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Fall 2020 Advanced Patho > Immune System Part 2 > Flashcards

Immune System Part 2 Flashcards

1
Q

Molecular Communication in the Immune System

Cytokines =

Pro-Inflammatory Mediators (3)

  • One way Cytokines are used to create a response
    • What are the cells that live in our bloodstream? and they are all ______ = constantly produced by bone marrow
    • During a bacterial infection, what do cytokines do?
A

Cell derived chemical mediators responsible for communication between immune cells (Cyto means cell)

IL1, IL6, TNF Alpha

  • Cytokines
    • Neutrophils, Eosinophils, Basophils, Monocytes - INDUCIBLE
    • Act on bone marrow to trigger increased production of neutrophils
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2
Q

Innate Immunity

  • Barriers to Infection (3)
  • In______
  • _____ cells
  • Plasma _____ systems (3)
  • _____ Phase Response
  • ____ ____ Cells and I_______
A
  • Physical, Chemical, Microbial
  • Inflammation
  • Phagocytic cells
  • Plasma Protein Systems: Clotting System, Complement System, Kinin System
  • Acute
  • Natural Killer Cells and Interferon

Physical Barriers: skin, epithelial and endothelial boundaries, mucous membranes

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3
Q

Routes of Infection for Pathogens

  1. Mucosal Surfaces
    • ​
  2. External Epithelia
    • ​
    • *
A
  1. Mucosal Surfaces
    • ​Airway (flu)
    • GI tract (contaminated food and water salmonella)
    • Reproductive tract (HIV)
  2. External Epithelia
    • ​External surface (Physical contact ie Athletes foot)
    • Wounds and Abrasians
    • Insect Bites (Vector that gets it across the epithelial like instects that inject ie Ticks)
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4
Q

Frontline of Defense: Barriers

(3)

Examples of each (3) (5) (1)

A
  1. Mechanical Barriers
    • Tight Junctions
    • Flow of air or fluid across barriers to prevent lingering of pathogens
    • Mucus and Cilia
  2. Chemical Barriers (reduce pathogenic microbial proliferation)
    • Low pH in stomach
    • Fatty Acids
    • Digestive enzymes in stomach
    • Lysozyme (salivary enzymes) in saliva
    • Antibacterial peptides
  3. Microbiome
    • Natural flora and microorganisms that live in our body
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5
Q

Second Line of Defense

=

Steps

  1. Damaged tissue releases _____ increasing ____ flow to the area
  2. Histamines cause capillaries to _____, releasing ______ and _____ factors into the wound
  3. Phagocytes _____ bacteria, dead cells, and cellular debris
  4. _____ move out of the capillary to ____ the wounded area
A

Inflammation

  1. Steps
    1. Histamines, blood
    2. leak, phagocytes, clotting
    3. Engulf
    4. Platelets, seal
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6
Q

Inflammation (Notes)

  • What needs to be present to cause an inflammatory response?
  • (2) Responses
A
  • Injury and Presence of a pathogen
  • Vascular Response, Cellular Response
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7
Q

Vascular Response (Notes)

What happens?

A

Vasospasm

Vasodilation

Increased Capillary permeability (redness, heat, edema)

Delated Vascular Stasis

“delivering blood and fluid to flush the wound and gets flushed into lymphatic system”

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8
Q

Cellular Response

What happens?

  • Chemotaxic _____ of ______ to area
    • ​First wave:
    • Second wave:
  • Transmigration =
A
  • migration of leukocytes
    • ​Neutrophils -> release reactive O2 species and lysosomal enzymes -> provides debridement
    • Monocytes that turn into macrophages will clean up the mess and switch to anti-inflammatory and healing response when things settle down
  • Leukocytes squeezing out of blood vessel to enter interstitial space
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9
Q

Inflammation Summary

I____ or _____ of a _____ triggers inflammation (how?)

  1. Injured tissue releases ______ that activate ______
  2. Injury activates ____ Cells which release?
  3. Macrophages detect/_____ pathogen then release?
  4. Activated ______ stimulate _____ cells to release?

