Systemic Lupus Erythematosus (SLE) is a devastating disease, which affects several organs and with poor therapeutic options. Cathelicin LL37 is an antimicrobial peptide (AMP) with pleiotropic functions on immune cells and parenchymal cells, which can be implicated in inflammatory pathways and in immune regulation. LL37, a stimulator of both the innate and the adaptive immune responses in psoriasis and related psoriatic arthritis (PsA), can represent a relevant model autoantigen to study the effect of irreversible post-translational modifications (PTM) in SLE, as compared to psoriasis and PsA. Being a relevant SLE antigen too, knowing whether irreversible PTM of a self-antigen play a role in SLE, can help shed light on SLE pathogenic mechanisms that contribute to disease, but remain underscored. This is of particular interest for SLE, a disease in the need of new therapy targets, although the concept necessarily also applies to PsA. For instance, the effect of PTM such as citrullination and carbamylation, usually studied in other diseases, especially in Rheumatoid Arthritis (RA), can shed light on new pathways favored by inflammation dominated by neutrophil infiltration, typical not only of RA, but in fact also present in SLE tissues, and not least, in the skin and joints of psoriasis and PsA, respectively.
Systemic lupus erythematosus (SLE); Post-translational modifications (PTM); LL37; antimicrobial peptides (AMP); Neutrophils