8% of WBC are located in tissue compartments
69
Q

Blood Smear

A
  • Most common lab test is a CBC
  • Second most common is a differential leukocyte count (DIFF)
  • Manual DIFF with CBC provides complete hematologic picture of the case, from morphologic standpoint
  • ZONE OF MORPHOLOGY: area looked at with a microscope.
  • Smear should occupy central area of slide
  • To be able to observe and recognize the different kinds of leukocytes, you must stain then with a GIEMSA STAIN
    • Giemsa stain is a mixture of BASIC STAIN METHYLENE BLUE and ACIDIC STAIN EOSIN

***** Blood Smear doesn’t allow differential count of B cells, T cells, and NK cells because all the cells appear the same. For this, techniques were developed based on the antibodies recognizing specific Ags, termed cluster of differentiation, which selectively expressed on each type of immune cell

70
Q

Blood Smear Count Levels (WBC)

A
  • Neutrophils: 40%-60%
  • Eosinophils: 1%-4%
  • Basophils: 0.5%- 1%
  • Monocytes: 2%-8%
  • Lymphocytes: 20%-40%
71
Q

Cluster of Differentiation (CD) of Phenotyping of Cells

A
  • T cell: CD3,4,8
  • B cell: CD19,20
  • Dendritic cell: CD11c, 123
  • NK cell: CD56
  • Stem cell/ precursor: CD34
  • Macrophage/Monocyte: CD14,33
  • Granulocyte: CD66b
  • CD are used for identification of leukocytes
72
Q

Direct and Indirect Fluorescent Microscopy

A
  • Direct (Used for high expression of molecules)
  • Indirect (Used for low expression of molecules)
  • How to tell what kind of cells you have in your blood. You can tell by the type of CD present
73
Q

Leukocytosis

A
  • Excess numbers of WBC are most often due to the normal response of bone marrow to INFECTION of INFLAMMATION (LEFT SHIFT):
    • Trauma
    • Gout
    • Rheumatoid Arthritis
    • Rheumatic Fever
    • Thyroditis
    • Acute Stress
  • In some instances, leukocytosis is a sign of more serious primary BONE MARROW DISEASE (Chronic Myelocytic Leukemies)
  • Storage of maturing cells in the bone marrow allows for rapid response to the demand for increased WBC
  • a 2 to 3 fold increase in circulating leukocytes is possible in 4 to 5 hours
  • Once a leukocyte is released into circulation and tissue, it remains there only a few hours, until the cell death occurs
  • Life span of a WBC is 11 to 16 days
74
Q

Leukopenia

A
  • A REDUCTION of circulating WBC
  • Usually characterized by Neutropenia (reduced number of circulating Neutrophils)
  • Neutropenia, if severe, can increase the risk of life threatening infection
  • Neutropenia is often cause by chemotherapy or radiation treatments
  • People with Neutropenia have frequent or unusual infections
75
Q

Mast Cells

A
  • Stained purple with methylene blue in Giemsa stain
  • TISSUE FIXED
  • Contribute to elimination of parasites
  • Key role in allergic and anaphylactic reactions
  • Contain basophilic granules with:
    1) Histamine, serotonin, heparin
    2) Cytokines and Chemokines
  • Among FIRST CELLS of immune response to interact with environmental antigens and allergens, invading pathogens or environmentally derived toxins
  • LONG LIVED
  • Have PAMP (pathogen) and DAMP (damage) receptors
  • Can amplify or suppress innate or acquired immune responses
    - Pro-inflamm, Anti-inflamm, immunosuppressive
  • Mast cells invite neutrophils and activate Macrophages to be made
76
Q

Basophils

A
  • Characteristic purple/green granules stained in methylene blue Giemsa staining
  • CIRCULATING IN BLOOD
  • Contribute to elimination of parasites
  • Key role in allergic and anaphylactic reactions
  • Contain basophilic granules with:
    1) Histamine, serotonin, heparin
    2) Cytokines and Chemokines
  • MUST BE SYNTHESIZED DE NOVO
77
Q