  • ________
    • Vasodilation, Increased permeability (redness, heat, edema), Delayed Vascular Stasis
  • _____ ______
    • Chemotaxic migration of leukocytes to area
  • ______ of ______
    • Pathogens phagocytized or destroyed via ________ killing
    • Phagocytic cells carry ____ through ____ fluid to the nearest?
A

Injury or Presence of a Pathogen

  1. cytokines -> macrophages
  2. Mas cells -> pro-inflammatory mediators
  3. ingests -> pro-inflammatory mediators
  4. Macrophages -> Mast Cells -> pro-inflammatory mediators
  • Vascular
  • Cell Migration
  • Attack of Pathogens
    • extracellular
    • antigen -> lymph -> lymph nodes
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10
Q

Inflammation Summary (Notes)

**Cellular Initiators of Inflammation** =

Edema happens due to?

Delayed Vascular Stasis =

Neutrophils will ___ but Macrophages carry antigens to lymph nodes and present to _____ _-cells (___) incase it needs to activate an immune response

A

Tissue Macrophages and Mast Cells

leaking of albumin (swelling)

Caused when fluid leaks out, what is left is very sluggish viscous fluid - which keeps leukocytes in the area (3rd response of inflammation in the cascade)

die, Helper-T cells (CD4)

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11
Q

How Macrophages are Inflammatory Mediators

Activated Macrophage Secretes a range of Cytokines

Key ones to focus on are? and their functions?

    1. 3.
A
  1. IL1 = activates mast cells
  2. TNF alpha = causes vasodilation and increased capillary permeability
  3. IL6 = important for the systemic inflammatory response
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12
Q

Things that Activate Mast Cells

(4)

A
  • Injury
  • Interleukin 1 (coming from macrophage or straight from injured cells)
  • IgE (allergies)
  • Complement Proteins (C3a and C5a)
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13
Q

2 Things that Happen When we activate Mast Cells

(2)

Definitions

A
  • Degranulation: Immediate response - of all the mast cell’s secretory granules, it releases all of the stuff in its granules
  • Synthesis of Leukotrienes and Prostaglandins: Long term response - make the inflammatory response painful (prostaglandins)
    • vascular effects -> increased permeability -> exudation
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14
Q

Degranulation

What is secreted? and what are their effects?

(3)

A
  • Histamine -> Vascular effects -> dilation, increased permeability -> exudation​ (potent vasodilator to increase permeability)
  • Neutrophil chemotactic factor -> attracts neutrophils to site -> phagocytosis
  • Eosinophil chemotactic factor -> attracts eosinophils
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15
Q

Vascular Events Location

Where do vascular events during inflammation happen?

Flow of blood?

_____ surrounds capillary bed

A

Microcirculation: capillaries, arterioles, venules

Arterioles -> capillary beds -> Drains into venules

Tissue

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16
Q

Events of Transmigration

(3)

A

Migration to site

Adhesion

Transmigration

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17
Q

General Cell Derived Chemical Mediators

  1. Histamine
    1. ​Source:
    2. Stimuli for release:
    3. Effects:
  2. Neutrophil, Eosinophil Chemotaxic factors
    1. ​Source
    2. Stimuli for release:
    3. Effects:
A
  1. Histamine
    1. ​Mast Cells, Basophils, Platelets
    2. Leukocyte inflammatory activation, platelet activation
    3. Increase Vasodilation, Increase Vascular Permeability
  2. Neutrophil, Eosinophil Chemotaxic factors
    1. ​Mast Cells, Basophils
    2. Inflammatory activation
    3. Attracts circulating neutrophils and eosinophils
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18
Q

General Cell-derived Chemical Mediators

  1. Prostaglandins
    1. ​Source:
    2. Stimuli for release:
    3. Effects:
  2. Leukotrienes
    1. ​Source
    2. Stimuli for release:
    3. Effects:
A
  1. Prostaglandins
    1. ​All leukocytes, Platelets, ECs, all injured cells
    2. Leukocyte inflammatory activation, platelet activation, cell injury
    3. Increased vasodilation, Increased vascular permeability, PAIN
  2. Leukotrienes
    1. ​All leukocytes, all injured cells
    2. Leukocyte inflammatory activation, cell injury
    3. Increased vasodilation, Increased vascular permeability
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19
Q

