III : Innate Immunology

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144 Terms

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Innate / Natural Immunity

• Non-specific Pathogens

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Innate / Natural Immunity

• 1st & 2nd line of Defense

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Innate / Natural Immunity

- the effect gear towards to non-specific pathogen.

- Our skin will protect us against any other pathogen.

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Adaptive / Acquired Immunity

• Specific Immunity

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Adaptive / Acquired Immunity

• 3rd line of Defense

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Adaptive / Acquired Immunity

- Acquire when exposed (to vaccines)

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Adaptive / Acquired Immunity

- We have the Lymphocytes – T cells (Cell Immunity) & B cells (Humoral Immunity) both of them can produce a memory cells therefore they can participate to anamnestic response.

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Innate Immune System

- Defense against infection that immediately act when a host is attacked by a pathogen.

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  1. External Defense System

  2. Internal Defense System

Innate IS is composed of 2 systems that work to promote phagocytosis which are

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physical, chemical, & biological barriers

External Defense System is composed of what barriers that work together to prevent infection from entering the body.

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External Defense System

- Anatomical barriers designed to keep microorganisms from entering the body.

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External Defense System

- Refers to the anatomical barriers represents the epithelial barriers (skin).

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Urine

helps remove potential pathogens from the genitourinary tract.

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keratinocytes

External Defense System

The physical barrier refers to the skin particularly

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Physical Barrier

refers to the skin particularly keratinocytes that is important for the keratin to make our skin dry.

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Physical Barrier refers to the skin particularly keratinocytes that is important for the keratin to make our skin dry.

Physical Barrier refers to the skin particularly - that is important for the keratin to make our skin dry.

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Physical Barrier

Another is respiratory (mucus and cilia) cilia e.g., pseudostratified ciliated columnar epithelium smoker more risk in getting covid 19 due to damaged cilia.

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F

Another is respiratory (mucus and cilia) cilia e.g., pseudostratified ciliated columnar epithelium smoker more risk in getting covid 19 due to damaged cilia.

Physical Barrier (t/f)

Another is respiratory (mucus and cilia) cilia

e.g., pseudostratified ciliated columnar epithelium smoker is at low risk in getting covid 19 due to damaged cilia.

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Gastric Acid

External Defense System

Chemical Barrier is composed of

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  1. coughing

  2. sneezing

External Defense System

Biological barrier is composed of what mechanisms that is helping us to expel the microbes.

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Internal Defense System

- Includes cellular responses that recognize specific molecular components of pathogens.

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inflammation

Internal Defense System

Another internal defense system that will allow localization of infection is -.

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Phagocytosis & inflammation

Internal Defense System

What are important mechanisms as part of our body defense.

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• P - Pathogen – recognition Receptors

• P - Phagocytosis

• A - Acute-phase Reactants

• I - Inflammation

• N - Natural Killer (NK) Cells

Internal Defense System is composed of

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Cellular Response

Internal Defense System

– appearance of phagocytosis

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<p>Skin </p>

Skin

External Defense System

- Physical barriers with secretions that discourage microorganism growth

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<p>5.6</p>

5.6

External Defense System

- Lactic acid & fatty acids maintain the skin at a pH of approximately - (maasim).

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<p>Psoriasisn</p>

Psoriasisn

External Defense System

– a small protein produced by skin cells, has antibacterial effects.

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<p>Epidermis</p>

Epidermis

External Defense System

– tightly packed epithelial cells coated in keratin.

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<p>Dermis</p>

Dermis

External Defense System

– connective tissue with blood vessels, hair follicles, sebaceous glands, sweat glands, & WBCs.

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<p>1 stratum cornium </p>

1 stratum cornium

External Defense System

- Skin layer: - (dead skin) composed of microorganism

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<p> sebum &amp; fatty acids </p>

sebum & fatty acids

External Defense System

Sebaceous Glands is composed of

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<p>sweat</p>

sweat

External Defense System

- Sweat Glands is composed of

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<p>Keratin</p>

Keratin

External Defense System

– keeps our skin dry.

