Y3 Immunology > week 2 - phagocytes > Flashcards

week 2 - phagocytes Flashcards

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1
Q

Innate vs adaptive immunity

innate

A

Rapid (minutes to hours)
Evolutionarily old
Relatively non-specific
No specific memory
Mostly driven by myeloid cells

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2
Q

Innate vs adaptive immunity

adaptive

A

Slower (days)
Found only in vertebrates
Highly specific
Highly specific memory
Driven by lymphoid cells

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3
Q

maturity of immune cells

A

Immune cells are specialized white blood cells (leukocytes) that originate from hematopoietic stem cells in the bone marrow.

Their maturation is a developmental process where they gain specialized functions, with lymphocytes maturing in central lymphoid organs (bone marrow or thymus) and myeloid cells maturing in the bone marrow or tissue. This maturation is crucial for distinguishing between self and non-self, ensuring effective defense without attacking the body’s own tissues.

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4
Q

maturity of immune cells

Key Immune Cell Types and Maturation Locations
* B Lymphocytes (B cells):

A

Originate and mature in the bone marrow. They specialize in antibody-mediated (humoral) immunity

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5
Q

maturity of immune cells

Key Immune Cell Types and Maturation Locations
* T Lymphocytes (T cells)

A

Originate in the bone marrow but migrate to the thymus to mature and undergo “education”. They are involved in cell-mediated immunity, specifically controlling intracellular pathogens.

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6
Q

maturity of immune cells

Key Immune Cell Types and Maturation Locations
* Natural Killer (NK) Cells

A

Originate from common lymphoid progenitors in the bone marrow, providing rapid defense.

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7
Q

maturity of immune cells

Key Immune Cell Types and Maturation Locations
* Myeloid Cells (Neutrophils, Monocytes, Dendritic Cells):

A

Formed in the bone marrow. Monocytes circulate in the blood and become macrophages in tissues.

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8
Q

maturity of immune cells

Key Immune Cell Types and Maturation Locations
* Dendritic Cells:

A

Mature upon encountering pathogens, becoming highly effective antigen-presenting cells (APCs) that bridge innate and adaptive immunity.

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9
Q

maturity of immune cells

Immune Cell Maturity and Education
* Thymic Selection:

A

Immature T cells (thymocytes) undergo rigorous positive and negative selection in the thymus, where only about 1–5% survive to become mature, functional T cells.

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10
Q

maturity of immune cells

Immune Cell Maturity and Education
* Self-Tolerance

A

During maturation, cells that react strongly to self-antigens are destroyed (negative selection) to prevent autoimmune disease.

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11
Q

maturity of immune cells

Immune Cell Maturity and Education
* Naïve to Effector

A

Mature lymphocytes that have not yet encountered their specific antigen are considered “naive”. Once they recognize a specific antigen, they activate, proliferate, and differentiate into effector cells (e.g., plasma cells, helper T cells).

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12
Q

maturity of immune cells

Immune Cell Maturity and Education
* Memory Cells

A

Some activated B and T cells differentiate into memory cells, which provide long-lasting immunity and faster, more vigorous responses upon re-infection.

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13
Q

maturity of immune cells

Maturity Over the Lifespan
* Birth to Infancy:

A

The immune system is functional at birth but matures rapidly in early childhood, with the most significant development occurring in the first three years. Infants rely on passive immunity from maternal antibodies initially.

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14
Q

maturity of immune cells

Maturity Over the Lifespan
* Adulthood

A

The immune system fully matures and is characterized by a balance of memory cells and specialized, quick-responding cells

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15
Q

maturity of immune cells

Maturity Over the Lifespan
* Aging (Immunosenescence)

A

The thymus shrinks (involution) after puberty, leading to a decreased production of new T cells. Older adults have fewer naïve cells and more memory/exhausted cells, reducing vaccine efficacy and increasing susceptibility to infection and cancer.

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16
Q

maturity of immune cells

Peripheral Lymphoid Organs

A

After maturation, lymphocytes travel to peripheral lymphoid organs (lymph nodes, spleen, MALT) to encounter antigens and initiate adaptive immune responses.