General Cell Derived Chemical Mediators

What are the 2 inflammatory mediators that cause the most of the Damage

  1. ________
    1. ​Source:
    2. Stimuli for release:
    3. Effects:
  2. ________
    1. ​Source:
    2. Stimuli for release:
    3. Effects:

What are the 2 major cells that release these inflammatory mediators?

A
  1. Reactive O2 Species (released extracellulary)
    1. All Leukocytes (especially neutrophils, macrophages), Platelets, ECs
    2. Leukocyte inflammatory activation, Platelet activation, Cell injury
    3. Main function is to destroy pathogens but also causes collateral damage to neighboring host tissue
  2. Lysosomal Enzymes
    1. ​Neutrophils, Macrophages
    2. Inflammatory activation
    3. Degradation/Digestion as a part of phagocytosis, also some release into extracellular space to cause pathogen injury (also results in host tissue injury)

Neutrophils and Macrophages

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20
Q

Cytokines

(3)

A

TNF alpha

IL1

IL6

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21
Q

TNF-alpha

  1. Source (4)
  2. Stimuli for Release:
  3. Local Effects
    1. Increased ______, Increased ______
    2. Increased leukocyte _______, m_____ and n_____ attraction and activation, promotes macrophage ________
  4. Systemic Effects
    1. Increased _ _ _, f____, decreased a______, increased liver production of? (ie. CRP, MBL)
A
  1. Activated Macrophages, NK cells, Mast cells, injured cells
  2. Inflammatory activation or cell injury
  3. Local
    1. vasodilation, vascular permeability
    2. adhesion, monocytes and neutrophils, phagocytosis
  4. Systemic
    1. CRH, fever, appetite, acute phase proteins
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22
Q

IL-1

  1. Source:
  2. Stimuli for Release:
  3. Local Effects
    1. Increased _______, Increased ________, increased leukocyte ______
  4. Systemic Effects
    1. Increased _ _ _, f_____, decreased ______, increased liver production of? (CRP, MBL)
A
  1. Activated Macrophages, Injured cells
  2. Inflammatory activation or cell injury
  3. Local
    1. vasodilation, vascular permeability, adhesion
  4. Systemic
    1. CRH, fever, appetitie, acute phase proteins
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23
Q

IL-6

  1. Source:
  2. Stimuli for Release
  3. Systemic Effects
    1. Increased _ _ _, f_____, decreased _____, increased liver production of? (CRP, MBL)
A
  1. Activated Macrophages, EC’s
  2. Inflammatory activation or cell injury
  3. Systemic
    1. CRH, fever, appetite, acute phase proteins
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24
Q

Plasma Protein Systems

(3)

