Innate immunity Flashcards
Neutrophils crossing activated vascular epithelium
Glycam-1 and CD34 (addressins) on neutrophils bind P-selectin or E-selectin on vascular epithelial cells, the neutrophils roll
LFA-1 on neutraphil binds iCAM
PECAM-1 (CD31) binds PECAM-1 and neutraphil enters between tight junctions
Phagocyte killing of microbes (oxidative burst)
axurophillic granules with antimicrobial properties bind
NADPH oxidase produces superoxide radicals which are later converted to H2O2
fusion of phagosome with lysosome and release of acid hydrolyses
increase in O2 consumption during this process
NETs
neutraphils undergo NETosis and expel their genome in undigested form so that it creates a web that entraps pathogens
endocytic PRRs
recognize carbohydrates and they promote phagocytosis
non-signaling
signling PRRs
Toll-like receptors(extracellular)
Nod-like receptors (intracellular-for bacterial RNA)
Rig-like receptors (intracellular-for viral RNA)
TLR2/6
recognize lipoteichoic acid and zymosan
TLR3
bind double stranded viral RNA
TLR4
recognizes LPS
TLR7/8
bind single stranded viral RNA
secreated PRRs
MBL, C-reactive protein, produced during acute phase response
cytokines produced by macrophages
IL1 IL6 TNF-alpha IL8(CXCL8) IL12
IL1
fever
IL6
IL6
produced by macrophages of liver
fever
production of recreated PRRs by hepatocytes
activate vascular epithelium
TNF-alpha
fever
activate vascular epithelium
contains localized infections by preventing dissemination via blood, increase platelet adhesion
CXCLA (il8)
neutrophil chemotactant
IL-12
activates NK cells
acute phase response cytokines
il1, il6, tnfalpha
B1B cells
respond to T-independent type 2 antigens cells can be induced to produce antibody (primarily IgM, with some programmed class-switching to IgG), but they do not clonally expand, undergo affinity maturation, and never class switch to any isotypes other than IgG a truly innate cell type and every exposure of a single host to any pathogen that “activates” these cells will result in an identical B1 B cell response found in secondary lymphoid tissues
3 effects of viral production of IFN-alpha and beta
- Induces a state of heightened resistance to viral infection and viral replication in all cells
- Induces increased expression of MHC class I and other ligands for the inhibitory receptors on NK cells
- Activation of NK cells to kill virus-infected cells
T/F When cell is infected it unregulated IFN-alpha and beta which binds to adjacent cells making them harder for viruses to infect and also causing them to up regulate MHC class 1
true
