Depletion of Gr-1+, but not Ly6G+, immune cells exacerbates virus replication and disease in an intranasal model of herpes simplex virus type 1 infection

IFNγ induces monopoiesis and inhibits neutrophil development during inflammation

“…54 Indeed, depletion of neutrophils with the Ly6G-specific Ab had no effect on the replication of HSV-1, whereas depletion with the Gr1-Ab exacerbated virus replication; this suggests an important role for monocytes in controlling this viral infection. 55 However, another recent study reported increased replication of influenza virus after depletion of neutrophils with the Ly6G-Ab, suggesting that the contribution of neutrophils in controlling viral infection may also depend on the type and/or site of viral infection. 56 In the present study, we have demonstrated that IFN␥ is an important cytokine in directing myelopoiesis during acute viral infection.…”

Emergence, origin, and function of neutrophil–dendritic cell hybrids in experimentally induced inflammatory lesions in mice

“…Two recent reports demonstrated complete lack of Ly6G expression by CD11c high DC populations in various tissues in mice. 12,13 Because neutrophil recruitment and local production of GM-CSF both take place at sites of inflammation, 14,15 we hypothesized that significant numbers of neutrophil-DC hybrids might emerge under inflammatory conditions. The present study was, therefore, conducted to test this hypothesis by using standard mouse models of inflammation.…”

Revisiting the protective and pathogenic roles of neutrophils: Ly‐6G is key!

“…Altogether these recently published reports [13][14][15] highlight the importance of the Ly6G mAb (clone 1A8) for investigating the functions of neutrophils. Furthermore, the findings [13][14][15] remind us that all previous studies that used the anti-Gr-1 mAb (clone RB6-8C5) to investigate the roles of neutrophils need to be revisited and their conclusions reconsidered.…”

“…Furthermore, the findings [13][14][15] remind us that all previous studies that used the anti-Gr-1 mAb (clone RB6-8C5) to investigate the roles of neutrophils need to be revisited and their conclusions reconsidered. Neutrophils have been implicated in the pathogenesis of many kinds of diseases, with both inflammation-initiating (harmful) [3,16,17] and antiinflammatory (protective) [4,5] functions being reported; however, the mechanisms that modulate this plasticity of neutrophils remain unclear.…”

“…These results of Carr et al [13] go against previous conclusions drawn regarding the roles of neutrophils in LM infection observed on the basis of anti-Gr-1 mAb-mediated depletion experiments, and reveal a precise role for neutrophils in controlling LM infection in the spleen and liver. Interestingly, Wojtasiak et al have shown in mice that specific depletion of Ly-6G 1 neutrophils does not modulate disease or alter virus replication following intranasal infection with HSV-1, whereas treatment of HSV-1-infected mice with the anti-Gr-1 mAb (clone RB6-8C5) leads to exacerbated virus replication and disease severity and increased mortality [14]. Furthermore, another study has shown that anti-Gr-1 mAb (clone RB6-8C5)-treated mice succumb to oral infection with Toxoplasma gondii at a similar level as that observed in Ccr2 À/À mice, which are deficient in monocyte recruitment to the inflammatory sites but, overall, have normal levels of neutrophils; in the same study, mice treated with the anti-Ly6G mAb (1A8) were able to control parasite replication and survived acute infection [15].…”