Eosinophils

A
  • Stained red with Acidic dye eosin in Giemsa
  • Comprise 2-5% of WBC
  • Contain granules with:
    1) Basic proteins
    2) Peroxidases
    3) Antimicrobial substances
  • Important in allergic reactions and defense against parasitic infections
  • Secrete granules for extracellular digestion of infections pathogens
  • Produce inflammatory mediators (cytokines, prostaglandins)
78
Q

Eosinophilia

A
  • Low peripheral Eosinophil blood cells count
  • Caused by:
    1) Allergic events
    2) Parasitic infections
79
Q

Infalmmatory Mediators of Mast Cells

A
  • Release:
    1) Histamine
    2) Heparin
    3) Proteases
    4) TNF
  • Recruitment and activation of Neutrophils, Basophils, and Eosinophils
  • They can release cytokines, cheekiness, angiogenic, and growth factors (macrophages are the only one cells that can do this)
80
Q

Mast Cell Strategic Locations

A
  • Widely distributed throughout tissues, especially in areas exposed to the environment (skin, airways, GI) ALWAYS PRESENT
  • Found in close proximity to blood vessels when can regulate vascular permeability and effector-cell recruitment
  • Can modulate the behavior of these and other neighboring effector cells through the release of mediators
81
Q

Mediators Released by Mast Cells

A
  • Histamine (Vasodilation)
  • Cytokines:
    • TNF-alpha
    • IL-8 (Attract Neutrophils)
    • IL-5
    • PAF
82
Q

Neutrophil Recruitment Cascade

A

1) Free circulating Neutrophils
2) Slow Rolling (selectin)
3) Firm Adhesion (integrin)
4) Intraluminal crawling (integrin and follow chemokine gradient)
5) Transmigration between endothelial cells

  • Rolling is SELECTIN-dependent
  • Adhesion, crawling and transmigration are INTEGRIN-dependent
  • Chemokin (IL-8) lining the luminal part of endothelium interacts with IL-8 receptor on neutrophils that induces conformational changes in neutrophil interns
83
Q

Neutrophil Blood Smear

A
  • Three to five connected lobules
  • 12 to 15 micrometer in diameter
  • Earliest phase of Inflammatory reactions
84
Q

Neutrophils

A
  • Produced in bone marrow and give rise to mononuclear phagocytosis
  • Production of neutrophils simulated by GRANULOCYTE COLONY-STIMULATING FACTOR (cytokine)
  • Circulates in blood for hours or few days
  • After entering tissue, they function 1 to 2 days
  • Comprise 60 to 70% of WBC
  • Professional Phagocytes
  • Produced inflammatory mediators- cytokines, prostaglandins
  • Cytoplasmic granules:
    • Proxidase
    • Lysozyme
    • Degrative enzymes
    • Defensins
85
Q

Granules in Neutrophils

A
  • Specific Granules: (stained with neutral dye)
    • Lactoferrin
    • Lysozyme
    • Secretory
    • Phospholiapse A2
  • Azurophil Granule: (stained with azure dye)
    • Elastase
    • Lysozyme
    • Myeloperoxidase
    • Cathepsin
    • Acid Hydrolases
86
Q

How Neutrophils Kill Bacteria

A
  • Phagocytosis (reactive oxygen species or antibact protein)
  • Degranulation (release enzymes just in their environment)
  • Neutrophil Extracellular Traps (NFTs)
    - Shoot out their DNA, which glues to pathogens, and then pulls the DNA (along with pathogens) back into the cell. Can continue their function during this whole time!
    - This function uses the histones and proteases from the inside of the Neutrophil
87
Q

Monocytes

A
  • Present 3 to 8% of WBC in blood
  • Important Phagocytes
  • Differentiate into macrophages
  • Main function of Macrophages is PHAGOCYTOSIS and DESTRUCTION of particulate material
  • Become macrophages as soon as they enter the tissue
88
Q

