Patients with SLE have lower levels of circulating HSCs and EPCs, even during clinical remission. The data suggest that increased HSC apoptosis is the underlying cause for this depletion. These observations indicate that progenitor cell-mediated endogenous vascular repair is impaired in SLE, which may contribute to the accelerated development of atherosclerosis.
Compared to the incidence of invasive pneumococcal infections in the Dutch population (15.6/100.000 patient years), the incidence in SLE patients is 13 times higher. This, in combination with the absence of a relation to use of immunosuppressive drugs, is a strong argument to recommend vaccination against S. pneumoniae in all SLE patients.
Background The soluble form of the interleukin 7 receptor (sIL-7R) is produced by fibroblasts after stimulation with proinflammatory cytokines. Increased sIL-7R serum and synovial fluid levels were recently demonstrated in patients with rheumatoid arthritis.
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