Another potential mechanism that would explain differences in neutrophil migration with similar concentrations of soluble KC is a difference in neutrophil chemotaxis of lpr and B6 neutrophils. However, our chemotaxis studied showed that, if anything, neutrophils from lpr mice have slightly increased chemotaxis to KC, strongly suggesting that differences in chemotaxis are not the reason for the attenuation in the neutrophilic response seen in the lpr mice. Neutrophil recruitment and migration appears to be partly dependent on the formation of anti-KC:KC immune complexes, which can bind Fcγ receptors in local leukocytes, enhancing the inflammatory response [22] . For example, the generation of anti-KC:KC immune complexes in the lungs of mice is followed by acute inflammatory lung injury, and this injury requires the presence of Fcγ receptors [21] . Furthermore, mice lacking γ chains show attenuated injury in response to LPS, suggesting that this process is relevant for inflammation secondary to bacterial products [21] . The human equivalent of anti-KC:KC complexes are anti-IL8:IL8 complexes, and these are present in the lungs of patients with ARDS [25, 26] . In our study, we found that there are less anti-KC:KC complexes in the lungs of the lpr mice, even though the concentrations of KC were similar to those in the B6 mice. Thus, it is possible that the lower numbers of neutrophils seen in the lpr mice were due to decreased formation and deposition of anti-KC:KC complexes in the lungs. Additional studies are necessary to confirm this hypothesis, and it remains possible that differences in other unmeasured chemotactic agents account for the differences in neutrophil recruitment. The mechanism linking the Fas/FasL system with impaired formation and deposition of immune complexes remains unclear. To date, lpr mice, particularly the MRL/ lpr strain are known to generate autoantibodies that can result in a lupus-like syndrome [27] .