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microvesicles) has been proposed as a mechanism of cellular communication between MSCs and CLCs, and not cell fusion or gap-junctional communication
doi: 10.1038/jid.2009.59 18 BenhadouFMintoffDDel MarmolV
In addition, HCs and KTRs controlling CMV infection responded with a stronger upregulation of G6PD and CD98 than noncontrollers (Figure 4C)
LL-37 antimicrobial peptide with very limited human safety data for systemic use [16]