Monocytosis and Monocytopenia

A
  • Monocytosis: Increased number of monocytes in the blood from:
    - Chronic infections
    - Autoimmune disorders
    - Certain cancers
    - Proliferation of macrophages can occur in tissues
  • Monocytopenia: low number of monocytes in the blood can occur in response to endotexemia, as well as in people receiving chemo
89
Q

Maturation of Mononuclear Phagocytes

A
  • Microphages can appear in the blood brain barrier from the HSC in a fetus
    • These HSC become macrophage precursors in the blood and can reach the brain, lungs, liver, and spleen
90
Q

Macrophages

A
  • Not found in circulation but reside in tissues
  • Various functions and morphologies in different tissues:
    • Histiocytes in connective tissue
    • Kupffer cells in liver
    • Alveolar macrophages in lungs
    • Microglial cells in the CNS
  • Macro are phagocytic cells and Antigen-presenting cells
91
Q

Function of Macrophages

A
  • Function in Innate and Adaptive Immunity
  • Express a variety of PRR, like TLRs and Scavenger receptors that recognize danger signals
  • Play an important role in the activation of Innate Immune Response
  • PRR also stimulate production of TNF and IL-1 beta
92
Q

Biology of Macrophages

A
  • Involved in wound repair
  • Secrete cytokines to regulate recruitment of cells to deposit extracellular metric components and sites of injury
  • Function as Antigen-presenting cells
  • Produce large amounts of TNF, IL-12, and IL-23, important for Th1 responses
  • Th1 derived IFN gamma, turns into feeb back for positive amplification of macrophages
  • Important drivers of chronic inflammatory and autoimmune diseases
93
Q

Macrophage functions in Innate Immunity

A
  • Phagocytosis of foreign material
  • Production of inflammatory cytokines and mediators:
    • Cytokines and chemokines
    • Reactive Oxygen Intermediates
    • Nitric Oxide
  • Produce cationic proteins and polypeps (defensins) mediate in killing of microbe
  • Produce and release enzymes:
    • Lipases, galactosidases
94
Q

Phagocytosis Requirements in Innate Immunity

A
  • Energy generates through glucose metabolism
  • Synthesis of additional cell membrane
  • An active cytoplasmic contractile protein system
95
Q

Steps in Functional Responses of Phagocytes

A

1) Rectuitment of cells to site of infection
2) Recognition of and activation by microbes
3) Ingestion of microbes by process of phagocytosis
4) Destruction of ingested microbes

96
Q

Movement of Phagocytic Cells

A
  • Amoebid Movement: migrate in and out of blood vessels and through tissues (diapedesis)
  • Chemotaxis: Move toward cells or organisms in response to chemotaxins.
    • Two important bacterial constituents:
      1) Lipopolysaccharide found in the outer membrane of gram neg bacteria
      2) N-formylmethionine from actuarial mRNA
97
Q

Chemotactic Factors

A
  • Neutrophil: Bact Lipoteichoic acid, formyl-methionyl peptides, Complement C5a, Fibrinogen, Leukotrin B4
  • Macrophage: Transforming growth factor beta, monocyte chemotactic protein 1
  • Lymphocyte: Cytokines—> Macrophage infalmmatory protein 1
98
Q

Phagocytosis

A

1) Phagocyte engulfs particle after coming into contact with it, and forms phagosome
2) Lysosomes fuse with phagosome to form phagolysosome
3) Engulfed material digested by enzymes contained in lysosomal granules
- Opsonins in plasma and tissue fluids enhance this process

99
Q

Opsins

A
  • Substances that bind to particles and make them more susceptible to phagocytosis. Opsonins found in serum include:
    1) Split products of the complement cascade
    - C3b, iC3b, C4b, and C5b
    2) Antibodies
    - Phagocytic cells have receptor for Fc portion of certain immunoglobulin molecules
    - Fibronectin, helps neutrophils stick to target
    - Leukotrienes, from Arachidonic acid, some leukotrienes are opsonins
100
Q

