Test 4 Flashcards
Steps in phagocytosis
- WBC find target by taxis
- Pseudopods surround particle and form a phagosome (the pouch formed when the particle is brought in)
- Fusion of phagosome + lysosome = phagolysosome
Phagolysosome
Fusion of the phagosome and the lysosome
-Where digestion of ingested materials occurs.
What happens after phagocytosis
Unique and recognizable parts (antigen) are processed and placed on the phagocytic cell surface. The WBC’s then show the level 3 defenses the antigen and they know who they need to look for.
*level 3 cells only recognize antigen when placed on a WBC surface
MHC-2
Major Histocompatibility Complex, which is the holder of the antigen.
Once a phagocytic WBC has an antigen on it what is it called
Antigen Presenting Cell (APC)
-cell has officially changed roles and will travel to lymph nodes and present antigen to level 3 cells.
APC is the ____ of all level 3 responses
Activator
Examples of bacterial antigens
- Cell wall/membrane
- Exoenzymes and exotoxins (proteins)
- Flagella, pili, or fimbrae
- Capsule or glycocalyx
Viral antigens
- Capsomeres
- If enveloped virus: peplomers
- Tegument
- Enzymes
Fungi/worms/protozoa antigens
- Cell surface protein
- Enzymes
Antigens
- Usually parts of proteins (complex)
exceptions: glycoproteins - Proteins on surfaces of abnormal “self” cells are also antigenic
Inflammation
Non specific process triggered by any damage to tissues (basophils and mast cells are the cells that respond)
Inflammation response
Release: Histamine, prostaglandins, leukotrienes, stored inside cells to have a local effect on capillaries.
What do the chemicals released due to inflammation cause?
-Increase arteriole dilation and increased capillary permeability
What is the leaving of blood from blood vessels called
Diapedesis
Result of inflammation
Number of level 2 cells increases in the tissue
Resulting signs of inflammation - latin and english
Rubor - Redness
Calor - Heat
Tumor - Swelling (accumulation of fluid and cells)
Dolor - Pain, due to increased pressure on nerve endings
Acute inflammation
Damage to tissues with good response of delivering white blood cells where they are needed
Chronic inflammation
Can cause actual damage to own tissues
Natural Killer Cells
- Come from T cell line
- Wandering WBC’s
- Use perforin to make pores
- Also use granzyme to trigger apoptosis to kill abnormal eukaryotic cells
- non-specific and destroy anything exhibiting abnormal behavior such as cancerous cells, infected self cells, protozoa/yeast
*protozoa/yeast = too large to phagocytize so once apoptosis happens, leftover pieces can be phagocytize and then APC’s can be made
Granzyme
An enzyme that causes spontaneous apoptosis to kill abnormal EUKARYOTIC cells
Interferons
- Released by infected cells to tell neighboring cells to be careful
- neighboring cells produce anti-viral proteins ahead of time (thanks to the warning from the interferons)
- Neighboring cells are thus protected from viral attack which slows down the viral passage
Complement proteins
- Created by liver and secreted into the blood
- Triggered to bind sequentially to form enzymes
- Level 2 trigger: pathogen molecule (esp. LPS in Gr- or capsule in Gr- and Gr+)
- -non specific (any Gr- or Gr+ or Gr+ with capsule)
Once complement proteins are triggered what are the results?
- Phagocytosis
- Inflammation
- Membrane attack
What do complement proteins enhance?
- Phagocytosis (opsonization) - helps get rid of small yeasts and bacteria..gives the WBC’s something to grab on to.
- Inflammation - complement proteins stik on tissues causing inflammation w/o tissue damage
- allows more phagocytes/killer T cells - Membrane attack complex - proteins form a channel in abnormal cells
- cell contents leak out causing lysis and cell death
Level 3 defenses
Command center: lymphoid organs
-Monitor body fluids
Lymphatic system
Series of vessel which drain body tissues
-punctuated by lymph nodes, which catch what is drained by the tissues
Cells involved in the level 3 defenses
T and B lymphocytes
-Both produced in the bone barrow, but mature in different locations
Where do T cells mature
The thymus
Where do B cells mature
In the bone marrow
-This is to destroy cells that would respond to antigens on our own cell surfaces so that the only ones left find antigens on foreign cells and then attack. Once mature dumped into circulation then jump into lymphatic organs (nodes, spleen, etc.)
