immunology Flashcards
components of the innate immune system
proteins and cells are already poised to defend
barrier defenses:
-skin
-mucous membranes
-secretions
Internal Defenses
-Phagocytic cells
-Natural Killer cells
-Antimicrobial proteins
-Inflammatory response
components of the adaptive immune system
humoral response:
antibodies defend against infection in bodily fluids
cell-mediated response:
cytotoxic cells defend against infection in body cells
What does the barrier defense include? How does it work
skin and mucus membranes (respiratory, urinary and reproductive tracts)
mucus traps microbes, low pH inhibits bacterial growth
How is mucus moved?
cilia movement helps to move mucus along
What are epithelial cells? What junctions are found?
Epithelial cells are the barrier between the outside world and the body
-tight junctions (blocks things out)
-desmosomes (connects the cytoskeletons of adjacent cells)
-gap junctions (lets small molecules move between cells, cytosol is continous)
Main types of phagocytic cells (2) and one other cell that has phagocytic properties but is an APC? what is their specificity? Where are they found?
Neutrophils and macrophages are the main cells. Dendritic cells are phagocytic but find their primary roles as antigen presenting cells.
They are generalists
Neutrophils are found in the blood until recruited
Macrophages reside permanently in the organs and tissue
What are the main receptors of phagocytic cells? Where can they be found?
Pattern recognition receptors
Found in the plasma membrane, internal membranes (like endosomes) and in the cytoplasm
What is an example of a pattern recognition receptor? How many pattern recognition receptors on one phagocyte
Toll like receptors are the pattern recognition receptors
Each cell has multiple TLRs of differing specificity:
TLR4 lipopolysaccharides
TLR5 Flagellin (protein of flagella - allows cellular motility)
TLR3 recognizes dsRNA
TLR9 recognizes unmethylated 5’-CpG-3’
TLR/Phagocytic Engagement (what are the steps? What)
1) pathogen gets to the surface of the phagocyte and pseudopodia surrounds pathogens
2) pathogens are engulfed by endocytosis
3) endosome forms
4) endosome and lysosome fuse
5) pathogens destroyed
6) debris from the pathogen is released
in other words
1) pathogen gets taken in by the phagocyte and an endosome forms
2) lysosome and endosome fuse and the pathogen is destroyed
3) (MACROPHAGE) can release signaling molecules. (THIS IS IMPORTANT FOR THE INFLAMMATORY RESPONSE)
Inflammatory response (How is it initiated and what happens)
1) barrier defenses are breached, and macrophage (TNF alpha) and mast cells (histamines) sitting below the barrier secrete signaling molecules
2) the endothelial cells of the capillary then sense the signaling molecules and they form gaps
what happens:
diameter increase, more blood flow at slower velocity. Vessel gets more leaky
pain, heat, redness and swelling
recruitment of more macrophages (from monocytes) and granulocytes from the blood
membrane attack complex/ complement proteins (how do they participate in the innate immune system)
1) complimentary proteins leak out of the capillaries (inflammatory response)
2) 20 compliment proteins form a membrane attack complex and can poke a hole in the membrane of a pathogen (IF THEY HAVE A MEMBRANE)
2a) (IF NO MEMBRANE PRESENT) complement proteins tag pathogen as garbage
How are leukocytes recruited from the blood? (How are they slowed down enough to be let out of the capillary?)
1) signaling molecule binds the receptor of the endothelial cell of the capillary
2)endothelial cells put up receptors facing the blood stream
3) the receptors (selectins) can allow for rolling adhesion!
steps of recruiting leukocytes from blood (4)
1) rolling adhesion along the selectin receptors
2) tight binding
3) diapedesis (cell squeezes between endothelial cells)
4) migration (towards higher concentration of chemokines)
4 characteristics of the adaptive immune system cells
1) cells are specific
2) they must have some way to achieve diversity. Only 20,000 genes in the genome and many more pathogens.
3) ability to not kill themselves (distinguish self from non self)
4) give rise to immunological memory
VJ (LIGHT) recombination steps
1) rag protein selects V and J segment and gets rid of all the DNA in between
2) DNA is transcribed into pre-mRNA
V-J-INTRON-C
3) intron is spliced, cap and poly A tail added
CAP-V-J-C-POLY A
4) mRNA is translated into a polypeptide
How diversity is achieved by VDJ recombination
Each B cell has different DNA!
1) random selection of segments ~8 million combinations
2) sloppy joining of segments that shifts the reading frame (8 million -> billions)
How do B and Tcells not KILL themselves? (How do they distinguish self from non self)
As lymphocytes (potential B/T cells) mature in the bone marrow and thymus, respectively, they get tested
some SELF REACTIVE B/T CELLS GET DESTROYED BY APOPTOSIS or PROGRAMMED CELL DEATH
the others just arent functional lol
B/T Cell binding (what biological molecules do they bind to )
B cells - anything w the right shape. Free floating
T cells - peptides only presented on an MHC (major histocompatibility complex)
Helper T cell CD4 activation (How do they recognize the peptide? What happens after recognition)
1) dendritic cell migration to the lymph nodes after ingesting pathogen. Macrophages already reside in the lymph nodes and ingest pathogens that come by the lymph nodes (NO MIGRATION REQUIRED).
2) after uptake of a pathogen. Antigen presenting cells place fragments of the pathogen on a MHC II.
3) T cell receptor binds the peptide fragment and the CD4 co-receptor strengthens the interaction
4) The activated T cell is selected for CLONAL EXPANSION
5) after clonal expansion the CD4 cells are differentiated into the activated CD4 population and the memory CD4 population.
CD4 function (what MHC does it correspond to? What happens after the CD4 T cell recognizes something? What cells are activated)
CD4 are the helper T cells
MHCII
cross activation of the APC and helper T cell. OR only one gets activated
CD4 either activates T cells (both CD4 and CD8) OR B cells. Each CD4 can only activate one type of cell.
CD8 function (what MHC)
CD8 are cytotoxic T cells (TOXIC8)
MCH I
1) CD8 recognizes peptide
2) CD8 aligns its cytoskeleton and cytoplasmic components for delivery into the infected cell
2) secretes Perforin (perforates the infected cell) and granzymes
3) cell undergoes apoptosis after proteases and cellular fluid comes in
What is the fundamental difference between naive and activated CD4? (… why is the activated one activated? What makes a CD4 specific to the cells it helps)
the fundamental difference lies in gene expression!
the genes they select confers specificity and differs between inactive/active forms
How does the constant region of the antibody come into play? WHY DO WE GIVE A SHIT ABOUT CONSTANT REGION (4 ways)
1) activates the complement protein system and holes can get poked into membranes or things can get tagged (IF NO MEMBRANE IS PRESENT)
2) agglutination/precipitation followed by uptake by a phagocyte (3 types- neutrophils and macrophages, and dendritic cells)
3) neutralizing the binding of a pathogen
B cell activation by an activated CD4 helper T cell
1) B cell binds the antigen
2) the antigen gets internalized into the B cell
3) endosome with the antigen fuses with another endosome housing the MHC II
4) peptide fragments get loaded onto the MHC II in the endosome and the MHCII:PEPTIDE migrates back to the plasma membrane
5) Now, B cell presents the peptide to an activated CD4 helper T cell.
6) Activated CD4 secretes cytokines
7) cytokines bind to the B cell and allows the B cell to go through clonal expansion and differentiation (plasma cells and memory B cells)