Granule Contents

A

1) Hydrolytic Enzymes
- Able to digest wall components of bacteria and some act on viral protein coats or envelopes
- Cathespin, glycosidase
2) Defensins
- Cationic proteins (large amount of arginine), kill microbes by interacting with microbial cell membrane to form channels through it
3) Nitric Oxide Synthase
- Combines oxygen with guanidine nitrogen of L-arginine to yield nitric oxide, which isotopic to parasites, fungi, and tumor cells

101
Q

Oxygen Dependent Intracellular Killing

A
  • Done by respiratory bursts
    that accompanies phagocytosis and produces several microbial oxygen metabolites
    1) Oxygen consumption
    2) Hexose monophosphate shunt activity stimulates
    3) Hydrogen peroxide production increases
    4) Superoxide anion is produced
102
Q

Superoxide Anion and by products

A
  • Superoxide anion is extremely toxic to bacteria and tissues and is unstable
    • Broken down to H2O2 by superoxide disputes
    • H2O2 broken down by Catalase
103
Q

Mononuclear Phagocyte System

A
  • Include circulating monocytes and resident tissue macrophages
  • Innate and adaptive role
  • Cells of macrophage lineage arise from committed precursors in bone marrow drive by M-CSF
104
Q

Functions of Monocyte/ Macrophage

A

1) Activation (IFN-gamma)
2) Chemotaxis, tissue inflammation (TNF-alpha, IL-1, IL-8)
3) Phagocytosis, scavenger function, tissue repair (Collagenase, Elastase)
4) Effection Function (Hydrolases, H2O2)
5) Antigen presentation (TNF-alpha)
6) Immunomodulation (IL-10, IL-12, Th1)

105
Q

NK cells

A
  • recognize and destroy variety of targets without any prior stimulation
  • Targets: virus, cancer, transplant
  • Secrete proforin (cytotoxic)
  • No specific Ag receptor
  • Innate immunity (cytotoxic activity)
  • Arise from bone marrow but distant lineage from B or T cells
  • Undergo differentiation in BM via precursor NK cells
  • NK are naturally occurring cytotoxic lymphocytes that exist in the body at birth
  • They are not induced by immunologic insult, although their numbers and activity can be increased by IL-15 and IL-2
106
Q

Functions of NK

A
  • Cytotoxic to tumor cells and coral infected host cells
  • Resistance role to bacterial, fungal, and parasitic infections
  • Secrete IFN-gama and IL-2 (Cytokines)
  • Major lymphocytic cells responsible for AB-dependent cellular cytotoxicity
    • Have membrane receptors for the Fc portion of IgG and interact with Ab-coated targets
  • DO NOT POSSESS ANTIGENIC SPECIFICITY and DO NOT ACQUIRE IMMUNOLOGIC MEMORY
107
Q

Antibody Dependent Cellular Cytotoxicity

A
  • Target cells are coated with specific Ab
  • Receptors fo Fc portion of IgG molecules on ADCC (anchor between cytotoxic cell and target)
  • ADCC play a role in antiviral, anti tumor, and anti-graft immunity
  • ADCC attributed to NK cells
  • Macrophages and neutrophils also participate in ADCC
108
Q

NK Mode of Action

A
  • Kills target by perforating cell membrane causing pores to form (perforins are responsible)
    1) Perforins released from granules are intimate cellular contact
    2) Perforin insets into target membrane and polymerize
    3) Depolarization, abnormal ion flux, and essential metabolite leakage from cytoplasm result
    4) Protectin protects NK from perforins by binding to it and prevent its insertion into NK (Spares NKs)
  • IL-2 and IFN enhance cytotoxic activity of NK cells
  • ** NK cells do not require that the NK cells recognize MHC molecules on the target cells
109
Q

Innate Immunity: Complement

A
  • Complement activation occurs in two phases:
    1) Activation of C3 component
    2) Activation of C5 component
  • Formation of the ‘attack’ of lytic sequence- MEMBRANE ATTACK COMPLEX (MAC)
110
Q

