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. 2020 Oct 29;7(1):e000437. doi: 10.1136/lupus-2020-000437

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© Author(s) (or their employer(s)) 2020. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.

This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/.

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This represents a proposed model for how genetic variants for the A20 binding inhibitor of NF-κB (ABIN1) gene TNIP1 (tumour necrosis factor-α-induced protein 3-interacting protein 1) contribute to the development and progression of SLE and lupus nephritis (LN). A number of TNIP1 single-nucleotidepolymorphisms have been identified in association with SLE and LN from large-scale genome-wide association study and replicate studies.^16–24 ABIN1 is ubiquitously expressed. It is possible that TNIP1 variants result in reduction or loss of ABIN1 cellular function and enhanced activation of nuclear factor kappa B cell (NF-κB). The findings presented herein suggest that loss of ABIN1 function mediates activation of adaptive immune and myeloid cells resulting increased circulating monocytes and elevated blood autoantibody and inflammatory modulator levels. This subsequently results in increased glomerular leucocyte infiltration and immune deposition in LN. iMo, inflammatory monocyte;pMo, patrolling monocyte.