A

Complement System

Kinin System

Clotting System

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Complement System ## Footnote 1. Source (1) 2. Stimuli for Release: (3) 3. Effects: Enhances vascular changes (increased \_\_\_\_\_, increased \_\_\_\_\_\_\_), aids leukocyte \_\_\_\_\_, chemo\_\_\_\_ and activation, promotes phagocytosis via \_\_\_\_\_\_, direct ____ of pathogens via ______ \_\_\_\_\_ \_\_\_\_\_
1. Liver 2. Presence of pathogen, Part of acute phase response, Part of adaptive immune response 3. vasodilation, vascular permeability, adhension, chemotaxis, opsonization, killing via membrane attack complex
26
Kinin System ## Footnote 1. Source: 2. Stimuli for Release: 3. Effects:
1. Liver 2. Activated by clotting system (in response to tissue injury and/or platelet activation, activated by neutrophils) 3. Incrased vasodilation, Increased vascular permeability, pain
27
Clotting System ## Footnote 1. Source: 2. Stimuli for Release: 3. Effects: Forms blood ____ to control bleeding, clotting enzyme ____ also promotes inflammation via increased leukocyte \_\_\_\_\_, increased p\_\_\_\_\_, increased _ \_ _ and _ \_
1. Liver 2. Tissue injury or platelet activation 3. clot, thrombin, adhesion, prostaglandins, PAF, NO
28
Overview of Complement System ## Footnote The complement system is made up of circulating _____ \_\_\_\_\_ that activate in a ______ of enzymatic _____ to accomplish (3) purposes **Is the most potent part of?**
plasma proteins, cascade of reactions 1. **Promotes inflammation** 2. **Directly Kills pathogen** 3. **Tag a pathogen for later killing (opsonization)** **Innate immunity** A plasma protein system that all starts as inactive proteins that goes through a cascade and activates each other
29
Purposes of the Complement System (Notes) ## Footnote **Directly Kill Pathogens =** **Opsonization =** **Opsons =**
Some of the proteins assemble wtih each other and turn into a **pore (big hole) aka Membrane attack complex** that inserts itself into the pathogen -\> water rushes in and cell dies **(Lyse) -**"these proteins flip a switch and kill bacteria like transformers" **Tagging a pathogen for later killing** **A protein tag** that attaches to the membrane of the pathogen and tags it for phagocytic killing by macrophage or neutrophil
30
Ways to Activate the Complement System (3)
1. Presence of Pathogen 2. As part of a Systemic Inflammatory Response 3. Can be activated by adaptive immunity (antibody-mediated) - B lymphocytes produce antibodies that attach to surface of pathogens and trigger activation of complement system
31
Systemic Inflammatory Response (Notes) ## Footnote AKA known as what response? In chronic inflammation, increased concentrations of **cytokines (3)** reach high levels start triggering a systemic response -\> f\_\_\_\_, increased \_\_\_\_, acts on **\_\_\_\_ to produce systemic inflammatory _____ (2)** - which triggers the complement system
**Acute phase response** **IL1, IL6, TNF alpha,** fever, wbc, **liver -\> proteins (CRP, MBL)**
32
The Kinin System ## Footnote * Activated Clotting Factor ____ synthesizes * _________ which converts ______ to \_\_\_\_\_ * Kinins then have 4 effects =
* Factor XII (XIIa) * **Kalikrein, Kinongens -\> Kinins (Bradykinin)** * 4 effects 1. **Stimulate complement system** 2. **Promote localized vasodilation and increased capillary permeability** 3. **Activate pain receptors** (along with prostaglandins) 4. **Act as chemotaxins** - to draw more neutrophils and macrophages to the area
33
The Kinin System (Notes) ## Footnote Another plasma protein system that intersects with the clotting system * Activated by ______ and potentiates inflammation by producing more inflammatory \_\_\_\_\_ * Inflammation -\> _____ arrive and release _____ -\> triggers blood ____ and **convert inactivated kininogens to active Kinins** * **​Kallikrein =** * **Kinins =** * (2) both cause the **pain** asctd with inflammation * Bradykinin also produces?