Timeline: Innate and Adaptive Immunity

A
  • Innate immunity happens from 0 to 12 hours after the infection has occurred
    - 90% of the pathogens are destroyed by the innate immune response
    - Have Toll Like Receptors
  • Adaptive Immunity occurs from 12 hours until 7 days after the infection
    - The adaptive response is extremely specific and is mediated by B and T lymphocytes
    - If the antigen in the cell mutates, then the Ab for the original protein won’t work for this new mutated pathogen
    - The adaptive immunity is really slow
111
Q

Adaptive Immunity

A
  • Adaptive immune response is ANTIGEN SPECIFIC
  • The Ag receptors are on the surface of B and T lymphocytes
  • B and T cell receptors are HIGHLY SELECTIVE towards particular Ag
  • The RESPONSE IS SLOW (days to weeks to mount)
  • Adaptive immunity has memory (memory B cells) therefore maturation of secondary response occurs faster—-> why we have vaccines
  • THE ANTIGEN MUST BE DELIVERED TO THESE CELLS
112
Q

Types of Adaptive Response

A

1) CELL-MEDIATED IMMUNITY: Based off of T lymphocytes (thymus)
- DIRECTED AGAINST VIRUSES OR INTERCELLULAR PATHOGENS
2) HUMORAL IMMUNITY: Based off of B lymphocytes (Bone marrow)
- DIRECTED AGAINST EXTRACELLULAR PATHOGENS

113
Q

Maturation of Lymphocytes

A
  • B lymphocytes develop from precursors DURING LIFETIME
  • All T lymphocytes are generated in the THYMUS DURING FETAL STAGE
  • Mature lymphocytes enter the PERIPHERAL LYMPHOID ORGANS, where they RESPOND TO FOREIGN AGs.
    - Peripheral lymphoid organs is where the lymphocyte gets exposed to foreign antigen (Lymph Nodes)
  • Enlarged Lymph Nodes demote an immune response in the lymph node
114
Q

B Lymphocytes

A
  • B cells express B Cell Receptor (BRC) for recognition of antigens
    - Each B cell has a different B Cell Receptor
  • An individual B cell expresses numerous BRCs where are identical
  • BRCs can recognize various Ags- protein, carbohydrates, lipids, and nucleic acids
  • The BRC determines the 3 Dimensional conformation of the molecules that it can bind to (key and lock)
115
Q

B cells (Plasmid Cells) Produce Antibodies (Abs)

A
  • Abs are secreted into the CIRCULATION and MUCOSAL fluids
  • NEUTRALIZE and eliminate extracellular MICROBES and microbial TOXINS
  • PREVENT DISSEMINATION of microbes (gaining access to host cells and connective tissue)
  • NOT EFFECTIVE against intracellular microbes that live and divide inside infected cells
  • PLASMA CELL: terminally differentiated B cells and produce a bunch of Ab until it dies
116
Q

T Lymphocytes

A
  • Ag Recognition by T cells:
    • T cell express T Cell Receptor (TCR) for recognition antigens
    • An individual T cell expresses numerous TCRs which are IDENTICAL
    • T cells can recognize PEPTIDE AGs (proteins) ONLY
    • T cells can NOT “see” Ags without the help of AG-PRESENTING CELLS (APC)
  • Two Types of T cells:
    1) HELPER T CELLS:
    - Activate macro
    - Inflammation
    - Activate proliferation of T and B lymphocytes)
    2) CYTOLYTIC T CELLS
    - Killing of Infected Cells
  • Defense against INTRACELLULAR MICROBES
117
Q

T Lymphocytes (Cytokines)

A
  • T HELPER lymphocytes produce cytokine called INTERFERON-GAMMA (IFN-gamma) that stimulates MACROPHAGES to destroy microbes in phagosomes
  • CYTOLYTIC T LYMPHOCYTES kill INFECTED HOST CELLS (intracellular microbes)
  • Macrophages can become APC and show the Th cells what to do which then amplifies the number of macrophages (looped amplification)
    - Macrophages can only attack pathogens released from cells
118
Q

