Novel pebbles in the mosaic of autoimmunity

Carlo Perricone,Nancy Agmon-Levin,Yehuda Shoenfeld

doi:10.1186/1741-7015-11-101

Abstract

Almost 25 years ago, the concept of the ‘mosaic of autoimmunity’ was introduced to the scientific community, and since then this concept has continuously evolved, with new pebbles being added regularly. We are now looking at an era in which the players of autoimmunity have changed names and roles. In this issue of BMC Medicine, several aspects of autoimmunity have been addressed, suggesting that we are now at the forefront of autoimmunity science. Within the environmental factors generating autoimmunity are now included unsuspected molecules such as vitamin D and aluminum. Some adjuvants such as aluminum are recognized as causal factors in the development of the autoimmune response. An entirely new syndrome, the autoimmune/inflammatory syndrome induced by adjuvants (ASIA), has been recently described. This is the new wind blowing within the branches of autoimmunity, adding knowledge to physicians for helping patients with autoimmune disease.

Highlights

Almost 25 years ago the concept of the ‘mosaic of autoimmunity’ [1] was introduced to the scientific community
This concept has been expanded by recent evidence of ‘familial autoimmunity’: is there familial aggregation for individual ADs [4,5], but there is a familial aggregation of diverse autoimmune diseases
Physicians should be aware that familial autoimmunity is a common finding, especially for some specific disorders, such as autoimmune thyroid disease and systemic lupus erythematosus (SLE), suggesting a stronger shared genetic influence in their development

Summary

Introduction

Almost 25 years ago the concept of the ‘mosaic of autoimmunity’ [1] was introduced to the scientific community. The chemokine CCL-2 seems to be implicated in systemic diffusion of aluminum particles captured by monocyte-lineage cells, and in the subsequent neurodelivery of these particles These various lines of evidence reinforce the idea that alum is neurotoxic, and that continuously escalating doses of this poorly biodegradable adjuvant in the population may become insidiously unsafe, especially in cases of over-immunization or immature/altered blood–brain barrier or high constitutive CCL-2 production. It is known to be an inducer of dendritic cells and complement activation, which is capable of increasing the levels of chemokine secretion at the injection site and of enhancing the secretion of key T-helper (Th) and Th17-cell polarizing cytokines such as interleukin-12 [28] All these effects lead to development of an autoimmune response. Anti-Rib-P was not clearly associated with any clinical condition, including NPSLE, in that study, the effects of these autoantibodies on the CNS

Alum may increase the levels of Tau protein

Conclusion