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  • DSI-2023-0026.R1 AAM

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Pericardial and mediastinal fat-associated lymphoid clusters are rapidly activated in an alkane-induced model of systemic lupus erythematosus

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Article numberkyad017
<mark>Journal publication date</mark>25/10/2023
<mark>Journal</mark>Discovery Immunology
Issue number1
Volume2
Publication StatusPublished
Early online date25/09/23
<mark>Original language</mark>English

Abstract

Summary Systemic lupus erythematosus (SLE) is an autoimmune disease predominated by auto-antibodies that recognise cellular components. Pleural involvement is the most common SLE-related lung disease. Natural antibodies are rapidly secreted by innate-like B cells following perturbation of homeostasis and are important in the early stages of immune activation. The serous cavities are home to large numbers of innate-like B cells present both within serous fluid and resident within fat-associated lymphoid clusters (FALCs). FALCs are important hubs for B-cell activation and local antibody secretion within the body cavities. Patients with SLE can develop anti-phospholipid antibodies and in rare situations develop alveolar haemorrhage. Utilising delivery of the hydrocarbon oil pristane in C57BL/6 mice as a model of SLE we identify a rapid expansion of pleural cavity B cells as early as day 3 after intra-peritoneal pristane delivery. Following pristane delivery, pericardial B1 B cells are proliferative, express the plasma-cell surface marker CD138, and secrete both innate and class-switched antibodies highlighting that this cavity niche may play an unrecognised role in the initiation of lupus pleuritis.