Ag- Presenting Cells

A
  • APC capture, process, and present Ags for recognition by T cells
  • Two types:
    1) PROFESSIONAL APCs: they are dendritic cells (DCs), macrophages (Mo), and B cells
    - When activated, professional APCs activate T Helper lymphocytes
    - Express CLASS I and CLASS II APC
    2) NON- PROFESSIONAL APCs: any nucleated cell in the body
    - When infected with intracellular pathogens, non-professional APCs activate CYTOLYTIC T LYMPHOCYTES
    - Express CLASS I APC ONLY!!!!!!!!
119
Q

Capture of Ags

A

1) Microbes enter through an epithelium and are captured by DCs RESIDENT IN THE EPITHELIUM
2) DCs transport Ags to the LYMPH NODE where protein Ags are displayed for recognition by T LYMPHOCYTES
3) BLOOD BORNE AGs are presented by APCs in the SPLEEN!!!

120
Q

Morphology of Lymph Nodes

A
  • LYMPH is drained by lymphatic vessels from the tissues to the lymph nodes and recirculate into the blood circulation
  • Lymph contains a mixture of substances absorbed from epithelia and tissues
  • Microbial Ag are carried by APCs
  • Ags are presented to T Lymphocytes congregated in the special areas called T CELL ZONES
  • Lymph delivers Ags to B cells congregated in the special areas called B CELL ZONES
121
Q

Morphology of Spleen

A
  • Each splenic arteriole is surrounded by the PERIARTERIOLAR LYMPHOID SHEATH (PALS)
  • PALS contain T CELL AND B CELL ZONES
  • PALS is attached to follicle containing a germinal center
  • The PALS and lymphoid follicles together constitute the WHITE PULP
  • White pulp is surrounded by the RED PULP, which is rich in vascular sinusoids
122
Q

APCs: Major Histocompatability Complex

A
  • T CELLS can only see protein Ags presented by APCs in association with molecules called MAJOR HISTOCOMPATIBILITY COMPLEX (MHC)
  • There are two MHC Classes: Class I and Class II
  • Non-Professional APCs express CLASS I MHC ONLY!!!
  • Professional APCs express both CLASS I and CLASS II MHC
  • Th cells express CD4+ that “directs” them to Ags presented by CLASS II MHC
  • Cytolyticl T Cells express CD8+ that “directs” them to Ags presented by CLASS I MHC
123
Q

Recognition of Microbial Ags

A
  • B cells do not need APCs
  • T helper cells recognize Ags presented by Professional APCs within CLASS II MHC
  • CTLs recognize Ags presented by Non-Professional APCs within CLASS I MHC
124
Q

How TCR Recognizes Ag

A
  • T cell receptor (TCR) recognizes a complex of a peptide Ag displayed by a MHC molecule
  • Peptides bind to the MHC molecules by ANCHOR RESIDUES
125
Q

Class I MHC Pathway of Ag Presentation

A
  • Class I MHC molecules are found on ALL NUCLEATED CELLS in the body (including professional APCs)
  • Class I MHC display INTRACELLULAR AGs including microbial Ags if cell is infected
  • Class I MHC presents processed peptides to CD8+ lymphcytes
  • If host cell infected, CTLs KILL INFECTED CELL after recognition of microbial Ags presented within class I MHC
  • NO AG-FREE MHC molecules are displayed on APCs
126
Q

Ag Processing and Presentation (MHC II)

A
  • Class II MHC molecules are found only on PROFESSIONAL APCs
  • Microbial AGs are taken up by professional APCs via PHAGOCYTOSIS (macrophages) or ENDOCYTOSIS (DC and B cells)
  • Protein AGs undergo ENZYMATIC DEGRADATION into PEPTIDES
  • Peptide Ags are loaded into CLASS II MHC and presented for recognition by CD4+ T HELPER LYMPHOCYTES
  • NO AG-FREE MHC molecules are displayed on APCs
127
Q

