Module 3- Immune System Flashcards
IgG
most abundant, antiviral, antibacterial, antitoxin, in all body fluids, crosses the placenta
IgA
second most common, secretory - in tears, colostrum, saliva, and bodily secretions to protect mucosal surfaces. Prevents attachment of viruses and bacteria onto epithelial cells
IgM
lysis of microorganisms, first antibody produced by the fetus and immature B lymphocytes, first produced in response to an infection
IgD
very low levels, functions unkown
IgE
least common, responsible in inflammation and allergic responses as well as combating parasitic infections
Type I Hypersensitivity Disorders
IgE Mediated
Allergic reactions
Type II Hypersensitivity Disorder
Antibody Mediated Disorders (cytotoxic mediated)
IgE and IgM - directed at tissues in the host
Cell lysis, inflammation, or injury
4 types:
1. Complement-Activated Cell destruction
2. Antibody-Dependent Cell Cytotoxicity
3. Complement and Antibody Mediated Inflammation - cellular destruction doesn’t occur, just inflammation. Antibodies activate the complement pathway and leads to inflammation
4. Antibody-Mediated Cellular Dysfunction - cells are not destroyed, the autoantibodies bind to cell surface receptors and form antibody receptor complexes
Type III Hypersensitivity Disorder
Immune Complex-Mediated
Immune complexes deposit in blood vessels or extravascular tissues activating the complement system and leading to inflammation
Lupus
Type IV Hypersensitivity Disorder
Cell Mediated
Delayed response carried out by T cells that damage tissues.
Types:
Direct cell-mediated toxicity: the CD8+ cells eliminate any cell presenting the antigen. Even if the cell is infected with an antigen that’s not going to harm the cell. For example, certain types of hepatitis, the damage to the liver comes from the T cells and not the hepatitis itself.
Delayed hypersensitivity reactions: occur on the skin and mediated by antigen presenting cells showing the T cell the antigen and their activation occurs via cytokines from the helper T cells. The antigens that penetrate the skin bind to self-proteins and then are displayed on the MHC proteins, triggering the immune response. It generally causes arrhythmia (redness) and itching on the skin.
Contact dermatitis, poison ivy
Cardinal signs of inflammation
Rubor - redness Calor - heat Dolor - pain Tumor - swelling Loss of function
Explain the vascular stage of acute inflammation
Vascular stage:
After injury, vasoconstriction followed by sustained vasodilation of the arteriole and venule (hyperemia) caused by histamine or nitiric oxide. Endothelial cells loosen their intercellular junctions and this makes the vessels leaky.
Exudate is pushed out of the capillaries into the interstitial space, creates an osmotic shift in the interstitial space.
Edema results in the interstitial space as water will move there because of the protein rich exudate. This causes the swelling at the site of the injury.
Then there will be blood clotting, slowing of the blood flow to the area as it becomes congested. This also isolates the area to stop the spread of microbes.
Explain the Cellular Stage of Acute Inflammation
Margination and adhesion - leikocytes accumulate on the wall of the vessel, they bind to the receptors on the endothelial cells, and mediators are released from the endothelial cells to allow leukocytes to attach.
Transmigration - the leukocyte attached to the endothelial cells signals to start breaking down intercellular junctions so they can squeeze through.
Chemotaxes - the leukocytes follow the chemical gradient of the chemoattractant mediators.
Activation - leukocytes are activated by the mediators, they find the microbes that have been marked via optimization or the complement system, they are now their targets, and they will phagocytose the particles so they’re no longer a threat.
Explain the mechanism for HIV
- Attachment - after exposure to the virus, HIV enters the bloodstream or is carried to lymphoid tissue by a dendritic cell or antigen presenting cell, where it will find a CD4+. HIV binds to the CD4+ receptors and GP120 and 41 viral proteins.
- Internalization & uncoating - the outer layer of the virus sheds so proteins and genetic info can be released into the cytoplasm.
- DNA synthesis via Reverse Transcriptase - the viral enzyme (reverse transcriptase - will take the genetic code stored in the viral mRNA and convert it to viral DNA.
- Integration: the viral DNA is integrated into the CD4+ cell’s own DNA using the virus enzyme integrase.
- Transcription - the host cell’s transcription factors will use the virus’ DNA to generate viral proteins
- Viral protein production - create polyproteins which are large proteins that need to be cut into individual proteins to activate.
- Cleavage - Use another viral protein called protease which acts like scissors on the polyprotein chain
- Assembly - put the new proteins and mRNA and package into our new virus particles which will go find other CD4 cells to infect, and this process will eventually kill our CD4 host cell.
What is innate immunity?
Innate immunity, also called natural immunity, is the first line of defense. This type of defense is in place before an infection takes place and can function immediately. It is comprised of physical, chemical, cellular, and molecular defenses.
How does the skin act as a physical barrier?
The skin’s design makes it a strong physical barrier. It has closely packed cells in multiple layers that are continuously being shed. Keratin covers the skin, which creates a salty, acidic environment inhospitable to microbes. It also contains antimicrobial proteins and lysozymes that inhibit microorganisms and help to destroy them.
What cells are involved in innate immunity?
The cells responsible for this response include neutrophils, macrophages, dendritic cells (DC), natural killer (NK) cells, and intraepithelial lymphocytes.
Describe each type of leukocyte and explain their function:
Neutrophils are the most abundant in the body and are an early responder in innate immunity and use phagocytosis to kill microbes. Eosinophils are active in parasitic infections and allergic responses. Basophils release histamine and proteolytic enzymes. Monocytes are the largest in size and are released from the bone marrow and mature into macrophages and dendritic cells where they engage in the inflammatory response and phagocytize foreign substances and cellular debris. Macrophages have a long life span, reside in the tissues, and are the first phagocyte that organisms encounter. Neutrophils and macrophages work together on behalf of the host’s initial defense system.
Describe adaptive immunity:
Adaptive immunity, also called acquired immunity, is the second line of defense and includes both humoral and cellular mechanisms that respond to cell-specific substances known as antigens. Adaptive immunity is acquired through previous exposure to infections and other foreign agents. It can not only distinguish self from nonself but can recognize and destroy specific foreign agents based on their different antigenic properties. This response takes more time but is extremely effective.
What are antigens?
Antigens are present on the surface of pathogens or other foreign substances that elicit the adaptive immune response.
What are the primary cells of adaptive immunity?
The primary cells of the adaptive immune system are the lymphocytes, APCs (antigen presenting cells), and effector cells.
