Immune system Flashcards
immune system responsible for?
complex system responsible for distinguishing self from non-self, for protecting against infections
primary and secondary lymphoid organs
primary lymphoid organs: bone marrow and thymus
(site of production and education of immune cells)
secondary lymphoid organs: spleen and lymph nodes (site of interaction immune system and foreign material)
lymph nodes and spleen function
what is lymph
lymph nodes and spleen monitor contents of fluid for potential pathogens
spleen filters blood
lymph nodes filter lymph
lymph is extracellular fluid that must be drained to prevent build up
less structured lymphoid tissue also exists, ie like tonsils, peyer’s patches
spleen is also site of WBC storage and destruction of old cells
WBCs make up what % of blood
1%
what proportion of WBCs are lymphocytes, monocytes, granulocytes
30% lymphocytes
5% monocytes
60% granulocytes
lymphocytes brief description
may live decades/ lifetimes
mostly found in lymph nodes and spleen
produce loads a day
B cells and T cells
monocytes brief description
circulate in blood 24 hours
if stimulated, develop into macrophages in tissue
granulocytes brief description
/polymorphonuclear leukocytes
only live a few days
neutrophil is the most common
neutrophils: multilobed nucleus, granules contain lysosyme, gransyme, defensins
eosinophils: bilobed nucleus, granules contain histamine, cytotoxic proteins
basophils: contain mainly histamine
contents of lymph nodes
where lymphocytes reside and first encounter foreign substances
T cells and dendritic cells in paracortex
B cells in outer cortex, germinal centre
what WBC do we see in tissues
low levels of T cells
dendritic cells if in contact w ext env
mast cells
macrophages
a leukocyte is?
another word for white blood cell
myeloid lineage?
haematopoietic stem cell myeloid progenitor cell: - (RBCs and platelets) - monocyte - eosinophil - neutrophil - basophil - mast cell
monocyte to
- macrophage
- dendritic cell
lymphoid lineage?
haematopoietic stem cell
lymphoid progenitor to
T cell progenitor to:
- helper T cell
- Cytotoxic T cell
- memory T cell
Natural Killer cell
B cell progenitor to:
- plasma cell
- memory B cell
stages of infection?
entry into body replication and spread disease exit from body reinfection of someone else
how are extra vs intracellular pathogens spread
intracellular pathogens spread by cell to cell contact
extracellular pathogen spread by lymph/ blood
innate vs adaptive immunity, time difference
innate: immediate protection
0-4h preformed mediators
4-96h recruit innate immune cells
adaptive: after 96h
becomes more specific with time
innate immunity consists of
physical barriers
anti-microbial factors
pro- inflammatory factors, fever
phagocytes and NK cells
where are physical barriers important
anywhere in contact with external, included GI and genitourinary
name physical barriers of
respiratory tract eyes GI skin genitourinary
respiratory: mucus, ciliated epithelium
eyes: tears (flush), lysozyme, lactoferrin
GI: stomach acidity, intestinal pH, flora, lysozyme, mech flushing
Skin: dead layer barrier, sweat and sebum (also flush), antimicrobials, low pH, commensal bacteria, shedding
Genitourinary tract: washing by urine, vaginal secretions, urine acidity, lysozyme
what are the anti microbial factors, give examples
lysozyme and lactoferrin found in many barriers
complement proteins lyse/coat bacteria in blood to be phagocytosed
cells of innate produce anti-microbial peptides AMPs
cytokines- IFN
if cells of the innate immune system do not recognise specific pathogens, how do they identify self vs non self
express pattern recognition receptors (PRR) that respond to broad pathogen associated molecular patterns (PAMPs)
there are 4 main types of PRR
what are the cells of the innate immune system
the granulocytes, so the
basophil
eosonophil
neutrophil
mast cell
monocyte
macrophage
dendritic cell
Natural killer T cells
what are phagocytes
WBCs/ tissue dwelling cells able to ingest and kill microbes
monocytes- in blood
netrophils- in blood (most of)
macrophages- in tissues (most effective)
granules are toxic so kill bacteria
after eat a few, die and turn to pus
natural killer cells?
large granular lymphocytes, activated by cytokines, recognise altered self cells
able to recognise and kill infected cells by apoptosis over miutes or hours. NK cell comes away unharmed
what are the 4 signs of inflammation
redness, swelling, heat, pain
how may infammation lead to a fever
inflammation is local to site of infection, if factors get into blood stream may develop an in parallel systemic infection- a fever
how is a fever caused and why
triggered by toxins from infecting organsim or by immune systems own inflammatory mediators
ie IL1 acts on hypothalamus (where thermostat)
higher temp inhibits bacterial growth and speeds metabolic actions- repair, antibody prod, phagocytosis
process of inflammation resulting from tissue damage?
- microbes gain entry to host via local epithelium, cause tissue damage as proliferate
- inflammatory mediators are released by macrophages- chemokines, cytokines, histamine. These diffuse through tissue into blood
- they cause vasodilation and incr permeability
- when exposed to inflamm mediators, neutrophils (instead of rolling along vesell wall w/o stopping) stop as adhesion molecule expression changes, stick to vessel wall
- neutrophils and macrophages squeeze through the now leaky vessel wall into tissue. Migrate up chemokine gradient coming from tissue damage to site of infection
- activated en route, arrive ready to phagocytose bacteria
serum proteins like clotting factors and RBCs also leak through causing swelling, oedema, redness
inflammation in response to tissue damage therefore involves
vasodilation and increased permeability accumulation of blood leakage of clotting proteins chemotaxis of neutrophils/ macrophages, phagocytosis death of phagocytes, pus initiation of tissue repair
adaptive immunity is?
a dedicated system of tissues, cells, molecules that act in concert to provide specific immune responses
3 cardinal characteristics:
specificity
memory
discrimination (btwn self and non)
what cells make up the adaptive immune response
lymphoid lineage, so
helper T cell
Cytotoxic T cell
memory T cell
NK cell
plasma B cell
memory B cell
how does the adaptive immune system have memory/ space for so many different pathogens
selective clonal expansion
each lymphocyte has unique receptors for specific pathogen, there are 100 million different cells with different receptors
clonal expansion on contact with pathogen= lymphocyte with complementary receptor binds to pathogen, causes lymphocyte to deivide and differentiate to produce daughter cells
rapid expansion of population specific to infection
selectiv clonal expression provides differentiated cells for antigen elimination, but what else?
immunological memory
a proportion of cells will become memory cells (long lived) whilst the others go on to become effector cells
how do T and B cells develop
from common precursor- haematopoietic stem cell- in bone marrow
virgin, antigen naive cells are released,
pre T cells go to Thymus
pre B cells go to Bone marrow
(primary lymphoid organs)
self reactive cells are deleted, the rest will mature and be released into circ
quick recap- what is innate immunity
a rapid response to a challenge. not antigen specific, does not change.
B cells are responsibly for what type of immunity?
humoral immunity, ie antibody mediated immunity
following encounter with specific pathogen, B cells activate and differentiate into plasma cells which produce antibodies
some will become memory B cells
plasma cell define
effector B cells with synthetic/ secretory machinery for manufacture and export of large amounts of specific antibodies
have receptor specifc to pathogen, then secrete antibodies basically
ie antibody producing factories
antibodies are
soluble effector molecules produced by B cells
also called immunoglobulins
all antibodies produced by an individual B cell will have identical antigen specificity
antibody basic structure
2 identical heavy chains
2 identical light chains
linked together by intermolecular disulfide bonds
hinge region gives flexibility
constant region on one end
variable region on other end (AAs differ) determines specificity