* inflammation -\> mediators * neutrophils, Kallikrein -\> blood clots * activated form of factor 12 which is the first protein in the clotting cascade * (similar in structure to bradykinin) * Bradykinin and Prostaglandins * Secondary area of pain (that's larger than the primary area ie skin around a cut also tender - zone of pain that protects against maniupulation of the damaged part) allodynia
34
The Clotting Cascade ## Footnote 3rd Plasma Protein system * Intrisic Pathway = damage to? * Extrinsic Pathway = damage to? * Starts with activation of? * Wherever you start, end point is a single reaction of **inactive _____ to active _____ -\>** which converts **\_\_\_\_\_\_ (individual strings of spaghetti)** to **\_\_\_\_\_\_ (spaghetti clumps)** * What does fibrin do? * What does thrombin do?
* Blood vessels * Tissues (outside vessels) * **Kallikrein (Factor 12)** * **​Prothrombin -\> Thrombin, Fibrinogen -\> Fibrin** * Traps rbc and wbc to create **Bloot clots** * Enhances **inflammation via Protease activated receptor-\> edema**
35
What is this a picture of?
Fibrin
36
Leukotrienes and Prostaglandins ## Footnote Role in Inflammation = Biosynthesis of Leukotrienes and Prostaglandins 1. **Arachidonic Acid =** 2. Arachidonic Acid interacts with either 1. **2 forms of \_\_\_\_\_\_** to produce **\_\_\_\_\_\_** 2. **2 forms of \_\_\_\_\_\_** to produce **\_\_\_\_\_\_**
Inflammatory mediators that are produced by all types of cells (when damaged) 1. Substance that all forms of leukotrienes and prostaglandins are derived from and is produced by our cell membrane phospholipids 2. interacts with 1. **Cyclooxygenase -\> Prostaglandins** 2. **Lipoxygenase -\> Leukotrienes**
37
Prostaglandins ## Footnote Functions * Some cause _____ and _____ vs. some cause \_\_\_\_\_\_ * Some inhibit and some ehance platelet \_\_\_\_\_\_ * Causes \_\_\_\_\_
* Vasodilation and Edema, Vasoconstriction * Inhibit platelet aggregation, Enhance platelet aggregation * Pain
38
Leukotrienes ## Footnote Function * Lipoxin A4 and AB * Vaso\_\_\_\_\_ * Inhibit neutrophil \_\_\_\_\_ * Stimulates _____ \_\_\_\_\_ * Leukotriene C4, D4, E4 * Vaso\_\_\_\_ * **\_\_\_\_\_\_\_\*\*** **Classic ______ is dt leukotrienes** * Increased \_\_\_\_\_\_
* Lipoxin * Vasodilation * Inhibits chemotaxis * Monocyte adhesion * Leukotriene * Vasoconstriction * **Bronchospasm\*\* - Anaphylaxis** * Permeability
39
Few Tools to Reduce Inflammation ## Footnote What are 2 major ones and how do they work?
**Steroids:** most potent anti-inflammatory durgs that act by blocking phospholipase - _synthesis of arachidonic acid -_\> blocks leukotrienes and prostaglandins...however have so many SE **NSAIDs (aspirin, indomethacin):** block cyclooxygenase (COX1 and COX2) however also have so many SE (ulcers/bleeding)
40
Interactions of Some Inflammatory Mediators ## Footnote No need to memorize - just shows the events of inflammation is all \_\_\_\_\_\_ No matter who starts the inflammatory response -\> it all potentiates very \_\_\_
interconnected quickly
41
Outcomes of Acute Inflammatory Response (3)
**Resolution** **Fibrosis +/- Abscess** **Chronic Inflammation**
42
**Resolution** ## Footnote * Clearance of (3) * _______ of injured cells * Function?
* injurious stimuli, mediators, and acute inflammatory cells * Replacement * Returns to normal Undergoes healing that replaces injured cells -\> tissue looks like nothing ever happened, is IDEAL, completely healed and normal function restored
43
**Fibrosis** = **Abscess** =
Loss of function, scar formation When certain bacteria colonize the area and are difficult to clear, causes continuous cycle of recruitment and death of neutrophils - **pus = dead neutrophils** -\> the abscess can eventually celar as well as cause a scar
44
Chronic Inflammation ## Footnote Caused by? What happens is? **"\_\_\_\_\_ \_\_\_\_\_\_"** * A\_\_\_\_\_ * Mononuclear cell \_\_\_\_ * _____ (scar) and ____ of function
**Persistent Injury :** ie. viral infections, chronic/autoimmune infections, HTN, hyperglycemia dt DM, smoking, HLD **"Frustrated Repair":** Active inflammation and Attempted healing occurs simultaneously * Angiogenesis * infiltrates * Fibrosis, loss of function Fibrosis of skin is diff, but in chronic inflammation you can get fibrosis of artery walls -\> athersclerosis
45
