BIOL255 FINAL KSU

non-specific, present at birth

innate defenses

specific, must be aquired

adaptive defenses

first and second line

innate defense lines

third line

adaptive defense lines

surface barriers

first line

protective cells, fluids in body (interferons/phagocytes)

second line

B and T cells

third line

physical, chemical (reproductive/GI tract), genetic, microbiome @ birth

4 categories of NON specific defenses

GI tract, target bacteria

chemical defense - BACTERIOCINS

skin, target bacteria + fungi

chemical defense - CATHELICIDIN

throughout body, target bactera + fungi + viruses

chemical defense - DEFENSINS

skin, target bacteria + fungi

chemical defense - DERMICIDIN

broad spectrum mediators, part of innate immunity, first line of defense, most target cell membrane

role of antimicrobial peptides (AMPs)

some hosts are gentically immune to pathogen (ex: CF immune to chlorea)

how does genetic variation play a role in immunity

biota competes with oppertunistic pathogens (ex: introducing normal flora to reduce c. diff populations)

role of microbiota as first line of defense

surviellence of body, recognization, and destroy

3 primary goals of immune system

mononuclear phagocytic system, EF, BS, lymphatic system

subdivisions of immune system

neutrophils, eosinophils, basophils, mast cells, monocytes, lymphocytes

list all types of WBCs

lobed nucleus

granulocytes

unlobed, round nucleus

agranulocytes

granulocytes: 1st response, most abundant

neutrolphils

granulocytes: destroy eukaryotic cells

eosinophils

granulocytes: inflammation + allergies

basophils

granulocytes: non motile, warning cells

mast cells

agranulocytes: largest WBC, macrophages + dendretic cells

monocytes

agranulocytes: B + T cells

lymphocytes

delevop from bone marrow, carry O2

erythrocytes

not whole cells, produced from MEGAKARYOCYTES

platelets

soak up ECF

lymphatic capillaries

one way toward heart

what way do capillaries return lymph

lymphatic origin + maturation, bone marrow (B-cells) + thymus (T-Cell)

primary lymphoid organs

lymph nodes + spleen (FILTERS BLOOD TO REMOVE OLD RBCs)

secondary lymphoid organs

signaling proteins produced by WBCs to act as messengers

cytokines

protein signal for coordinating immune response between cells

interleukins

kind of cytokine, stimulate movement of WBCs

chemokine

cytokine produced by WBCs w/ antiviral activity, bind to surface and induce expression of antiviral proteins + cancer expression

interferons purpose

extravasation, WBCs squeeze through BV walls and enter tissue

diapendesis

motile amoeboid cells, craw along BV surface and change shape

properties that allows WBCs to survey tissue

redness warmth swelling pain

4 symptoms of inflammation

vasoconstriction (BV narrowing), BV dilluate and increased flood flow, edema + pus (NETosis), resoltion/scarring

major inflammatory response after splinter injury

initiated by pyrogens

what causes a fever

liberated by monocytes, macrophages, neutrophils (from immune system)

endogenus pyrogens

product of infectious agent (outside body)

exogenus pyrogens

cause hypothalamus to release PROSTAGLANDINS (trigger increase heat from muscles, vasoconstriction)

pyrogens

survey, ingest, extract immunogenic info from forgien

purpose of phagocytes

neutrophils (general purpose), eosinophils (parasitic/eukaryotic), macrophages (prepare info for B + T cells)

types of phagocytes + purpose

pathogen associated molecular patterns

what does PAMP stand for

molecules typically on pathogens

PAMPs

LPS/peptidoglycan on bacterial cells, flagella, microbial DNA/RNA

PAMPs examples

receptors on WBCs from PAMPs

pattern recognition receptors (PRRs)

protein receptors on cell membrane of macrophage called toll-like (TLRs), dectect foreign and signal macrophage to produce chemicals to stimulate immune response

