Chapter 15 (adaptive immune responses) Flashcards
Lymphocytes
25% of WBC. easy to find
Natural killer cells function in (NK)
innate response. 2. anti anything foreign 3. secrete apoptosis. 4 sprays foreign with perferin and inject with granzymes (> apoptosis)
T and B lymphocytes
acquired/ adaptive imunity. 2, first exposure = dangerous. 3. naive = doesnt know which nonself to destroy. 4. if microbes change = 2nd exposure still dangerous. 5. cell specific
Cell specific (regarding T and B cells)
- until exposure = naive 2. once exposed = memory cells and antibodies to recognize foreign object
Vaccines (regarding to memory cells/ antibodies)
first exposure so resistance is acquired
Antigenic shift
DNA or RNA change. T & B cells have difficulties adjusting (why we are susceptible to flu and cold)
Gamaglobulin
using someone elses antibodies to rx disease (works temporarily for hepatitis)
T Lymphocytes
born in bone marrow and mature in thymus gland.
T lymphocytes training
learn to differentiate between self and non-self in thymus gland. release into blood one differentiation is initiated
T lymphocytes circulation
from thymus gland to blood to lymphatic system and tissue. still not exposed to foreign antibodies
T lymphocytes memory cell production
exposure to foreign antibodies (but still specific dificulties making vaccine for cold and flu virus)
T memory cells product of
clonal selection
Pre- Clonal selection steps
- virus infects cell. 2. cell with nucleus produce MHC1 protein (protein of self) 3. produce abnormal proteins 4. shows fragment of self and foreign protein. (looks like wiener in hot dog bun)
Cytotoxic T cells
attracted to MHC1 displays.
Clonal selection steps
and memory cell formation
- Cytotoxic T cells visits MHC1 “nice bun, not the weiner) 2. upon exposure lymphocytes undergoes clonal selection (reproduction of picture)
Cytotoxic T cell poisoning steps
- intracellular antigen required 2. MHC1 display 3. destroys infected cell via clonal selection 4. secretes perferin 5 secretes granzymes and 6 kills host cells
Perferin
enzyme that burns hole in cell membrane then injects granzymes into cell
Granzymes
kills cell
Cell mediated immunity
(equal to Cytotoxic T cell poisoning) T Lymphocyte attacks only an intracellular antigen results in destruction of infecttion & host cell.
Autoimmunity
T lymphocytes confusing self protein for foreign protein and destroys self
Diabetes mellitus and autoimmunity
Cytotoxic T cells attack and destroy insulin producing cell of pancreas (proof from medical history, onset usually brought on by mysterious infection < cytotoxic failed to differentiate)
product of clonal selection
formation of helper cells, (not the same as memory or cytotoxic cells)
Antibody production
produced against EXTRAcellular antigens
B lymphocytes production and mature
in bone marrows (10% of lymphocytes) naive
macrophages and dendritic cells
naive B lymphocytes against Extracellular antigens
Humoral Immunity
B lymphocytes/ macrophage and dendritic cell in action consumes extracellular foreign thing
B Lymphocytes/ Macrophages/ and dendritic cells produce
MHC2 identity tags
T helper cell function in Humoral Immunity
takes place in Lymph nodes. After B Lymphocytes/macrophages/dendritic cells consume extracellular foreign thing and destroys, places own display of MHC2 protein and foreign protein.
t helper cells secretes
Interleukins (chemical msg between white blood cells) “tattle tale” to other B lymphocytes
B lymphocytes action after t helper cells
- undergo clonal selection based on t helper info. 2. form B memory cells (> immunity for life). 3. produce plasma cells
Plasma cells release
antibodies against specific antigen. (about 150K cells per second) .
Ingredients in immunity
1, memory cells produced 2. antibodies produced
Antigent Antibody Complex
Antibodies made by plasma cells made to fit molecular composition of a specific antigen (hand to a glove)
Do antibodies destroy
nope, just bind to antigen
Gamaglobulin assistance in immunity (8 steps)
- antibodies we have made as we encounter foreign objects. 2. Macrophage eats them. 3. makes display. 4, t helper cells inspect display 5. comunicate to B lymphocytes 6. produce plasma cells 7. make antibodies 8 circulate in blood and always clear
outcomes of antigen antibody formation
antibodies occupy binding site of foreign thing. if cant attach then cant infect so wont cause problems. activates complement
what is agglutination
how antibodies work: clumping of antigens so agents of immune system can destroy antigens
Activation of Complement (4 types)
“get it done” 1. Inflamation (hyperemia) 2. Opsonization phagocytosis PBJ 3. causes AAC antigen destruction in spleen via RBC4. MAC:(membrane attack complex) lysis of antigen
8 steps of destroying antigen
- CD4, B lymphatic, macrophage, dendritic cell 2. antigen presentation 3. CD4 t helper inspection 4. Interleukin release 5. clonal selection of b Leukocytes (B memory and B plasma) 6. Plasma cells > antibodies > antigen AAC 7. AAC activates complement (expose complement binding cite) 8. complement (Inflamation, phagocytosis, antigen destroyed in spleen, MAC)
HIV and T helper cells
HIV is an autoimmune disorder which kills T helper cells, if T helper cells are below 200 there is little to no resistance to anything
Gamaglobulin RX
when “Y” (antigen binding cite) lacks antibodies gamaglobulin rx is shorter but helpful