Phases of Adaptive Response

A
  • Sequential:
    1) RECOGNITION of Ag by specific lymphocytes
    2) ACTIVATION of lymphocytes (clonal expansion and differentiation)
    3) EFFECTOR PHASE (elimination of Ag)
  • All immune responses are SELF-LIMITED and decline as the infection is eliminated
  • The response DECLINES as ANTIGEN IS ELIMINATED and most of the Antigen-stimulated lymphocytes die by apoptosis
  • The Ag specific cells that survive become MEMORY CELLS
  • These principles APPLY TO B and T LYMPHOCYTES
128
Q

AB Structure and Functional Domains

A
  • Ab is tetramer of two pairs of indexical HEAVY AND LIGHT CHAINS
  • Both heavy and light chain molecules have VARIABLE and CONSTANT DOMAINS
  • The variable region, FAB2 confers AG RECOGNITION
  • DISTINCT BIOLOGICAL ACTIVITIES attributed to each heavy chain molecule
  • The heavy chain contains A HINGE domain that confers flexibility to allow OPTIMAL AG BINDING
129
Q

Ab Classes and Isotypes

A
  • Antibodies are CLASSIFIED according to their HEAVY CHAINS
  • The constant region of the heavy chain confers antibody function, representing FIVE DIFFERENT CLASSES or isotopes
  • The isotopes IGM, IGD, IGG, IGE, and IGA each have characteristic properties
  • IGG has four subclasses of IGG called IGG1, IGG2, IGG3, and IGG4
  • IGA has two SUBCLASSES called IGA1 and IGA2
130
Q

Properties of Major Ab Isotypes

A

1) IgA:
- DIMER
- IgA1,2
- Mucosal Immunity, Neonatal Passive Immunity
- Has SECRETORY COMPONENT

2) IgD:
- Naive B cell Antigen receptor

3) IgE:
- MONOMER
- Mast Cell activation (immediate hypersensitivity)
- Allergic reaction

4) IgG:
- MONOMER
- IgG1-4
- Opsinization, complement activation
- Antibody dependent cell-mediated cytotoxicity
- Neonatal Immunity
- Feedback Inhibition of B cells
- MOST ABUNDANT!!!!!!

5) IgM:
- PENTAMER
- Naive B cell antigen receptor
- Complement activation

131
Q

Antibody: Effector Mechanisms

A

1) Neutralization - Abs neutralize viruses, bacterial toxins (LPS) and other harmful substances by blocking their interaction with cell surface receptors
2) Agglutination - Cross-linking occurs because Abs possess two identical Ag-binding sites—> microbes can be agglutinated into mesh-like structures called immune complexes
3) Activation of Complement- Abs can trigger an activation of complement cascade via classical pathway
4) Opsinization - Abs can bind Fc receptors on Macrophages and Neutrophils that enhances phagocytosis
5) Antibody- Dependent Cell Mediated Cytotoxicity (ADCC) - Fc receptors on NK cells —> Ab- tagged killing of tumor cells and virus-infected host cells
6) Degranulation - of mast cells, basophils and eosinophils - IgE binding to Fc receptors on the cells

132
Q

Which Cells express MHC, BRCs and TCRs

A
  • Macrophages and DC express both CLASS I and CLASS II MHC
  • T Cells express the TCR and CLASS I MHC
  • B Cells express BRCs and both CLASS I and CLASS II MHC molecules
  • Granulocytes (neutrophils, mast cells, eosinophils, and basophils) express CLASS I MHC only!!!!!
  • Erythrocytes (RBC) DO NOT EXPRESS MHC, BCRs, or TCRs
133
Q

Papain on Antibodies

A
  • Cuts and isolates the Ag binding sites of the Antibodies

- Produces 2 subunits of each one of the Fab regions on the Antibody

134
Q

Pepsin on Antibodies

A
  • Cuts the Heavy chain (in half) and forms one subunit with both Fab regions but some of the Fc is missing

Immunology (6 decks)

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