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ORIGINAL RESEARCH article

Front. Immunol.
Sec. Autoimmune and Autoinflammatory Disorders : Autoimmune Disorders
Volume 15 - 2024 | doi: 10.3389/fimmu.2024.1475073

Interleukin-32 positive immune and resident cells in kidney samples from lupus patients: a pilot study

Provisionally accepted
Simona Truglia Simona Truglia 1Francesco Ciccia Francesco Ciccia 2Silvia Mancuso Silvia Mancuso 1Antonella Capozzi Antonella Capozzi 3Aroldo Rizzo Aroldo Rizzo 4Francesca Romana Spinelli Francesca Romana Spinelli 5*FULVIA CECCARELLI FULVIA CECCARELLI 1Tania Colasanti Tania Colasanti 1Cristina Garufi Cristina Garufi 1Francesca Miranda Francesca Miranda 6Maurizio Sorice Maurizio Sorice 3Cristiano Alessandri Cristiano Alessandri 1Fabrizio Conti Fabrizio Conti 1
  • 1 Division of Rheumatology, Department of Clinical Internal, Anesthesiological and Cardiovascular Sciences, Faculty of Medicine and Dentistry, Sapienza University of Rome, Rome, Lazio, Italy
  • 2 Department of Precision Medicine, University of Campania Luigi Vanvitelli, Naples, Campania, Italy
  • 3 Department of Experimental Medicine, Faculty of Medicine and Dentistry, Sapienza University of Rome, Rome, Lazio, Italy
  • 4 Pathology section, Azienda Ospedaliera Ospedali Riuniti Villa Sofia Cervello, Palermo, Sicily, Italy
  • 5 Sapienza University of Rome, Rome, Italy
  • 6 Rheumatology Unit, ASL Roma1, Rome, Italy, Rome, Italy

The final, formatted version of the article will be published soon.

    Introduction Lupus nephritis (LN), caused by immune complexes produced in situ or deposited from the bloodstream, is one of the most severe features of Systemic Lupus Erythematosus (SLE) leading to an increased morbidity and mortality. Toll like receptors (TLRs), such as TLR3, TLR7 and TLR9, may play a key role in its pathogenesis. , a cytokine involved in both innate and adaptive immune responses, has been widely considered in autoimmune-inflammatory rheumatic diseases. This study aims to evaluate the IL-32 role in LN, also investigating the effect of LN patients IgG (LN-IgG) on IL-32 production via TLR3.In LN patients, IL-32 was detected in sera samples by ELISA KIT and in kidney tissue by immunohistochemistry. HEK293/T3 cells were incubated with LN-IgG and analyzed for TBK1, phospho-p65 NF-κB and IL-32 by Western blot.We demonstrated IL-32 presence in LN patients compared to SLE patients without renal involvement, observing a direct correlation between IL-32 serum levels and disease duration (p=0.02; r 0.2978). Moreover, IL-32 was strongly expressed in renal samples of LN patients. Phosphorylation of TBK1 resulting in NF-κB activation and IL-32 increase was observed in HEK293/T3 cells following LN-IgG treatment, TLR3 inhibitor using induced a significant reduction in the expression of these molecules.These results showed that IL-32 is up-regulated in the kidney of LN patients suggesting that in renal tissue IL-32 expression could be induced through TLR3 activation by the LN patients' antibodies. This study may indicate a possible role for IL-32 in the pathogenesis of LN.

    Keywords: Lupus Nephritis, Toll like receptor 3, interleukin-32, Lupus Nephritis IgG, resident renal cells. 2

    Received: 02 Aug 2024; Accepted: 12 Dec 2024.

    Copyright: © 2024 Truglia, Ciccia, Mancuso, Capozzi, Rizzo, Spinelli, CECCARELLI, Colasanti, Garufi, Miranda, Sorice, Alessandri and Conti. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence: Francesca Romana Spinelli, Sapienza University of Rome, Rome, Italy

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