Dimitrios Boumpas and colleagues recently published a study in Annals of the Rheumatic Diseases

Most cells participating in the pathogenesis of systemic lupus erythematosus (SLE) originate from bone marrow (BM) haematopoietic stem and progenitor cells (HSPCs). HSPCs actively respond to inflammatory stimuli by myeloid skewing, but this may lead to exhaustion, decreased function, increased risk for inflammation, decreased adaptive immunity and increased cardiovascular mortality. In SLE, we provide evidence of deregulation of hematopoiesis with skewing towards the myeloid lineage at the expense of lymphopoiesis and priming of HSPCs that exhibit a ‘trained immunity’ signature. Abnormalities of immune cells in SLE can be traced back in the BM HSPCs, a disease where stem cell therapy has been considered for refractory cases. Re-establishment of the appropriate myeloid versus lymphoid balance and alleviation of cell exhaustion may improve transplantability of HSPCs and may restore immune function. This could also decrease risk of infection and atherosclerosis and attenuate inflammation, decreasing the risk of flare.

Transcriptome reprogramming and myeloid skewing in haematopoietic stem and progenitor cells in systemic lupus erythematosus.
Grigoriou M, Banos A, Filia A, Pavlidis P, Giannouli S, Karali V, Nikolopoulos D, Pieta A, Bertsias G, Verginis P, Mitroulis I, Boumpas DT.
Ann Rheum Dis. 2019 Nov 28. pii: annrheumdis-2019-215782. doi: 10.1136/annrheumdis-2019-215782.