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17
Q

THE PHAGOCYTIC CELLS

Macrophages

A
  • Tissue-resident macrophages are sentinels of infection
  • Specialised, dependent on tissue (e.g. alveoli and stomach, different macrophages)
  • They:
    o Tackle the primary infection
    o Raise the alarm
     In a sense, constant surveillance
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18
Q

THE PHAGOCYTIC CELLS
Macrophages: recognition

A
  • Recognise foreign particles via:
    o Endogenous ligands on the pathogen surface (PAMPs)
    o Host factors that are deposited onto the surface
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19
Q

THE PHAGOCYTIC CELLS

Macrophages: phagocytosis

A

More on this in later lectures
Happens at the same time as the alarm
Digesting and potentially providing antigens to the adaptive immune system

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20
Q

THE PHAGOCYTIC CELLS

Macrophages: the alarm:

A
  • Particle uptake triggers release of alarm molecules:
    o Cytokines
    o Chemokines
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21
Q

THE PHAGOCYTIC CELLS
Macrophages: the alarm:
CYTOKINES

A

general name for secreted proteins that affect nearby cells)

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22
Q

THE PHAGOCYTIC CELLS
Macrophages: the alarm:
CHEMOKINES

A

(specific class of proteins that trigger chemotaxis in some cell types – help bring in neutrophils and other cells)
 Gradient of chemicals
 Adhesion proteins expressed on inside of vessels – stopping immune cells
 TNFalpha
 IFNgamma

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23
Q

THE PHAGOCYTIC CELLS

Macrophages: the alarm:

PROCESS

A

bacteria trigger macrophages to release cytokines and chemokines

vasodilaton and increased vascular permeability cause redness, heat and swelling

inflammatory cells migrate into tissue releasing inflammatory mediators that cause pain

