Immunity Flashcards
-Activates vascular endothelium
-Activates lymphocytes
-Local tissue destruction increases of effector cells
-produces IL-6
-leads to shock and fever
IL-1B
-Activates vascular endothelium
-increases entry of complement and cells to tissue and fluid drainage to lymph nodes
-Activates fever and shock
-Activates mast cell degranulation
-Activates mobilization of metabolism
TNF-a
-Acute phase protein production by hepatocytes
-Activates CRP and fever
-Activates complement components and serum Amyloid A cox
IL-6
Chemo-attractant for neutrophils
IL-8
-Found in tissue
-Recognize microbial products and has IgE antibodies
-Activated by trauma, IgE cross linking, C3a and C5a (leukocyte activators)
-Release histamines
Mast cells
-Cell distress with no MHC-1 leads to lysis with Perforin and granzymes
-cells distress with MHC-1 signal NO lysis
-will secrete IFN8 in setting of infection d
-prevents autoimmune disease
NK cells
-2nd responders
-secrete ROS, NO, & lysosomal enzymes
-IL-1, IL-12, IL-23 and chemokines
Macrophages
Bump on gram negative bacteria that activates TLR 4
LPS
Infection seen-> release soluble mediators->vasodilation(rubor, calor)->vascular leakage and increased osmotic pressure (tumor, dolor)-> extravasation of fluid & leukocyte influx(chemokine controlled)->phagocytosis & toxin release-> eliminate infection & repair / resolve tissue
Inflammatory response
Homeostasis return vs scaring (from high macrophage #)
-vascularization: high vs low
-cellular infiltration: abscess vs granuloma
-stromal: low edema vs fibrosis
Acute vs. chronic
Degrade basement membrane proteins
-collagenases
-elastases
Proteolytic enzymes
- Edema (shortest)
- Neutrophil arrival
3.Macrophage recruitment (longest)
Phases of acute inflammation
Rolling (selections), Adhesion (integrins), Arrest (chemokines), Diapedesis (junction adhesion molecules, integrins)
RAAD SIC-JAI
Another name for WBCs precursor
PMN
- Initiates
- Sensors
3.mediators (control point, TGF & IL-8)
4.target tissues
Regulation inflammation
In mucus membranes and secretions
-trancytosis
-local defense
-neutralization, agglutination
IgA
1st responder and best complement
-neutralization & agglutination
-5days after exposure (1.5 week life)
-expressed by B cell
IgM
Least abundant in serum and initiates mast cells and basophils
IgE
Cross placenta
-optimize, neutralize, agglutination
- most abundant
-works with NK
-15days after exposure(30day life)
-abundant in 2nd response
IgG
Recognizes non-infected MHC-1 marked cells
NK inhibitory receptor
Antibodies and complement unite for measurement
-positive (when complement isn’t left to lyse RBCs)
Assay
Located on infected cells
Stress proteins
Several of these determinants in an antigen
Epitopes
Varies
-self vs non-self Ag recognition
-cause transplant rejection
Human leukocyte Ag
-1(kill virus infected cell/ see MHC1&peptide)
-2(make other cells see it)
Major histocompatibility complex