how does a macrophage recognize a pathogen

chemotaxis (phagocytes follow gradient of stim products), binding TLRs to PAMPs, ingestion, phagolysome formation, destruction, elimination

process of phagocytosis

consists of 26 blood proteins that work to destroy pathogens

complement

stim inflammation, opsonization (flagging to engluf), membrane attack

3 ways complement can aid in destruction

specificity, memory

main 2 goals of adaptive (specific) immunity - third line

major histocompatibility complex, receptors on all cells except RBCs

explain MHC class 1 and class 2 molecules

unique characteristics of self, required for T lymph

MHC class 1

found on antigen presenting cell (APCs), present antigen to T cell

MHC class 2

any sub that elicits immune reponse

antigen

antigentic determinants, small molecular group recognized by lmphocytes

epitome

complex molecule w/ several epitope (foreign + large)

good immunogen

small, simple molecules not attached to carrier molecule

bad immunogen

too small to elicit immune response, hapten serves as epitope

what is special about immunogenicity of

haptens

only trigger response when binded to larger poteins in the body (ex. poision ivy)

example of hapten

surface marker that occue in some members but not others, determine blood group

alloantigen

potent T cell stimulators (cytocine storm)

superantigen

self tissues where tolerance is inadequate

autoallergens

mature in bone marrowm, immunoglobin + MHC 1/2, low # in BS, do not require antigen present with MHC, produce antibodies

B Cells

thymus maturation, CD mol, MHC 1 receptor, high # in BS, requires antigen present, regulate kill and syn cytokines

T cells

CD4, activated by MHC 2, activates other CD4 or CD8 cells, promote inflammation and reg immune, form memory cells

Help T Cells

CD8, activated by MHC 1, can destory cancer cell, form memory cells

Cytotoxic T Cells (Tc)

perforins and granzymes

how do Tc cells destory pathogen

macrophages, b cells, dendretic cells (abundant)

what cells can serve as APCs

depends on what set of cytokines is released from APCs

what determines if a TH cell turns into TH1 or TH2

TH cell

more prevelent t cell in BS

TH1, TH2, TH17, Treg, Tcytotoxic

types of T cells

CD4, MHC 2, activates other CD4 or CD8 cells

TH1

CD4, MHC 2, b-cell proliferation

TH2

CD4, MHC 2, increase inflammation

TH17

CD4 or CD25, MHC 2, decrease immune system

Treg

CD8,requires mhc 1 for activation, destroys via lysis

TC

large glycoproteins that serve as specific receptors of b cells and as ANTIBODIES

immunoglobins

y arrangement, 4 polypeptide chains (2 heavy + 2 light), wide range of bind sites at end of fork

immunoglobin structure

colonal selection + antigen binding, antigen presentation on MHC 2, helpter t cell interaction, clonal expansion, plasma/memory b cell

b cell naive to activated

b cell undergoes proliferation (mitosis) into large clump of genetically identical b cells, after expansion diff into plasma or memory cell

steps:

• antigen enters body

• b cell binds to antigen

• b cell recieves help from t cell

• expansion or proliferation

• differentiation

clonal expansion

long term memory, react with same antigen

memory cells

short lived release antibodies, NOT CLOTTING

plasma cell

more unique epitopes

antibodes are better with…

complement fixation, osponization, neutrilization

3 main anibody-antigen interactions

activation of complement pathway can result in rupturing of cells and some viruses

complement fixation

coating microrganism w/ specific antibodies for easy recognization by phagocytes

opsonization

antibodies fill surface receptors to prevent attachment

neutrilization

cross link into large clumps

agglutination

4 peptide chains connected via DISULFIDE bond

immunoglobin structure/bond

IgG, IgA, IgM, IgD, IgE

isotypes of immunoglobins

most prevelent immunoglobin

IgG

circulating in BS, secretions

IgA

synthesized after Ag encounter

IgM

receptor of B cells

IgD

allergic reactions

IgE