Abstract
Challenging the Role of Diet-Induced Anti-Neu5Gc Antibodies in Human Pathologies.
Highlights
The thematic issue of Frontiers in Immunology, entitled “Human Antibodies Against the Dietary Non-Human Neu5Gc-Carrying Glycans in Normal and Pathological States,” benefits from an extensive fundamental review of previous studies on N-glycolylneuraminic acid (Neu5Gc) in humans [(1) for recent review and citations therein] and from studies on anti-Neu5Gc antibodies (A-GcAbs) in Cmah−/− mice that, similar to humans, lack a functional cytidine monophosphate N-acetylneuraminic acid hydroxylase (CMAH), thereby allowing Neu5Gc synthesis [2]
Not many studies have been performed to date in humans, and these studies have not yet unambiguously demonstrated that A-GcAb-related xenosialitis could contribute to major diseases in humans
Xenosialitis, which is restricted to human pathologies in this opinion article, has been proposed as a “logical” basis for deleterious effects that would result from in situ interactions of A-GcAbs, which are present in human sera and diet-derived Neu5Gc deposits on certain human cells [1]
Summary
The thematic issue of Frontiers in Immunology, entitled “Human Antibodies Against the Dietary Non-Human Neu5Gc-Carrying Glycans in Normal and Pathological States,” benefits from an extensive fundamental review of previous studies on N-glycolylneuraminic acid (Neu5Gc) in humans [(1) for recent review and citations therein] and from studies on anti-Neu5Gc antibodies (A-GcAbs) in Cmah−/− mice that, similar to humans, lack a functional cytidine monophosphate N-acetylneuraminic acid hydroxylase (CMAH), thereby allowing Neu5Gc synthesis [2]. The first [17] suggests there is an activation of umbilical ECs that develop a white blood cell binding phenotype after incubation with A-GcAbs-containing whole serum These first experiments used several extra-physiological conditions; for instance, the Neu5Gc loading among ECs far exceeding the levels naturally observed in human ECs and the high anti-Neu5Gc titer of the serum tested. Large artery ECs that undergo physiological loading levels of Neu5Gc were used [9] This last study [9] was restricted to the complete transcriptomic patterns and apoptosis of stimulated ECs, it is interesting that the activation patterns triggered either by purified diet-derived human A-GcAbs or by rabbit IgG-elicited A-GcAbs in these more physiological conditions did not present a classical “inflammation-like” activation of ECs. In contrast, the observed patterns are consistent with the concept that A-GcAbs may contribute to the homeostasis of ECs [9]. The late loss of transplant function that is associated with the highest elicited A-GcAb titres in patients who received rabbit IgGs [in Supplementary Data of [25]] is yet anecdotal,
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