Two types of Healing ## Footnote **Primary Intention** **Secondary Intention**
* Minimal tissue loss, clean closely apposed wound edges * Involves sealing (epithelialization) and wound shrinkage (contraction) * More tissue damage - open wounds * Involves more extensive and prolonged epithelialization, scar formation, and contraction
46
Healing by First vs. Second Intention ## Footnote 1. First Intention 1. **Reconstruction phase:** 2. **Maturation phase:** 2. Second Intention 1. **Reconstruction phase:** 2. **Maturation phase:**
1. Neutrophils -\> Macrophages that continue inflammation -\> 2nd wave of macrophages that turn off inflammatory response triggers healing (reconstruction phase) * Healing macrophages: release cytokines that cause tissue regeneration, healing 2. Wound tightens up and matures 1. Reconstruction phase takes longer with a larger wound (more susceptible to infection -\> more likely to leave a true scar) 2. Large amounts of granulation tissue and wound contraction
47
Another Flow Chart of Healing ## Footnote Example of ______ -\> chronically inflamed liver will cause _____ of liver (which is the definitionof cirrhosis) - and liver loses its ____ -\> have to take away ___ before liver becomes fibrotic
Cirrhosis -\> fibrosis -\> loses function -\> alc
48
Causes of Chronic Inflammation (3) + Examples of each
**Persistent Infections** microorganisms like tubercule bacilli, treponema pallidum (syphilis), viruses, fungi, parasites **Prolonged exposure to potentially toxic agents** (endogenous or exogenous) **Autoimmunity** ex) RA Endogenous source: DM hyperglycemia damages tissues that line vessels and nervous tissue Exogenous sources: air pollution, smoking, vaping
49
What is the immune cell responsible for switching inflammatory response to a healing response? By releasing what ____ factors
**Macrophages** **growth factors** In chronic inflammation macrophages are going to release both inflammatory and healing mediators -\> frustrating both processes and resulting in fibrosis
50
**Persistent recruitment to and/or immobilization of Macrophages at site will cause ____ sets of mediators to be released concurrently leading to "\_\_\_\_\_ \_\_\_\_\_"**
**"frustrated repair"**
51
Persistent Stimulus (Chronic Inflammation) ## Footnote Development of fibrosis in chronic inflammation. The persistent stimulus of chronic inflammation activates _____ and \_\_\_\_\_, leading to production of ____ factors and \_\_\_\_\_, which increases the synthesis of **\_\_\_\_\_.** Deposition of collagen is enhaced by decreased activity of m\_\_\_\_\_\_\_.
macrophages, lymphocytes -\> growth factors,cytokines -\> collagen, decreased activity of metalloproteinases = decreased collagen degradation
52
Major Histocompatibility Complex (MHC) = * MHC often used to refer to self-antigen or ____ antigen * MHC is actually the?
**Most important set of proteins that are self-antigens** * HLA * set of genes that codes for HLA antigen
53
MHC 1 ## Footnote * Found on which cells? * Recognized by which cells? * Function =
* All cells except for RBCs * Cytotoxic T and NK cells * Indicates virus infected, non-self, or abnormal self cells
54
MHC II ## Footnote * Found on which cells? * Recognized by which cells? * Function =
* Antigen presenting Cells (Macrophages, Dendritic Cells, B cells) * Helper T cells * Involved in antigen presentation and activation of adaptive immune response
55
MHC 1 (Notes) ## Footnote Self antigen found on all cells EXCEPT \_\_\_\_ * The most _____ from one person to the next * Start as ______ proteins -\> before it travels to _____ it binds to other proteins produced by the cell -\> then displays that protein on membrane _____ (**Self _____ + Abnormal \_\_\_\_\_)** * Signals to you that? * Signals read by (2) - cells that are responsible for identifying abnormal cells (ie virus or cancer cells) * Ex) If a host cell is virus infected, MHC 1 will bind to the ____ protein before it gets to the membrane and ____ the viral protein in the air and signals "this is a host cell that belongs to my body and it is making viral protein"
