MCP 34: Lymphoid I Flashcards
three immune defense mechanisms
physical/chemical barriers, innate (non-specific) immunity, acquired (specific) immunity
physical/chemical barriers
tears, skin, mucus/cilia, commensals, gut acid
commensals
bacteria that help fight off infection, our body doesn’t destroy them
innate (non-specific immunity)
attacks anything that the body recognizes as foreign in a non-specific way, innate immunity is ancient
cells that participate in innate immunity
neutrophils, eosinophils, macrophages (from monocytes), natural killer cells
acquire (specific immunity)
T-cell immunity and B-cell immunity; much younger evolutionarily than innate immunity, sharks oldest animal to demonstrate acquired immunity
cell-mediated (T-cell) immunity
mediated by T-lymphocytes, don’t secrete antibodies but recognize antigens through T-cell receptor, TCR interacts with MHC-I on infected cell
humoral (B-cell) immunity
mediated by B-lymphoctes that originate from and mature in the bone marrow
fetal B-cells
precursors may come from the liver
mechanism of humoral immunity
mature B-cells leave bone marrow, has IgD antibody on membrane, and await activation by pathogen, once activated divide in plasma cells and memory cells, plasma cells release IgM antibodies into blood stream
plasma cells
synthesize IgM antibodies that release them into blood
memory cells
become a reservoir on activated B-cells in case the body becomes infected again
antibodies
immunoglobins, 4 subunits; 2 light chains and 2 heavy chains held together by disulfide bonds, has a variable portion and a constant portion,
variable portion of antibody
conference specificity to an antigen for a specific antigen,
somatic recombination
random shuffling on DNA sequence that encodes for variable portion, occurs during B-cell development
secondary response from memory cells
more rapid than primary response, magnitude of antibody release is greater, IgG antibodies released instead of IgM antibodies
5 mechanisms by which antibodies neutralize a pathogen
1.) agglutination 2.) opsonization 3.) neutralization 4.) cytotoxicity 5.) complement activation
agglutination
antibodies bind to antigens, forming aggregates and reducing the amount of free antigens
opsonization
binding of antibodies to the microorganism stimulates phagocytosis
neutralization
binding of antibody to microorganisms blocks their adhesion to cells and inactivates toxins
cytotoxicity
antibodies adhering to the surface of macrophages and eosinophils and inducing them to liberate chemical agents that attack the surface of the antigen
complement action
the binding of antibodies to the initial protein of the complement system triggers the complement cascade and causes cell lysis
maturation of T cells
originate in bone marrow, mature in thymus
major histocompatibility complexes
MHCs takes pieces from inside cell and displays them to the outside world
MCH-I
all cells have these, if cells is infected with virus, piece of the virus will show up in MCH-1, targeted for destruction by killer T-cells
MCH-II
found on antigen presenting cells (i.e macrophages), present material that has been brought by the APC (via phagocytoses), helper T-cells recognize as non-self and secrete interleukins, stimulates humoral immunity
cytotoxin T-cells
killer T lymphocytes, CD8+ cells monitor MHC-1 molecule
how killer T-cells kill cells
1.) lysis with perforin and granzyme 2.) activating Fas-mediated apoptosis
helper T-cells
CD4+ recognizes MCH-II molecules on APCs, secretes interleukins that stimulates humoral immunity
target of HIV infection
affects helper T-cells (CD4+ cells)
IgD
monomer, extremely low amounts in serum
IgG
monomer, largest percentage in blood
IgM
pentamere, 5-10% in blood
