immunology Flashcards
name the types of non specific immune cells
phagocytic cells, monocytes, neutrophils, macrophages, natural killer cells
difference between monocytes and macrophages?
monocytes: circulate in blood, eat invaders
macrophages: in tissues . eat everything that is not self
types of immune cells / new blood from bone marrow
RBC’s, neutrophils, monocytes etc
what do neutrophils do?
consume invaders. Die after attack. Accumulation of pus = dead neutrophils. Release fibrous traps. Kill w/ “NET’s”
what do natural killer cells do?
Kill EVERYONE. Punch holes in bad cells 2 kill. (perforin)
note that they are their own cell type
stimulated by cytokines
Interferons
proteins secreted by virally infected self. It’s a signal saying “SAVE YOURSELVES IM INFECTED!” causes other cells to alter their metabolism; reduces transcription of local cells, shorten ½ life of RNA.
pyrogens
fever inducing signal
why is a slight fever good for the body when there’s an invader?
sequester iron in liver - unavailable to microorganisms
high temp slows bacterial growth
increases activity of phagocytic cells
Complement System- how is it different from natural killer cells?
both punch holes and both are stimulated by cytokines, but the complement system is a bunch of peptides led by a peptide called C3 that assemble into MAC (membrane attack complex) versus natural killer cells which are actual cells
specific immune cells
refer to t cells and b cells only!
Mast cells and their consequence:
release histamines. Results:
• Erythema (redness), edema.
• Neutrophils rush over. Jump on the splinter, out of blood stream, : process is called “diapedesis” cells leaving circulation to enter the tissue spaces.
• Neutrophils jump on their NETS , then die, and you get pus
first line of defense
unbroken skin
All openings are protected by some mechanism:
respiratory system, macrophages
A. urogenital tract system: protect with acidity (why u drink cranberry juice)
B. digestive tract: lymphoid centers, Peyer’s Patches
C. tonsils- act as lymphoid barrier
o pharyngeal tonsils-adenoids, palatine tonsils, lingual tonsils
second line of defense
Cellular proteins and other mechanisms A. lymphatic system B. Immune Cells C. Non specific immune cells D. other (fevers, interferons etc)
third line of defense
Active/adaptive immunity
antibodies, T-cells (4 kinds!)
Antibody:
proteins with binding sites for specific targets. Binding site = antigen.
• Clusters of Differentiation aka “CD” markers
• markers on surface of immune cells
o >100 known. CD4, CD8. Most important.
o Way to tell populations of cells apart from each other
Immune Cells
Have immune receptors on them to recognize invaders
ex: lymphocytes, T cells, B-lymphocytes
T-lymphocytes- whats special about their education
“educated” in the thymus. Selected for those that do not recognize ‘self.’
4 types of T cells:
- Helper T cells: all have CD4 marker. Work with other cells to make immune response more efficient. TH1 and TH2.
- Inducer T cells: stimulate replication of more T cells. CD4.
- Cytotoxic T cells: (Tc) CD8 marker. Killing cells.
- Regulating/suppressor t cells: turn down immune resp
B-Lymphocytes
educate in periphery . (originate in chicken gut, bursa of fabricius) hence the name ‘B’ from Bursa. And they really come from bone marrow so it works.
- Can also be activated; puff themselves up with Rough Endoplasmic Reticulum. Aka, protein synthesis. Making antibodies! When B cells become activated, make + secrete antibodies.
- When activated: “plasma cell”
discuss the incidence of class 1 vs class 2 MHC HLA
type I MHC HLA on everything, type II MHC HLA on nearly everything
how do MHC HLA’s contribute to difficulty of tissue transplants?
HUGELY POLYMORPHIC. Everyone’s HLA markers are different. This is why tissue transplants are so difficult.
Autologous transplant
get your own tissue, like a hair transplant
heterologous transplant
someone else’s tissue that has matched MHC markers to yours. Ex: siblings donating skin to siblings.