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24
Q

THE PHAGOCYTIC CELLS

Dendritic cells

A
  • Tissue resident (early cells in infection as in the tissue)
  • Phagocytose and destroy pathogens
  • Constitutively macropinocytose
  • Then use the pathogenic material that they have collected to activate T-lymphocytes
    o The major ANTIGEN PRESENTING CELLS
     A key link between innate and adaptive immunity
  • Membrane extensions (dendrites)
    o Act like fishing nets to scoop in and sample extra cellular matrix (taking up traces)
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THE PHAGOCYTIC CELLS Dendritic cells Difference with macrophages
- Macrophages stay - Dendritic cells about antigen presenting cells
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THE PHAGOCYTIC CELLS Dendritic cells Not all DCs are the same
- There are actually many subsets (although many go to the lymph not all do) - E.g.: the CD103+/- populations of dendritic cells (Varol, 2009 & Bogunovic 2009) o CD103+ DCs migrate to lymph nodes for antigen presentation o CD103- DCs remain tissue based and promote local T cell and inflammatory responses - Role of CD103+ DCs in gut tolerance (Scott, 2011)
27
THE PHAGOCYTIC CELLS Neutrophils
- Frontline of attack, responding rapidly to cytokines and chemokines - Migrate rapidly to the infection site, phagocytose and kill the pathogen then self-destruct - Growing evidence of a complex role in resolving inflammation (Cassatella 2009)
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THE PHAGOCYTIC CELLS Neutrophil chemotaxis:
- Attracted to a range of chemoattractants o C5a o IL-8, IFNgamma  E.g. ATP attracts them to uninfected tissue damage (McDonald, 2010) from diagram - Pocket of dead cells in middle - Can see red ATP being diffused out (see ppt for gradient that neutrophils follow)
29
THE PHAGOCYTIC CELLS Phagocytes: some exceptions
- In humans, a specialised sort of T-cell, the gamma-delta T-cell, is also phagocytic (Wu, 2009) - B-cells in bony fish and Xenopus also appear to phagocytose (Li 2006)
30
THE PHAGOCYTIC CELLS Phagocyte defects are severe
- E.g. chronic granulomatous disease (CGD) o Defect in the oxidative burst, used by phagocytes to kill pathogens. o Highly susceptible to infection (including organisms usually thought of as non-infectious)
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THE NON-PHAGOCYTIC CELLS Eosinophils Deal with
large pathogens (e.g. parasitic worms) that are too big to phagocytose
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THE NON-PHAGOCYTIC CELLS Eosinophils contain
a range of toxins/enzymes that are released in response to antibody (esp. IgE) coated pathogens) o IgE antibody most likely to recognise parasites o Quick directive response
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THE NON-PHAGOCYTIC CELLS Eosinophils also found in
- Note that eosinophils are also found in invertebrates but how they work is unclear
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THE NON-PHAGOCYTIC CELLS Eosinophil granules
- Major basic protein 1 (MBP1) - ECP/RNase3 - EDN/RNase2 - EPX/EPO
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THE NON-PHAGOCYTIC CELLS Basophils compared to Eosinophil
- More unknown
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THE NON-PHAGOCYTIC CELLS Basophils - Contain range of
toxins/enzymes and are frequently found close to internal parasites (e.g. worms) or exoparasites (e.g. tick bites)
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THE NON-PHAGOCYTIC CELLS Basophils only known function is in
allergy
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THE NON-PHAGOCYTIC CELLS Basophils controversial data
- Some controversial data suggests a role in Th2 antigen presentation (Leslie 2010) - Review on “amateur antigen-presenting cells” (Schuijs, Hammad and Lambrecht, 2019) o Thought to be involved in lots so harder to pin down
39
THE NON-PHAGOCYTIC INNATE IMMUNE CELLS Mast cells
- Major orchestrator of inflammation - Degranulate in response to IgE (within seconds) - Releasing inflammatory mediators
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THE NON-PHAGOCYTIC INNATE IMMUNE CELLS Mast cells release inflammatory mediators Class of product: Enzyme
Examples: Tryptase, chymase, cathepsin G, carboxypeptidase Biological effects: Remodel connective tissue matrix
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THE NON-PHAGOCYTIC INNATE IMMUNE CELLS Mast cells release inflammatory mediators Class of product: Toxic mediator
Examples: Histamine, heparin Biological effects: Toxic to parasites Increase vascular permeability Cause smooth muscle contraction
42
THE NON-PHAGOCYTIC INNATE IMMUNE CELLS Mast cells release inflammatory mediators Class of product: Cytokine
Examples: IL-4, IL-13 Biological effects: Stimulate and amplify Th2-cell response Examples: IL-3, IL-5, GM-CSF Biological effects: Promote eosinophil production and activation Examples: TNF-α (some stored preformed in granules) Biological effects: Promotes inflammation Stimulates cytokine production by many cell types Activates endothelium
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THE NON-PHAGOCYTIC INNATE IMMUNE CELLS Mast cells release inflammatory mediators Class of product: Chemokine
Examples: CCL3 Biological effects: Attracts monocytes, macrophages, and neutrophils
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THE NON-PHAGOCYTIC INNATE IMMUNE CELLS Mast cells release inflammatory mediators Class of product: Lipid mediator
Examples: Prostaglandins D₂, E₂; Leukotrienes B₄, C₄ Biological effects: Cause smooth muscle contraction Increase vascular permeability Stimulate mucus secretion Examples: Platelet-activating factor Biological effects: Attracts leukocytes Amplifies production of lipid mediators Activates neutrophils, eosinophils, and platelets
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THE NON-PHAGOCYTIC INNATE IMMUNE CELLS Mast cells Local Reponses to infection
- Mast cells are present in all the bodys surfaces - They constitutively bind IgE antibody on their surface - Binding of the cognate antigen triggers cytokoine and chemokine release
