immune system and defend against disease

Pathogen

Disease causing organism

Resistance (immunity)

Body’s ability to ward off disease

Susceptibility

Lack of resistance

Leukocytes

• Neutrophils, eosinophils, basophils

• Monocyte → macrophages

• T lymphocytes (T cells), B lymphocyte (B cells) and natural killer cells

Location of leukocytes

• Lymphatic system

• Certain organs

• Skin epithelium

• Mucous membranes

• Connective tissue

Interleukins

Regulate immune cells

Tumor necrosis factors

Destroy tumor cells

Colonies stimulating factors

Stimulates Leukopoiesis

Interferons

Antiviral, inflammation

Innate (nonspecific) immunity

bodies defense against a wide variety of foreign substances and pathogens

• Immediate, broad (nonspecific) protection against many pathogens at once

• Present at birth

• Fast response

• No memory of pathogens

Adaptive (specific) immunity

• Fight a specific pathogen

• Develops overtime

• Slower response

• Has memory of pathogen and will respond faster if exposed again

Body’s first line of defense

External, prevent entry

Examples:

• Skin - physical barrier

• Mucus membrane - lines body cavities exposed to outside

• Tears - protect eyes

• Urine - cleans urethra

Body second line of defense

Internal

• Neutrophils - phagocytosis

• Monocytes - change into macrophages to perform phagocytosis

• Bails and mast cells - secret histamine inflammatory and allergic reaction

• Natural killer cells - type of lymphocyte that is able to kill a wide variety of infected cells in some tumor cells

• Eosinophils - fight, parasites, involved in reducing allergic reactions

Antimicrobial proteins (in blood)

• Discouraged, pathogen growth

• Interference which reduce spread of viral infection infections

• Compliment - group of proteins that protect against bacterial infections

Inflammation

A nonspecific response to tissue damage / injury

Functions of inflammation

• Eliminate pathogens and harmful substances

• Prevent their spread

• Prepare damaged area for tissue repair

Causes of inflammation

• Pathogens (infections)

• Trauma, surgery

• Chemicals

• Extreme temperatures

• Ischemia

Stages of inflammatory response

1. Release of chemicals

2. Vascular changes which include vasodilation, increased vessel, probability, cell adhesion, molecule display

3. Leukocyte recruitment - neutrophils and macrophages leave blood and enter damaged tissue to perform phagocytosis

   • Neutrophils arrive first

   • Wandering macrophages arrive later

   • Margination - leukocyte CAMs stick to vessel CAMs

   • Diapedesis - leukocyte squeeze out of the vessel walls and into the tissue

1. tissue repair

Vasodilate blood vessels

Increased blood flow to damaged area which causes redness, heart, and pain

Increase vessel permeability

Allow substances normally found in blood to move into damaged tissue, which causes swelling

Exudate

Fluid in cell buildup that washes the affected area

Inflammatory chemicals

• Histamine

• Prostaglandins

• Chemotactic factors

• Serotonin

• Nitric oxide

Histamine effects seen in allergies

• Bronchoconstriction - difficulty breathing

• Increased mucus production

• Stimulates nerve endings which causes itching in pain

Leukotriene effects in asthma

Constrict airway

Prostaglandins

Contribute to fever

Signs and symptoms of inflammation

• Heat

• Redness

• Swelling

• Loss of function (sometimes)

• Pain

Acute inflammation

Has rapid onset and lasts less than two weeks

Chronic inflammation

Can have rapid / slow onset, less more than two weeks, may result in scarring, occurs when tissues are unable to overcome injury

Pus

Normal buildup of dead phagocytes, damaged tissue, and fluid

Abscess

Accumulation of pus in a confined space

Ulcer

An open store accompanied by pus and tissue necrosis

Cellulitis

A a serious spreading inflammation of subcutaneous or connective tissues

Tissue repair steps

1. Macrophages secret growth factors which stimulate fibroblasts

2. Fibroblasts produce a collagen framework

3. Cells replaced damage damaged cells

Factors affecting tissue repair

• in adequate blood supply is needed

• Adequate protein and vitamin C are needed

• Healing is faster than young people, slower in the older and diabetics

• If the wound is large or the cells cannot undergo mitosis, scar tissue forms

• If scar tissue joins tissues, together abnormally, the result is an adhesion

Fever

In elevated body temperature that helps the body fight infection

Pyrogen

Fever producing substance

Fever production

Pyrogens cause hypothalamus to produce prostaglandins

Prostaglandins reset the hypothalamic thermostat

Onset - chills and shivering, raise his body temp to new fever temp

Stadium - time when fever is maintained

Crisis occur occurs when pyrogen is gone in body reduces fever by sweating and vasodilation

Benefits of fever

• inhibits reproduction of microbes

• Promotes interferon activity

• Increases immune response

• Accelerates tissue repair

Complications of fever

• Dehydration

• Seizures

• Coma

• Permanent brain damage

• Potential death

Adaptive (specific) immunity

Body’s defense against a specific pathogen or foreign substance

Immunology

Study of the bodies response to antigens

Antigen

Foreign substance that provokes an immune response. Example, bacteria, viruses, toxins.