Allogenetic transplant
someone else’s tissue entirely. Unmatched MHC markers. Likelihood of success varies- fine in cornea, not fine in bone marrow
danger: graft vs host disease (killed boy in bubble)
Two arms of immune response:
cell mediated immunity (t cells) and antibody/humoral mediated immmunity (b cells)
cytokines
immune signaling molecule
describe cell mediated immunity cascade
After a macrophage has processed an antigen, releases Interleukin 1, which signals helper T cells (Cd4) to bind to the antigen-MHC protein complex. This triggers helper t cell to release IL2, which stimulates the multiplication of cytotoix t cells . Body cells that have been infected by the antigen are destroyed by the cytotoxic t cells.
cascade for antibody-mediated immunity
Signal for phagocytosis – put MH2, display on surface, helper t cell w/ t cell (CD4) receptor, recognizes it.
Releases signal molecule which then stimulates these B cells.
IL2/4 released, activates these B cells
function of antibodies?
mark stuff for destruction
what happens once antibodies bind to surface of infected cells?
macrophages destroy them
interleukin (1/2) activates B cells and cytotoxic t cells
2
Ways that having antibodies stuck on you helps lead to your destruction:
- Increase rate of phagocytosis
- Increase attack by complement system (immflation increases)
- Increase attack by natural killer cells (increased cell lysis)
Opsonization:
the process of enhancing phagocytosis by marking with antibody
What does HIV do?
• HIV targets CD4 TH (helper T) cells. Killing off helper T cells makes you get all sorts of weird diseases. You can die from weird forms of pneumonia. Kaposi’s sarcoma: only really see it in AIDS patients.
5 antibody classes and what they do
IgM- first. pentamer. agglutination. short lived
IgG- second. monomer. MAIN HUMORAL RESPONSE immunoglobulin.
IgD- present on surfaces of B cell receptors
IgA- antibody in body sections (breast milk). dimer.
IgE - release of histamine
Self Tolerance mechanism in T cells (when immune system recognizes a ‘self’ antigen but knows not to respond to it)
requires 2 signals:
- binding of an antigen to T cell receptor
- B7 protein
‘co stimulation’ allows for self tolerance. why baby animals can get skin grafts.
autoimmune mimicry hypothesis
when infected cell displays foreign antigen- overlap, just by chance, so that same T cell receptor which normally recognizes self now sees this thing and recognizes it
So basically its trained to attack “yellow green blue” as foreign- and if itself happens to have that , it will also attack itself
Myasthenia gravis:
attack on neuromuscular junctions. Ach receptors
causes ‘droopy eye’
removal of thymus halts progression
why can’t microorganisms mimic MHC markers to escape detection?
b/c MHC markers are far too diverse
describe how celiacs disease works
o Undigested gluten fragments interact with epithelial cells. Epithelial cells held together by tight junctions. When ep cells encounter gluten, release ‘zonulin’ protein. Tells cells to release their tight junctions. Opens up spaces between epithelial cells, normally sealed- gluten gets through – secretion of cytokines- then attack the epithelial cells. “TTG enzyme” released by damaged cells- display of gluten molecules on HLA, release other cytokines, helper t cells kill off some of these epithelial cells
o People start making antibodies against TTG , and HLADG2/8
hygiene hypothesis
Little exposure to parasites- our immune system never learns to deal with them. Unemployed actors in the immune system sit around with nothing to do and start attacking normal things- get allergies, autoimmune disorders.
cd markers and function : cytotoxic and helper t cells
cytotoxic t cells- cd8- only form immune synapses to MHC1
helper t- cd4- only form immune synapses w/ cells w/ MHC2 (macrophages + B-cells). connect to B7 protein as well to prevent anergy (co- stimulation)
describe what happens (regarding neutrophils) when you get a splinter.
neutrophils attracted to the scene by inflammation- once there, release cytokines to attract other components of the immune response. kill using NETS. die in the process of killing the invader (apoptosis) and accumulate as pus. part of innate immune system
imagine an infection has occurred - what do antibody molecules do to further the response?
mark for destruction by: complement, phagocytosis, killer cells
(describe how they punch holes + kill it!)
what happens to an antigen floating free in blood?
helper t activates B cells into plasma cells
plasma cells synthesize antibodies
B cells undergo clonal selection to make more antibdoies
from what cells are IgE molecules produced?
made by B cells which have been ACTIVATED INTO PLASMA CELLS BY HELPER T CELLS
