A common gene signature in tolerance to renal allograft

To the Editor: We read with great interest the article by Baron et al.1 regarding a meta analysis of five studies, which showed 20 biomarkers that could identify patients with tolerance in renal allografts. While it is accepted that the B-cell pool are the effector cells involved in development of tolerance and that depletion of these B cells could result in graft loss, it is also held that antibodies against a graft can protect a graft by blocking immune recognition.2 These ‘enhancement antibodies’ can regulate complement and induce changes causing acquisition of graft tolerance. I would like to enquire if the authors in their assessment of the functional and cellular components and discriminating biomarkers have noticed whether there were present certain antibodies among the recipients of Tolerance grafts that may also contribute to graft enhancement and acquisition of tolerance. In like manner, perhaps among their patients with no Tolerance, those with chronic rejection, while they could detect the absence of the 20 biomarkers, perhaps they may also find that these ‘enhancement antibodies’ are also absent. These antibodies if present may also contribute to the identity of the common gene signature if their genetic linkage could be further established.