RBC's * varied * intracellular -\> membrane, surface (**self** **recognition + abnormal protein)** * "I belong to your body and I am making this type of protein right now" * **NK and CD8 T cells** * **​**viral protein, wave ​
56
MHC II (Notes) ## Footnote Self antigens found only on (3) cells -\> bc they carry out specific job of? which is the key first step in? * Recognized by? * ex) macrophage digests a pathogen and binds it to MHC II -\> MHC II presents antigen to CD4 T cell -\> CD4 T cell recognizes MHC II as self and antigen as virus then initiates adaptive immune response
**Macrophages, Dendritic Cells, B cells -\>** **Antigen Presentation** -\> Adaptive immune responses * **CD4** **Helper Cell T cells** **MHC II:** secondary MHC protein found on these 3 cells and is key in communicating with CD4 T cell to trigger adaptive immune response
57
Overview of Adaptive Immune Response ## Footnote **APC =** * Presents _____ (red triangle) attached to MHC __ to ____ cell (red receptor) * Triggers either __ or __ cell response * **B Cell Response:** * **T Cell Response:** * Each response creates a * ​**Banked set:** * **Effector set:**
**​**Antigen Presenting Cell (Macrophage, Dendritic Cell, B lymphocytes) * Antigen, MHC II, CD4 Helper T cell * B or T * CD4 T cell has to find the complementary **B lymphocyte** and once triggered B cell to make copies of itself * CD4T will find the **complementary CD8 T cell** and once triggered will make copies of itself * 1 set is banked as **memory cells** to sit in lymphatic system for next time we encounter this pathogen * B cells that will undergo terminal differentiation that will secrete the antibodies to fight the infection vs. T cell set that goes off and attacks the pathogen in the plasma (adaptive immune response)
58
Steps in Development of the Adaptive Immune Response ## Footnote 2 major steps * **Generation of Clonal Diversity:** * Key aspect: * **Clonal Selection:**
Initial process of developing our huge library of B and T cells that can respond to any antigen we encounter, happens mostly in early development We produce all these B and T cells before we EVER encounter the pathogen Selection, proliferation, and differentiation of individual B or T cell that specifically **complements the antigen,** and eventually fights the pathogen
59
Production of T and B cell Library T cells * Produced in ___ \_\_\_\_ as \_\_\_-T lymphocytes and migrate to the ____ gland * Acquire ___ and ___ surface _____ that will determine their \_\_\_\_ * Also requires a T cell ____ that indicates the cell's ____ (what antigen this T cell can fight)
* Bone marrow, pre, Thymus * CD4 or CD8, surface markers, function * receptor, specificity
60
Why can we produce T cell receptors against antigens we've never encountered? **(3)** Basic Sets of Genes that code for T cell receptors
**Random Rearranging of genes** that code for a variety of T cell Receptors ## Footnote **V gene** **J gene** **C gene**
61
Risk of Randomization ## Footnote Risk: **Clonal Deletion:** **Central tolerance:**
Randomization can produce **Autoreactive T cell receptor** that binds to self-antigen and kills our own cells Process that **Kills autoreactive cells** done by self-antigen epithelial cells throughout the thymus gland -\> this produces **Central Tolerance (**bc happens within central lymphoid structures)- our first level of protection against autoimmune disorders
62
B Cells ## Footnote Process is almost identical B cell development happens in the?
Bone Marrow
63
Genetics of the B cell Receptor ## Footnote Coded by a set of genes (**3)** that are randomaly rearranged to produce a wide variety of B cell receptors * And in the bone marrow we have epithelial cells that display self-antigen -\> so if any newly formed B cells bind to self antigens, they are ______ = **\_\_\_\_\_ \_\_\_\_\_**
**V, D, J genes** deleted = **Central Tolerance** **Conclusion:** The mature B and T cells leave the bone marrow and thymus gland, carry B and T cell receptors that are naive but capable of fighting pathogens they have not yet encountered and are hopefully not auto-reative.

Fall 2020 Advanced Patho (15 decks)

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