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Review
. 2009 Nov 17;120(20):2012-24.
doi: 10.1161/CIRCULATIONAHA.108.771170.

Mechanisms of immune complex-mediated neutrophil recruitment and tissue injury

Tanya N Mayadas  1 , George C Tsokos, Naotake Tsuboi
Affiliations
Review

Mechanisms of immune complex-mediated neutrophil recruitment and tissue injury

Tanya N Mayadas et al. Circulation. .
No abstract available

PubMed Disclaimer

Conflict of interest statement

Disclosures None

Figures

Figure 1
Figure 1. Structure of human and mouse neutrophil FcγRs
Human neutrophils express FcγRI associated with the ITAM containing signaling Fcγ-chain, the single polypeptide FcγRIIA with its own ITAM motif and the GPI-linked FcγRIIIB. Murine neutrophils express three activating receptors FcγRI, FcγRIII and FcγRIV which require the common Fcγ-chain for expression and signaling. Whether the FcγRIIB inhibitory receptor containing the ITIM motif is present in human neutrophils requires further clarification.
Figure 2
Figure 2. Model of neutrophil FcγRIIIB and FcγRIIA dependent functions in homeostasis and disease
Left panel: Intravascular ICs trigger transient accumulation of neutrophils which internalize the immune deposits and return to the circulation. Neutrophil FcγRIIIB present on microvilli tether to ICs under physiological flow and clear them without damaging the vasculature. Right panel: When mechanism(s) of clearance are overwhelmed or defective, or during persistent IC generation, ICs translocate and accumulate in extravascular tissues. ICs, sensed by FcγRs and receptors for complement components (triangle) on resident mast cells triggers the release of inflammatory mediators (e.g. LTB4 and TNF). These directly or indirectly activate the endothelium, promote FcγRIIIB shedding and increase the capacity of FcγRIIA to promote neutrophil recruitment and signal. Tissue accumulated neutrophils release inflammatory mediators (e.g. ROS, proteases, eicosanoids and cytokines) which activate resident cells. Moreover, they produce cytokines and chemokines which promote their own recruitment and the recruitment of other circulating leukocyte subsets. These actions together perpetuate inflammation and tissue damage.
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