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Dysregulation of immune checkpoint molecules as a characteristic of autoimmune congenital heart block
  1. Ana-Luisa Stefanski1,2,
  2. Hector Rincon-Arevalo1,2,3,4,
  3. Iris Dressler-Steinbach5,
  4. Nadja Nomovi5,6,
  5. Alma Mackert5,
  6. Arman Aue4,
  7. Jacob Ritter1,2,
  8. Annika Wiedemann1,2,
  9. Franziska Szelinski1,2,
  10. Eva Schrezenmeier2,4,
  11. Anja A Kühl7,
  12. Andreia C Lino2,
  13. Wolfgang Henrich5,
  14. Thomas Dörner1,2
  1. 1Department of Rheumatology and Clinical Immunology, Charité Universitätsmedizin, Berlin, Germany
  2. 2Deutsches Rheuma-Forschungszentrum (DRFZ), Berlin, Germany
  3. 3Immunologia cellular e immunogenetica, Universidad de Antioquia, Medellin, Colombia
  4. 4Department of Nephrology and Intensive Medical Care, Charité Universitätsmedizin, Berlin, Germany
  5. 5Department of Obstetrics, Charite Universitätsmedizin, Berlin, Germany
  6. 6Department of Obstetrics, Ernst von Bergmann Hospital, Potsdam, Brandenburg, Germany
  7. 7iPATH, Core Unit of Charité, Charité Universitätsmedizin, Berlin, Germany
  1. Correspondence to Dr Ana-Luisa Stefanski, Rheumatology and Clinical Immunology, Charite Universitatsmedizin Berlin, Berlin, Germany; ana-luisa.stefanski{at}charite.de

https://doi.org/10.1136/ard-2024-226176

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    Autoimmune congenital heart block (CHB) represents a severe manifestation of neonatal lupus syndrome due to placental transfer of maternal anti-Ro/SS-A ± anti-La/SS-B autoantibodies, whereby type-I-interferon (IFN) activation is recognised as a significant risk factor for CHB development.1 2 However, only about 2% of children born to mothers with the respective antibodies are affected, indicating a disturbed feto-maternal tolerance in CHB pregnancies, which is still not entirely understood. Recent findings suggest a significant involvement of placental immune checkpoint molecules (CPM) in the induction of feto-maternal tolerance, in particular via the inhibitory molecule PD-L1, which is constitutively expressed in placental syncytiotrophoblasts juxtaposed to maternal blood and tissue.3 4 In line with this, the levels of soluble PD-L1 (sPD-L1) in the serum of pregnant women are higher than in non-pregnant women and are supposed to suppress maternal immunity.5 6 This study aims to assess the contribution of co-inhibitory and co-stimulatory checkpoint molecules in CHB affected and at-risk mothers positive for anti-Ro/SS-A ± anti-La/SS-B autoantibodies.

    Therefore, in a first step, we analysed plasma from 12 pregnant women with CHB pregnancy and 23 with antibodies against Ro/SS-A ± La/SS-B without a CHB …

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    Footnotes

    • Handling editor Josef S Smolen

    • Contributors Guarantor: Ana-Luisa Stefanski. The concept of the study was developed by ALS, ACL and TD. Patient’s samples were collected by ALS, IDS, NN, AM, ES and JR. Data were obtained by ALS, HRA, AA, FSZ and JR. Data were analysed by ALS, HRA and AK. The theoretical framework was developed by ALS and TD. The work was supervised by ACL, HH and TD. All authors developed, read and approved the current manuscript.

    • Funding This study was funded by Charité Berlin (Rahel-Hirsch-Scolarship).

    • Competing interests None declared.

    • Patient and public involvement Patients and/or the public were not involved in the design, conduct, reporting or dissemination plans of this research.

    • Provenance and peer review Not commissioned; externally peer reviewed.

    • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.