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<p>F</p><p>External Defense System</p><p>-	Severely burn skin is at <strong>high risk</strong> from getting infected. </p><p></p>

F

External Defense System

- Severely burn skin is at high risk from getting infected.

External Defense System (t/f)

- Severely burn skin is at low risk from getting infected.

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<p>Respiratory Tract </p><p>-	<strong>Mucous secretion</strong> block bacteria from adhering to epithelial cells </p><p></p>

Respiratory Tract

- Mucous secretion block bacteria from adhering to epithelial cells

Respiratory Tract

what block bacteria from adhering to epithelial cells

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<p>Coughing/sneezing</p>

Coughing/sneezing

Respiratory Tract

what moves pathogens out of tract

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<p>pseudostratisfied ciliated columnar epithelium</p>

pseudostratisfied ciliated columnar epithelium

Respiratory Tract

- The lining of our trachea is made up of - .

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<p>Goblet cells </p>

Goblet cells

Respiratory Tract

- The lining of our trachea is made up of pseudostratisfied ciliated columnar epithelium. This pseudo stratified has - this cells produced mucus that block & trap bacteria.

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<p>hydrochloric acid</p>

hydrochloric acid

Digestive Tract

What acid in the stomach keeps the pH as low as 1, prohibiting microorganism growth.

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<p>pH 1 </p>

pH 1

Digestive Tract

- Stomach’s hydrochloric acid keeps the pH as low as -, prohibiting microorganism growth.

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<p>Normal Flora / Microbiota</p>

Normal Flora / Microbiota

Digestive Tract

– Helps to keep pathogens from establishing themselves in these areas.

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<p>E. coli</p>

E. coli

Digestive Tract

can produce bacteriocins (prevent bacteria from growing) on the mouth

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<p>bacteriocins</p>

bacteriocins

Digestive Tract

o E. coli can produce - (prevent bacteria from growing) on the mouth

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<p>Clostridium defficile</p>

Clostridium defficile

Digestive Tract

o – associated with antibiotic diarrhea

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Pathogen-Recognition Receptors (PRRs)

- Recognize molecules unique to infectious organisms. (has marked in order to identify)

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Pathogen-Recognition Receptors (PRRs)

- Encoded by host’s DNA to sense extracellular infection.

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Pathogen-Recognition Receptors (PRRs)

- Recognize pathogen-associated molecular patterns (PAMPs) on microorganisms

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phagocytic cells.

Pathogen-Recognition Receptors (PRRs)

- When bound to a pathogen, activate -

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• Macrophages

• Dendritic cells

• Neutrophils

• Eosinophils

• Monocytes

• Mast cells

• T cells

• Epithelial Cells

Pathogen-Recognition Receptors (PRRs) is found on

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• Neutrophils

Pathogen-Recognition Receptors (PRRs)

– cannot attack/phagocytize by neutrophil because they are too big.

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• Eosinophils

Pathogen-Recognition Receptors (PRRs)

– attack large microorganisms like parasites.

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Toll-like Receptors (TLRs)

example of Pathogen-Recognition Receptors (PRRs)

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10 types

How many types of Toll-like Receptors (TLRs) are found in humans

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cell surface & in cytoplasm

Majority of Toll-like Receptors (TLRs) are found on the

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phagocytosis

Toll-like Receptors (TLRs)

Glycoproteins that bind to particular substances, activating cytokine & chemokine production & other processes to enhance -.

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T

Toll-like Receptors (TLRs) (t/f)

- Can destroy most pathogens that humans are exposed to before disease sets in.

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phagocytosis

Toll-like Receptors (TLRs)

- Most important in promoting & enhancing -.

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• C-type Lectin Receptor (CLR)

• Retinoic Acid

• Nucleotide-binding oligomerization domain (NOD) Receptor

Other Receptors in Internal Defense System

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C-type Lectin Receptor (CLR)

binds to mannan & β-glucans found in fungal cell walls to activate cytokine & chemokine production. The outcome is to minimize/prevent fungal infection.

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minimize/prevent fungal infection.

C-type Lectin Receptor (CLR) binds to mannan & β-glucans found in fungal cell walls to activate cytokine & chemokine production. The outcome is to -

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Retinoic Acid

– inducible gene-l like receptor (RLR)

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Acute-Phase Reactants

- Soluble factors found in serum.

