Intro to Immunology (Week 2 Lecture 3) Flashcards
When did immunity first start being studied?
study began in the late 18th century with small pox outbreak (‘protection from diseases’)
What is immunity?
host’s defense against destructive forces from outside and within the body
* A versatile and coordinated defense system.
* Recognition (of something foreign) and Response (attack back)
Role of the immune system
- Defense against infection.
- Defense against tumors (can induce their own immune response)
- Recognition of newly introduced molecules (proteins, transplants).
- Source of inflammation (part of healing, inflammatory disease or autoimmunity).
What are the two immune responses?
- innate
- acquired
innate immune response
First immune response from birth which doesnt need to what the invading thing is to work effectively
* First response
* Immediate response
* Short term
* Non-specific (viruses, bacteria, etc.)
* Directs and initiates adaptive response
Acquired (adaptive) immune response
Aquiring the immunity is based on the characterisitics of what the infection is
* Second response
* Delayed response (days)
* Long term
* Requires exposure
* Has memory
* Specific and selective
Types of innate immunity
- anatomic barriers
- physiological barriers
- eating cells
- other cells
anatomical barriers
- Skin
- Mucous membranes
- GI and respiratory tract (eat and breath in many toxins)
physiological barriers
- Fever (growth inhibition)
- Low pH (Stomach)
- Chemical mediators
Eating cells
Phagocytes/ Endocytes are recruited to sites of infection where they recognize foreign molecule and ingest it (intracellular killing)
* Monocytes/Macrophages
* Neutrophils.
other cells (innate)
- Dendritic cells, mast cells: Recruited to sites of infection, recognize and engulf
- Natural Killers: surveillance/ killing/ transformed “self” cells (important for tumour surveillance to recognize self cells that have mutated)
Types of adaptive immunity
- cell mediated immunity
- humoral immunity
cell mediated immunity
Uses T-cells which are a type of white blood cell called lymphocytes. They help your immune system fight germs and protect you from disease.
* CD4 helper cells
* CD8 cytotoxic cells
CD4 helper cells
Help coordinate the immune response by stimulating other immune cells, such as macrophages, B lymphocytes (B cells), and CD8 T lymphocytes (CD8 cells), to fight infection.
* 5 subsets of CD4 cells (Th1, Th2, Th17, Treg and Tfh)
* IL-2, IFN- g cytokines (messengers between cells)
* targets intracellular bacteria
CD8 cytotoxic killer cells
Can directly kill cells harbouring pathogens, such as viruses
* TC1/ TC2 cells
* IL-4, IL-5, IL-10 cytokines (messengers between cells)
* extracellular bacteria antibody production
humoral immunity
Produces B cells which make antibodies to eliminate/ neutralize microbes outside the normal cell
* deals with antigens from pathogens that are freely circulating, or outside the infected cells.
Organs involved in the immune system
- Bone marrow: Origin and development (hence B cells)
- Thymus and Spleen, GI tract: Education and selection
- Lymph nodes: Reservoirs, circulation and traps
- Lymphatic vessels, blood vessels: transportation
Effect of nutrition on the immune system
One of the most sensitive systems in the body to changes in nutritional status
* measures of immune function are used to assess nutritional status
What is the leading cause of immunodeficiency worldwide?
protein energy malnutrition
futile cycle of immunity and poor nutrition
Continuum of Immune Responses
need a balance of:
* cytokines: innate (IL-2, IFN- g) and adaptive (IL-4, IL-5, IL-10)
* eicosanoids, oxylipids
* hormones (corticosteroids/stress)
* other mediators
The good of inflammation
Inflammation is essential for normal defense against pathogens and repair of tissue damage
* Redness, heat, swelling and pain
* Keeps us alive
* Means immune system is working effectively
The bad of inflammation
sustained inflammation disrupts metabolic pathways and suppresses immune response:
* Excessive tissue damage
* Induce insulin resistance by disrupting insulin signalling
* Impair ability to defend against future infection
Acute inflammation
Healing of tissue
* Immediate defense to tissue damage/injury
* Usually < 3 wks
* Neutrophils recruited to site
* Variable systemic effects
* Not necessarily associated with tissue destruction
* Followed by healing and repair
* Inflammation resolves
Chronic inflammation
Low grade inflammation is constantly on and production can be disruptive systemically
* Excessive activation and/or insufficiently regulated immune system
* Sustained duration
* Macrophages, T-lymphocytes & their mediators predominate
* Significant tissue damage
* Systemic effects
Commonly Measured Mediators
- Glucocorticoid (stress hormones)
- Interleukin-6 (IL-6)
- Tumor Necrosis Factor (TNF-α)
- Interleukin-1 (IL-1)
- Interleukin-8 (IL-8)
- Eicosanoids (prostaglandins)
Bolded are pro inflammatory
Metabolic changes with chronic inflammation (tumor)
- Liver (center of metabolism): ↑ Acute phase, ↓drug metabolism
- Muscle: ↑ proteolysis, ↓ synthesis
- Hypothalamus: ↓ appetite, ↑ sympathetic activity, ↑ REE, ↑ cortisol, ↓ testosterone
- Gut: early satiety
- produces C-reactive protein (non-specific)
- Fat: ↑ lipolysis, ↓lipoprotein lipase
- Brain: depression