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THE NON-PHAGOCYTIC INNATE IMMUNE CELLS allergy
Eosinophils/Basophils can also be recruited to the same sites and have a role in allergic reactions
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THE NON-PHAGOCYTIC INNATE IMMUNE CELLS Natural killer cells
- Lymphoid-derived but still a major player in innate immunity - Act early in infection to kill infected host cells - Killing is mediated by the release of toxic granules and the induction of apoptosis in the target cell
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THE NON-PHAGOCYTIC INNATE IMMUNE CELLS Natural killer cells process
MHC class I on normal cells is recognised by inhibitory receptors that inhibit signals from activating receptost - NK cells does not kill the normal cell altered or absent MHC class I cannot stimulate a negative signal. the NK cell is triggered by signals from activating receptors - activated NK cell releases granule contents inducing apoptosis in teh target cell
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THE NON-PHAGOCYTIC INNATE IMMUNE CELLS Killing of tumour cells by NK cells
- Natural Killer (NK) cells are innate lymphocytes that eliminate tumor cells by balancing activating and inhibitory signals, acting as a crucial first line of defense against cancer. They detect "missing-self" (low MHC-I) or "induced-self" (stress ligands) on cancer cells, triggering direct lysis via perforin/granzymes and apoptosis through death receptors (TRAIL/FasL).
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THE NON-PHAGOCYTIC INNATE IMMUNE CELLS Killing of tumour cells by NK cells Mechanisms of NK Cell-Mediated Tumor Killing
- Direct Cytotoxicity - Death Receptor-Mediated Apoptosis - Antibody-Dependent Cellular Cytotoxicity (ADCC): - Cytokine Production:
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THE NON-PHAGOCYTIC INNATE IMMUNE CELLS Mechanisms of NK Cell-Mediated Tumor Killing - Direct Cytotoxicity
: Upon recognizing abnormal cells, NK cells release cytotoxic granules containing perforin (which creates pores in the target cell membrane) and granzymes (which enter the pore to induce apoptosis).
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THE NON-PHAGOCYTIC INNATE IMMUNE CELLS Mechanisms of NK Cell-Mediated Tumor Killing - Death Receptor-Mediated Apoptosis
NK cells express ligands like TRAIL and FasL, which bind to corresponding death receptors on the surface of cancer cells, triggering cell suicide.
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THE NON-PHAGOCYTIC INNATE IMMUNE CELLS Mechanisms of NK Cell-Mediated Tumor Killing - Antibody-Dependent Cellular Cytotoxicity (ADCC)
NK cells use their CD16 (FcγRIII) receptor to recognize the Fc region of antibodies bound to tumor cells, activating a potent, targeted killing response.
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THE NON-PHAGOCYTIC INNATE IMMUNE CELLS Mechanisms of NK Cell-Mediated Tumor Killing - Cytokine Production:
NK cells produce tumor-priming cytokines, such as interferon-γ (IFNγ) and tumor necrosis factor-α (TNFα), which facilitate the maturation of dendritic cells and strengthen the immune response.
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COORDINATING THE INNATE IMMUNE RESPONSE Detecting infection
- First line of defence (skin, AMPs, etc.) are constitutively active - Once bypassed, the first cell to be activated is the tissue macrophage - The macrophage o Releases inflammatory signals o Phagocutoses and destroyes the pathogen o Acts as an antigen presenting cell to trigger adaptive responses (locally)
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COORDINATING THE INNATE IMMUNE RESPONSE Detecting infection process: the macrophage
the macrophage expresses receptors for many bacterial consitiuents bacteria binding to macrophage receptors initate the release of cytokines and small lipid mediators of inflammation macrophages engulf and digest bacteria to which they bind
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COORDINATING THE INNATE IMMUNE RESPONSE Phagocytes: raising the alarm
cytokines produces by macrophages cause dilation of local small blood vessels leukocytes move to periphery of blood vessel as a result of increased expression of adhesion molecules leukocytes extravasate at site of infection blood clotting occurs in the microvessels
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COORDINATING THE INNATE IMMUNE RESPONSE Inflammatory cytokines:
- Increase vascular diameter - Activate endothelial cells - Attract leukocytes
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COORDINATING THE INNATE IMMUNE RESPONSE Phagocytes
destroy the primary infection - Neutrophils (and additional macrophages), summoned by inflammation, engulf pathogens - Also extracellular trapping by neutrophils (brinkmann 2004) o Debated if this is something that we are seeing in lab
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COORDINATING THE INNATE IMMUNE RESPONSE Activation of adaptive immunity
- DCs migrate to lymph nodes - Present antigen to naïve T-cells, activating them
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COORDINATING THE INNATE IMMUNE RESPONSE Activation of adaptive immunity APCs
APCs deliver three kinds of signals to naive T cells 1. activation 2. survival 3. differentiation
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Innate defences – a summary - Constitutive defences
(barriers, defensins etc.)
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Innate defences – a summary - Macrophages
(first line of attack; raise alarm)
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Innate defences – a summary - Neutrophils
(main attack; kamikaze approach)
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Innate defences – a summary - Dendritic cells
(primary antigen presenting cell)
66
Innate defences – a summary - Natural killer cells
(hybrid adaptive/innate cell)
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Innate defences – a summary - Mast cells
(trigger local inflammation)
68
Innate defences – a summary - Eosinophils and basophils
extracellular destruction)
69
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