Immunology Flashcards
CD14
It is a TLR present on macrophages that recognizes LPS
Activation of TLRs leads to what
Upregulation of NF-kappa B
Actions of prostaglandins
Vasodilation of arteriole
Increased vascular permeability
Fever and pain (PGE2)
Leukotrienes
Attract and activate neutrophils
Also mediate vasoconstriction, bronchospasm, and increase vascular permeability
What process allows for increased vascular permeability?
Contraction of endothelial pericytes
Activation of classic complement pathway
Binds an IgG or IgM that are bound to an antigen
Activation of the alternative complement pathway
Complement directly to microorganisms
Activation of lectin complement pathway
MBL binds mannose on microorganisms
C3a and C5a
Trigger mast cell degranulation
C5a
Chemotactic for neutrophils
C3b
Opsonin for phagocytosis
MAC (C5b-C9)
Lyses microbes by creating holes in cell membrane
Bradykinin actions
Pain, vasodilation, and increased vascular permeability
What leads to fever during acute inflammation?
Pyrogens –> macrophages to release IL1 and TNF –> increase COX activity in hypothalamus –> increased PGE2
Steps of neutrophil entry into tissue
Margination: vasodilation slows blood so neutrophils flow to the periphery
Rolling: SLX on neutrophils bind selectins which slow neutrophil movement
Adhesion: Integrins (CD18) on neutrophils bind ICAM 1 on endothelial cells
Transmigration (PECAM-1)
Chemotaxis (bacteria, leukotrienes, C5a, IL-8)
Leukocyte Adhesion Deficiency
Deficiency in CD18 (integrin)
Delayed separation of the umbilical cord, increased circulating neutrophils, recurrent bacterial infections
Chediak-Higashi Syndrome
Protein trafficking defect characterized by impaired phagolysosome formation
Increased pyogenic infections, neutropenia, giant granules in leukocytes, albinism, peripheral neuropathy
Chronic granulomatous disease
Defective NADPH oxidase –> poor O2 dependent killing
Granulomas are caused by catalase-positive organisms
Anti-inflammatory mediators
IL-10 and TGF-beta (secreted by macrophages)
IL-8
Released by macrophages to call more neutrophils to the site of inflammation