Patients with SLE with an expanded autoantibody profile and raised BLyS levels at baseline had shorter clinical responses to BCDT. This may reflect a greater propensity to, and degree of, epitope spreading in such patients and suggests that treatment regimens beyond BCDT may be necessary to induce long-lasting clinical remissions in these individuals.

Diminished peripheral blood memory B cells and accumulation of memory B cells in the salivary glands of patients with Sjögren's syndrome.

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FcγRIIIa is a cytokine‐inducible IgG Fc receptor implicated in the activation of macrophages by imm_une complexes. Differential expression of FcγRIIIa by macrophages in different tissues may therefore modulate local imm_une responsiveness. FcγRIIIa expression in normal human tissues was assessed semiquantitatively using microdensitometry. Synovial intimal, serosal, alveolar, salivary gland and placental macrophages, Kupffer cells, and macrophages in mechanically stressed dermis expressed high levels of FcγRIIIa. Less consistent expression was seen in skeletal muscle and lymphoid organs. No significant expression was observed in brain, thyroid, spine, intestine, myocardium, prostate, uterus, flexor forearm dermis, uterus, or kidney. Staining for FcγRIII was also observed on extracellular matrix, and co‐localized with both complement decay‐accelerating factor and fibrillin‐1. It is proposed that differential levels of both cellular and extracellular FcγRIIIa, by modulating the response to imm_une complexes, may contribute to relative tissue susceptibility to infection and autoimm_une disease.

No abstract