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This study was designed to determine the association between complement depletion and T-cell immunosuppression.
Complement depletion induced by CVF significantly reduced post-ischemic cerebral infarct volume and atrophy in adult and neonatal rats.
Complement depletion commonly occurred in septic patients, but this problem was often underestimated during the treatment process.
Therefore, experiments were designed to test the effect of complement depletion on cerebral infarct volume in adult rats and cerebral atrophy in neonatal rats.
And in rats, complement depletion during passive transfer at the lung stage significantly reduced protection, thus generation of C3a and C5a by antibody/antigen fixation of complement may play a role [7].
Moreover, complement depletion or inhibition demonstrated beneficial effects in animal models of hemorrhage, and therefore they represent an interesting novel treatment option [ 162] in the clinical arena.
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A plasmid expressing FtsZ-mEos2 was transformed into JKD7-2/pKD3a [67] to examine if FtsZ-mEos2 is able to complement the depletion of wild-type (wt) FtsZ expressed from the temperature sensitive plasmid pKD3a at 42°C.
The failure of the BubR1 gain-of-function mutant to complement the depletion of wild-type BubR1 strongly suggests that the evolutionary divergence of Bub1 and BubR1, with its specific effects on kinetochore recruitment, is functionally relevant.
It has been demonstrated that experimental autoimmune uveoretinitis (EAAU) can be caused by activation of the complement system, and depletion of the host's complement system can completely inhibit the EAAU [[54],[55]].
At all IPTG concentrations tested no growth was detected at 42°C, indicating that FtsZ-mEos2 did not complement the conditional depletion of wt FtsZ.
As a complement to the depletion of different subsets of immune cells in normal BALB/c mice, tumour rejection experiments were also performed in CD4−/− single, CD8−/− single, or CD4−/−CD8−/− double knock-out C57Bl/6 mice.
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