Lymphoid organs
- Lymph nodes
- Spleen - filters blood, important in septicemia infections
- Mucosal associated lymphatic tissues (MALT) - tonsils, adenoids, peyers patches, appendix (catch pathogens at mucus membranes)
What happens if the pathogen gets into lymph organs without being processed
Phagocytosis won’t occur in lymphoid organs, so the pathogen is basically home free to reproduce
What are the 2 types of MHC holders? what do they do?
Class I MHC - all nucleated cells (except RBC’s)
-display for: recognition and ID of abnormal cells. (T&B cells don’t respond to an antigen held in MHC 1)
Class II MHC - Antigen presenting cells
-macrophages, dendritic cells, B-lymphocytes.
-Are on cells that carry antigen to lymph nodes.
Once a Th0 cell is converted to a Th1 what do the secreted cytokines do?
- Cause APC cells to kill better/faster
- Activate T cytotoxic (Tc0) to rapidly clone info about antigen which results in a huge number of T cytotoxic cells
Majority: Tc Clones are active currently and go to the bloodstream and tissues using chemotaxis to find Antigen bearing cells.
Minority (small amount): Stay dormant, don’t work during first exposure, but work later on in another exposure to the pathogen, wander around
How do T cytotoxic cells find specific infected or abnormal self cells?
Chemotaxis - antigen in MHC -1
-Use perforin and granzyme to destroy specific abnormal eukaryotic cells which includes: infected self cells, cancerous self, yeast, protozoa, worms
When the pathogenic threat is over what happens to cloned Tc Cells and Th1 cells? and memory cells
Die - they are short lived
Memory cells live forever however some research has shown that as someone ages, Tm cells decline.
What happens in a second exposure to the same pathogen?
All primary responses at normal time
- Tm cells = no need for APC
- -touch antigen to activate and become active T cytotoxic cells within minutes (the pathogen won’t have much time to reproduce/create enzymes, toxins etc - ends up saving a lot of time - host may never even feel symptoms)
Humoral immunity steps
Activation of B cells
-MHC-2 or B cell receptors in membrane
T dependent activation (most common)
-APC enters lymph nodes
–Stimulates Th0 to create Th2
—Th2 activates virgin B-cells to clone (bind to MHC-2 on B cell surface)
Cloned B-cells differentiate into:
-Majority: plasma cells which secrete antibodies which travel into plasma
-Minority: become B-memory cells - dormant plasma cells, don’t respond during first exposure.
Humoral immunity activates ____ cell while cell mediated initiates
B;T
When threat is over humoral immunity/second exposure
Antibodies last about 1-7 weeks, broken down and recycled
- plasma cells die within several days
- Bm cells remain in lymph node for potentially ever in preparation for second exposure to pathogen
Second exposure:
- Primary response plus:
- -Bm respond to antigen quicker w/o APC
- -form plasma cells which secrete antibodies in 1-2 days
Antibody structure
Globulin group of proteins (Y shaped) known as gamma globulins or immunoglobulins (Ig)
- All antibodies have Y shape/combinations of monomers
- Each has 2 long amino acid chains, and 2 short amino acid chains
Tips of Y on antibody
Fab
- Fraction which is Antigen Binding
- Variable (specific to antigen, so can change)
Base of Y on antibody
Fc
- Fraction which is crystallizable or constant
- does not change
Antibody Types
IgG IgA IgM IgE IgD
IgG Antibody
- highest percentage in circulation in blood at any time
- monomers
- found in blood and tissues, works against local, focal, septicemia
- can cross placenta to protect fetus, anything mother is exposed to the baby will also get IgG….maternal antibodies can persist for up to 6 months after birth
IgA
- 10-15% of circulating antibodies (in an active form)
- Present as monomers, get combined in glandular secretions where they turn into a dimer and then become active
- Any surface that is covered in mucus there is IgA
- Found in blood, tissues
- Transported through glands for release in secretions (found in saliva, nose, vagina, resp. lining)
- Absorbed directly w/o being broken down (babies) - helps protect them from focal/local infections because baby can absorb them in dimer form
What type of infections would IgG protect from
local, focal, septicemia
What antibody can cross the placenta?
IgG
IgM
- 5-10% of circulating antibodies
- pentomer
- primarily found in circulation (blood stream)
- works well against septicemia, but not focal or local
IgE
- less than 1% of circulating antibodies
- monomer
- found in blood and tissues
- involved in allergies
- found and bind to inflammatory cells (mast, basophils, eosinophils)
- allergies are not inherited, some of us have more B cells that then create IgE to cause allergic reaction
- a lot of things can affect production of IgE
Which antibody is involved in allergies and allergic responses
IgE