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Sir, We read with interest the review article entitled ‘Consequence of neo-antigenicity of the ‘altered self ’’ [1], where the authors discuss the importance of oxidation-specific protein adducts in plasma membranes. We would like to point out that we have also shown the importance of 4-hydroxynonenal (HNE), a lipid eroxidation by-product, modified Ro 60 (SS-A) autoantigen in the rapid development of autoimmunity in an animal model of SLE [2] and the role of oxidatively modified proteins in autoimmune diseases [3]. Ro 60 RNP is a common target of autoantibodies in both SLE and SS. This structure is made up of a 60 kDa protein non-covalently associated with at least one of four short uridine-rich RNAs (the hY RNAs) [3, 4]. These hY RNAs are also associated with the 48 000 molecular weight La (or SS-B) autoantigen. Anti-Ro is found in 25–40% of patients with SLE, while anti-La is found in substantially fewer patients [3, 4].  Tolerance against Ro 60 and other autoantigens was abrogated faster and strongly in the HNE-Ro 60-immunized animals compared with the Ro 60-immunuzed animals. Immunization with HNE-modified Ro 60 induced a rapid intramolecular epitope spreading (within the Ro 60 molecule) and a rapid inter-molecular epitope spreading to other autoantigens. Such a scenario envisages developing antibodies to 60 kDa Ro and thus autoimmunity to the entire Ro RNP particle after an initial immune response to oxidized Ro 60.  We studied oxidative modification of Ro 60 since we and others observed free radical mediated peroxidative damage in SLE and other diseases [5–9]. Significantly higher HNE-modified protein levels have been found to occur in children with SLE [7].  Thus, we believe that oxidative modification of proteins is important in the generation of autoantibodies and thus brings about autoimmunity.    Disclosure statement: The authors have declared no conflicts of interest.

4-Hydroxynonenal-modified Ro 60 autoantigen accelerates autoimmunity in experimental animals