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Acute-Phase Reactants

- Increase rapidly in response to infection, injury, or tissue trauma.

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Acute-Phase Reactants

- Facilitate contact between microbes & phagocytic cells.

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Acute-Phase Reactants

- Mop up & recycle important proteins after phagocytosis

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C-rp

example of Acute-Phase Reactants

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C-rp

indicator for infection & inflammation

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C-reactive Protein

Association of HLA Alleles & Disease

Response Time (hours) : 4 – 6

Normal Concentration (MG/DL): 0.5

Increase: 1000x

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• Opsonization

• Complement Activation

Association of HLA Alleles & Disease

Function of C-reactive Protein

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Serum amyloid A

Association of HLA Alleles & Disease

Response Time (hours) : 24

Normal Concentration (MG/DL): 5

Increase: 1000x

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Activates monocytes & macrophages

Association of HLA Alleles & Disease

Function of Serum amyloid A

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Alpha1-antitrypsin & Fibrinogen

Association of HLA Alleles & Disease

Response Time (hours) : 24

Normal Concentration (MG/DL): 200 – 400

Increase: 2 – 5x

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Protease inhibitor

Association of HLA Alleles & Disease

Function of Alpha1-antitrypsin

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Clot formation

Association of HLA Alleles & Disease

Function of Fibrinogen

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Ceruloplasmin

Association of HLA Alleles & Disease

Response Time (hours) : 48 – 72

Normal Concentration (MG/DL): 20 – 40

Increase: 2x

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Binds copper & oxidizes iron

Association of HLA Alleles & Disease

Function of Ceruloplasmin

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Complement C3

Association of HLA Alleles & Disease

Response Time (hours) : 48 – 72

Normal Concentration (MG/DL): 60 – 140

Increase: 2x

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• Opsonization

• Lysis

Association of HLA Alleles & Disease

Function of Complement C3

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Opsonization

an immune response process which uses opsnonin’s to tag foreign pathogens for elimination by phagocytes. Without an opsonin, such as an antibody, the negatively-charged cell walls of the pathogen & phagocyte repel each other.

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Crp

is the most common nonspecific indicator for inflammation/infection.

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Ceruloplasmin

copper transport protein & can oxidize iron.

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C3

most abundant/dominant form of complement.

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Process of Inflammation

body’s overall reaction to injury/invasion by an infectious agent.

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• Redness/ Erythema – Rubor

• Swelling / Edema – Tumor

• Heat – Calor

• Pain – Dolor

• Funciolasse – loss of function, 5th cardinal sign

Cardinal Signs & Symptoms of Process of Inflammation

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Rubor

Redness/ Erythema

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Tumor

Swelling / Edema

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Calor

Heat

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Dolor

Pain

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Funciolasse

loss of function, 5th cardinal sign

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<p>simple squamous epithelium</p>

simple squamous epithelium

Process of Inflammation

- Our blood vessels is made up of endothelial cells (-)

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<p>diapedesis</p>

diapedesis

Process of Inflammation

- Process called _ – the leukocytes can crawl between endothelial cells

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<p>T</p>

T

Process of Inflammation (t/f)

• Localize the infection which means there is no systemic infection, because when it is already systemic this will be hard to control.

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<p>T</p>

T

Process of Inflammation (t/f)

• Important for tissue repair (healing)

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<p>T</p>

T

Process of Inflammation (t/f)

- Pimples may pus cells. This pus cells will protect then and localize the infection.

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Neutrophils

– #1 cell to attack due to their small size.

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Phagosome

characterized by the presence of vacuole in the cytoplasm.

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Lysosome

granulated (acid hydrolase) then they are released/emptied

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<p>I - Initiation  </p><p>C - Chemotaxis</p><p>E - Engulfment </p><p>D - Diapedesis </p>

I - Initiation

C - Chemotaxis

E - Engulfment

D - Diapedesis

Phagocytosis

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<p>Natural Killer (NK) Cells               </p>

Natural Killer (NK) Cells

- 1st line of defense against:

• Cells that are virally infected