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50 Cards in this Set

  • Front
  • Back
what is immunology?
the science of self-nonself discrimination
functions of immunology
1. recognition mediated by MHC
2.effector (t-cells and b-cells)
what is 'self'
dictionary - material that is part of an individual organism

the body does not normally mount immune responses against its self antigens, at least not in quantities sufficient to harm the body
what is 'nonself'
dictionary - material that is foreign to the body of an organism
what are the 4 threatening situations that individuality is jeopardized?
1. parasitism, which is a threat to the individual's survival
2.organ and tissue damage, which is a threat to the organism's integrity and individuality
3.neoplasia, which is a threat to both uniqueness and survival
4. fusion of genetically disparate individuals in colonial animals
an abnormal, incompetent growth in a tissue or organ, typically forming a separate mass. Such a growth is called a neoplasm, also known as a tumour.
Elie Metchnikoff
russian embryologist, first presented his phagocytosis theory of host defensed
providing the cellular basis for immunological specificity
shown to orchestrate cellular communication, to promote and/or regulate most immunological reactions, and to play key roles in promoting host defense and immunopathology
what is the single progenitor that leads to all effector cells?
pluripotent hematopoietic stem cell in the bone marrow
bone marrow progenitor stem cell leads to....
3 lineages
1. lymphatic
2. myeloid/macrophage

need all lineages to reach professional APCs
what is MSG?
macrophage specific gene
needed to produce macrophages
what are the steps of clonal selection?
-each lymphocyte bears a single type of receptor with a unique specificity
-interaction btw a foreign molecule and a lymphocute receptor capable of binding that molecule with high affinity leads to lymphocyte activation
-the differentiated effector cells derived from an activated lymphocyte will bear receptors of identical specificity to those of the parental cell from which that lymphocyte was derived
-lymphocytes bearing receptors specific for ubiquitous self molecules are deleted at an early stage in lymphoid cell development and are therefore absent from the repertoire of mature lymphocytes
Nature of the antigen is the major variable...
charlie janeway
broad categories of disease-causing microbes (pathogens)
1. viruses
2. bacteria
3. fungi - eukaryotes
4. parasites - unicellular and multicellular eukaryotes
key difference btw antibodies and t-cell receptors (TCRs)
TCRs are bound to the cell membrane
what are the professional APCs?
Dendritic (myeloid)
Macrophage (myeloid)
B lymphocyte (lymphoid)
activated function of dendritic cell
antigen uptake in peripheral sites

antigen presenting

phagocytosis and initiation of immune response
what kills the infected cells?
CTLs - cytotoxic t lymphocytes
what does a viral cell target in the host?
ribosomes, to create more viruses
What kind of antigens are presented by MHC I
what kind of antigens are presented by MHC II
activated function of macrophage
phagocytosis and activation of bactericidal mechanisms

able to process antigens and produce peptide antigens

antigen presentation
what is the precursor for macrophages?
the antigen receptors found on the macrophage are apart of which immune system?
what are receptors found on the macrophage?
LPS (CD14)
where are lymphocytes activated?
int he lymph node, then head back to site of infection
how are t lymphocytes activated?
immature dendritic cells reside in peripheral tissues

then migrate via lyphatic vessels to regional lyphm nodes

then mature dendritic cells activate naive t cells in the lymphoid organs (lymph node)
how do lymphocytes and lymph return to the blood
via the thoracic duct
antigen binding region of MHC I
only alpha chain used, still has beta chain
antigen binding region of MHC II
made up of both alpha and beta chain
pathway for cytosolic pathogens
degraded in the cytosol

bound by MHC I found on any cell then presented to EFFECTOR CD8 T cells leading to the death of the infected cell
pathway for cross-presentation of exogenous antigens
broken down in the cytosol by retrotranslocation

bound by MHC I and presented to naive CD8 t cells

the presenting cell, usually dendritic, activates the CD8 cell
pathway for intravesicular pathogen
degraded in the endocytic vesicles with a acidic pH

bound by MHC II found on macrophage then presented to CD4 T cells

leads to activation to kill intravesicular bacteria and parasites
pathway for extracellular pathogens and toxins
degraded in the endocytic vesicles by acidic pH

bound by MHC II and presented to effector CD4 t cells

activation of b cells then occurs to secret immunoglobins to eliminate extracellular bacteria/toxins
what happens after a virus infects the cell?
viral proteins are synthesized in the cytosol

peptide fragments of the viral proteins are bound by MHC I in the ER

bound peptides are transported by MHC I to the cell surface
how do you get the peptide into the ER
must produce peptides that degrade the virus so they can be transported into the ER
adaptations of viruses that block the immune response
blocking the peptide from entering the ER (block/inhibit TAP from binding the peptide)

retention of MHC I in the ER (in hibitor of tapasin, block tapasin)

degradation of MHC I

binds MHC I at cell surface which interferes with recognition by APCs
peptide transporter that allows antigen peptides to enter the lumen
what is different about the immunal proteosome vs the constitutive?
has 2 p28 caps on the end

3 substituted beta subunits:
lmp-1, lmp-2, mecl-i
2 ways antigens enter cell for binding with MHC class II
bacterium infects macrophage and enters into a vesicle, producing peptide fragments that become bound by MHC II, and are then transported to the surface

antigen bound by b-cell surface receptor becomes internalized and degraded to peptide fragments. The fragments bind to MHC II and are transported to the cell surface.
vesicular pathway for pathogens
antigen is taken up front he extracellular space into the intracellular space encasing it in a vesicle.

in the stages the vesicle is of neutral pH, which keeps the endosomal proteases inactive

acidification of vesicles activates proteases to degrade antigen into peptide fragments

the vesicle containing the peptides fuses with vesicles containing MHC II
what is the invariant chain?>
binds in the groove of MHC II while in the ER.

the chain is then cleaved twice leaving a small fragment (CLIP) bound to the MHC

it blocks the binding of peptides and misfolded proteins
How is the invariant chain cleaved to leave CLIP behind?
through acidic situations in an endosome
what is the purpose of the CLIP peptide?
there are endocytosed antigens that are degraded to peptides in the endosomes and CLIP blocks the binding of these peptides to the MHC II molecule
how is the CLIP peptide removed from MHC II?
HLA-DM binds to the MHC II molecule, releasing the CLIP allowing other peptides to come in and bind with MHC, after which the MHC complex moves to the cell surface.
where do the stages of the invariant chain take place?
it first binds the MHC II in the ER

it is cleaved forming CLIP in the endosome

CLIP is removed in the endosome
CD8 T Cells
cytotoxic (killer) t cells or CTLs

endogenous pathogens

binds to MHC I + antigen
CD4 T Cells
TH1 and TH2 cells (helper)

interacts with infected macrophages and B-cells

exogenous pathogens
difference btw TH1 and TH2
TH1 - proinflammatory and activates macrophages

TH2 - b-cell helpers