Immuno U1 Flashcards
Antigens
Foreign substances that induce the host reponse
Immunity
Having resistance towards an infection
Attenuation
Making a pathogen less virulent
Innate immunity
The first response to something foreign, no prior exposure, no memory cells
Adaptive immunity
The next responses (after innate), prior exposure needed, memory cells available
Neutrophils
Destroy foreign particles
Eosinophils
Kill parasites, phagocytose, releases cytokines
Basophils
Releases histamine for allergic reactions
Monocytes
Eats foreign material and removes dead cells
Macrophages
Innate - phagocytise and kills microbes
Adaptive - brings antigens to T cells and makes cytokines
Tissue cells
Kills microbes, eradicated intracellular parasites, secrete cell mediators
Mast cells
Enhance and suppress the adaptive response - in tissues
Innate lymphoid cells
CD16 and CD56
Kills virus cells and tumor cells
Helps with tissue remodeling
Dendritic cells
Most potent phagocytic cell and an effective APC
Lymphocytes
B, T, NK cells
B cells
Antibody production
CD19, CD20, CD21
matures in BM
Differentiates into plasma cells which secrete antibodies
T cells
CD3
mature in thymus
Helper T - CD4, make cytokines for antibody production
T reg - CD4, inhibit immune responses
Cytotoxic - CD8, destroy virus cells and tumor cells
Primary lymphoid organs
BM and thymus
BM
Source of HSCs, matures B cells
Thymus
Matures T cells
Second lymphoid organs
Spleen, lymph nodes, MALT/CALT
Spleen
Destroys old RBCs, rich in macrophages
Lymph nodes
Collects lymph fluid
MALT
on mucosa surfaces, GI, respiratory, urogenital tracts
main port of foreign antigens
macrophages and lymphs
CALT
found on skin and eyes
monos, macrophages, dendritic, T cells
innate immune system
internal and external defense system
external defense system
anatomical barrier
skin, respiratory tract, GI tract, stomach, tears and saliva, microbiota
skin
physical barrier with secretions that limit microorg growth
epidermis - epi cells coated in keratin
dermis - covered in blood vessels, hair follicles, sebaceous and sweat glands, WBCs
resp tract
mucous secretions block bacteria from attaching to epi cells
coughing and sneezing remove potential pathogens
cilia clears out deposited material
GI tract
flushes out potential pathogens by maintaining pH of 5 with lactic acid
stomach
prohibits microorg growth with hydrochloric acid which keeps pH at 1
tears and saliva
lysozymes attack walls of GP bacteria
microbiota
takes up space in the body so pathogens cannot land establish a spot
internal defense system
cellular responses recognize certain molecular components
PRRs, acute-phase reactants, inflammation, phagocytosis, NK cells
PRRs
recognize unique molecules associated with the infection
TLRs
binds to particular substances
activates cytokines
makes chemokines that enhance phagocytosis
destroys pathogens before the disease sets in
CLRs
binds to mannan and B-glucans on fungal cells
activates cytokine and chemokine production
acute-phase reactants
rapidly responds to infection
limits host destruction cause by proteolytic enzymes
recycles minerals for inflammation
CRP
response time: 4-6 hrs
increased by: 1000x
function: complement activation (an opsonin)
fibrinogen
response time: 24 hrs
increased by: 2-5x
function: forms a clot
haptoglobin
response time: 24 hrs
increased by: 2-10x
function: binds hemoglobin
inflammation
body’s reaction to injury or infection
cardinal signs - redness, swelling, heat, pain
phagocytosis
process of ingesting pathogens - adheres, engulfs, makes phagosomes, granule contact, makes phagolysosome, digests enzymes, excretes
enhance by opsonins
cells involved - macrophages, dendrites, neut, mono
oxidative burst
HMP shunt converts NADP to NADPH
also converts O2 to H2O2 and OH
O2 independent pathway
cell pH is altered resulting in activation of lytic enzymes
NK cells
recognizes damaged cells and removes them
this gives adaptive immunity time to respond with specific T and B cells
first line of defense - virally infected or tumor cells
cytotoxic mechanisms can be inhibited, activated, or alternative
CD 56
adaptive immune system
cell-mediated immunity and humoral immunity
cell-mediated immunity
key component - T cells (CD 3)
role of T cells
circulate in bloodstream looking to activate APCs to start the adaptive response
T cell differentiation flow
double negative (CD 4- and CD8-)
double positive (CD 4+ and CD8+)
single positive (CD 4+ or CD8+)
mature T cell (Th, Th1, Th2, Treg, Tc)
double negative
driver: chemokines
shotgun: thymocytes (gets to choose which genes can be made into unique binding sites)
kids: a/B chains (seeks out antigens)
double positive
negative selection - thymocytes that fail to bind or bind too strongly to MHC antigens will die from apoptosis
positive selection - thymocyte TCRs that moderately recognize the MHC antigens can move on
single positive
when selection happens, the thymocyte gets to choose a profession - express CD 4 or CD 8
thymocytes that end up binding with self antigens undergo apoptosis instead
mature T cell
cytokines help differentiate the thymocyte into a specific T subset
T helper
makes antibodies and activates adaptive response
CD 4+ and CD 3+
Th1 - activates cytotoxic lymphs and macro for direct killing
Th2 - helps B cells with making antibodies
T regulatory
suppressed the immune response towards self antigens and secretes inhibitory cytokines
CD 4+, CD 3+, CD 25+
cytotoxic T
binds and destroys infected cells with cytotoxic granules
CD 8+ and CD 3+
humoral immunity
key component - B cells and antibodies
role of B cells
make antibodies and can be either T-independent or T-dependent
T-independent
does not need helper T cells
makes ONLY IgM
no memory cells are made
polysaccharides link with BCRs
T-dependent
needs helper T cells
can switch from making IgM to other immunoglobulins
memory cells are made
increased BCR affinity
B cells differentiation flow
pro-B cell
pre-B cell
immature B
mature B
pro-B cell
made from rearranged genes that code for heavy and light chains, once a heavy chain is made, the cell can become a pre-B cell
pre-B cell
heavy IgM chains + short Iga and IgB chains = pre-BCR
heavy chains express with surrogate light chaints
immature B cell
pre-BCR is replaced with a functional BCR
composed of 2 heavy and 2 light chains
variable region
determines specificity and is an antigen receptor
B cell surface proteins
BCR, CD 21, CD 40, MHC II
central tolerance
eliminates B cells with self-reactive receptors
if the immature B cell can survive central tolerance, move to next stage in spleen
mature B cell
once stimulated, B cell enters antigen-dependent phase to become either memory cells or plasma cells
develops in the spleen
exhibits both IgM and IgD
plasma cell
found in BM and lymphoid organs
make antibodies
no surface Ig, only cytoplasmic Ig
CD 38 and CD 138
marginal B cell
remains in spleen
fast response to bloodborne pathogens
follicular B cell
migrates in lymph nodes and other SOs
recirculates