Antibody (immunoglobulin)

Protein produced by immune system in response to an antigen period antibody will bind to inactivate that specific antigen

Two features of adaptive immunity

• Specificity - target a specific antigen and also has to recognize self from non-self

• Memory- if exposed to the same antigen again, immune system system recognizes it, and will launch a faster attack

Active immunity

Produce your own anti antibodies and memory cells

Natural active immunity

Exposure to an antigen causes production of antibodies

Artificial active immunity

Vaccination

Vaccination

Exposed body to weakened / in active form of antigen. Body launches immune response and creates memory cells. If ever exposed again to that same antigen, immune response is much faster and you won’t get sick.

Natural passive immunity

Maternal antibodies passed to infant through placenta or breastmilk

Artificial passive immunity

Patient given injection of antibodies ( in potentially high risk exposure situations)

Naturally occurring (genetic) immunity

Produce blood group anti antibodies for antigens we don’t have

Species immunity

Reason why we don’t get many animal diseases and vice versa

Development of lymphocytes (T cells and B cells)

1. Both are produced by red bone marrow. B cells mature here.

2. T cells mature in the thymus

3. Both types of lymphocytes are tested for immunocompetent, and self tolerance

4. B cells + antibody mediated immunity anti T cells - cell mediated immunity

5. Lymph organs - where mature B and T cells reside until needed in the lymph nodes, spleen, tonsils, MALT

Major Histocompatibilty complex antigens

• Embedded in cell membranes of muscle cells, different for each person

• MHC antigens help T cells recognize self from non-self

• MHC antigens are responsible for transplant. Rejection. In rejection, T cells don’t recognize foreign MHC anti antigens, and will attack transplanted organ

• To prevent rejection, match as many MHC antigen as possible between donor and recipient and give immunosuppressant drugs to recipient for life

Helper T cells

Secrete interleukins and help increase the number of T cells in B cells

Cytotoxic T cells

Destroy cells containing foreign antigens

Memory T cells

Remember the antigen and react quickly, if the body ever encounters the same antigen again

Regulatory T cells

Suppress them in response contribute to self tolerance

Plasma cells

Produce antibodies

Memory B cells

Remember the antigen and react quickly, if the body ever encounters the same antigen again

An APC

1. Phagocytizes the foreign antigen

2. Combines it with MHC-ll antigen

3. Then displays the combination on its cell membrane. This is called antigen processing.

Activation of T cells

To become activated, a T cell binds its TCR to the antigen-MHC complex and also is caused cumulated by interleukin-2. The binding and chemicals are both required for activation.

Clonal selection

When’s activated, large numbers of tea cells are produced, which differentiate into either cytotoxic, helper, or memory T cells

Elimination of invader

Cytotoxic T cells destroy cells containing the foreign antigen

Activation of B cells

Helper T cells in interleukin-4 are required to activate B cells

Clonal selection

After activation, large numbers of memory cells and plasma cells are produced. Plasma cells produced antibodies.

Elimination of invader

Antibodies bind to an inactivate the foreign antigen. This antigen antibody complex, then gets phagocytized by macrophages

Ig G

Most abundant, protects against bacteria and viruses, crosses the placenta

Ig M

First antibody released after an infection, high levels, indicate a recent infection

Ig A

Helps protect mucous membranes, levels decreased during stress

Ig D

Serves as the B cell receptor, involved in B cell activation

Ig E

Helps protect against parasitic worms, involved in allergic reaction when level levels are high (most common)

Primary response

First encounter with antigen, slow increase in number of antibodies (can take days)

Secondary response

Second encounter with same antigen, faster, and stronger response than primary because memory cells are present

Age

Babies - need to develop immunity, breastmilk is beneficial in disease prevention

Elderly - decreased number of T cells in B cells, T cells become less responsive to infections

Autoimmune diseases

• immune system doesn’t recognize normal cells “self” and attacks them

• Twice as common in woman

AIDS

• caused by HIV

• Transmission through infected body fluid

• No cure, some success with end of our drugs, ending the process to aid

• Prevention - use universal precautions, use latex condoms, avoid IV drug use

Hypersensitivity / allergy

Immune system overreacts to a substance tolerated by others

Allergen

Antigen that causes an allergic reaction

Types of reactions

1. Types l or igE mediated reactions

   • Most comic allergic reaction

   • Signs- watery eyes, runny nose, sneezing, itchiness, inflammation, hives, or difficulty breathing

   • Example: be venom, latex, cat, dander, mold, pollen, dust

First exposure to allergen : sensitization

Allergen stimulates production of IgE which then binds to mast cells

Second exposure : response

Same allergen attaches to IgE already present, which causes a mass cells to release histamine, which then has inflammation effects

Anaphylactic shock

Life-threatening, systemic, allergic reaction, results and difficulty breathing and symptoms of shock

Type ll or cytotoxic reactions

Produce antibiotics against normal antigens on blood cells / tissues, these antibodies attached to normal sub, engine and cell and mark the cells for destruction. Example: incompatible, blood transfusion, Graves’ disease, drug allergies.

Type lll or immune complex reactions

• antigen, antibiotic complex escapes, phagocytosis, and inflamed tissue. Example: celiac disease.

Type lV or cell mediated reactions

• happens 12- 72 hours after exposure to allergen

• T cells involved in tissue destruction

• Example: tuberculosis, poison ivy, toxin, auto immune disease, transplant, rejection