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Objective. To identify B cell subpopulations participating in the lymphocyte infiltrate of salivary glands from patients with primary Sjögren's syndrome. A special emphasis was placed on those B lymphocytes included in the ectopic germinal centers (GCs).Methods. The presence of B cells in salivary glands and their polyclonality were ascertained by phenotyping and reverse transcription-polymerase chain reaction in salivary gland samples from 18 patients. Their phenotype was thoroughly analyzed using a number of double-staining combinations. The results obtained in tissue sections were confirmed by fluorescence-activated cell sorting analysis of B cells eluted from salivary glands, and these findings were compared with those in tonsils.Results. Memory-type B cells were defined as CD20؉,CD27؉ and were seen in all specimens, whereas GCs were found in only 7 specimens. Furthermore, B cells found in these GCs lacked certain characteristics of centroblasts and centrocytes. Instead,

The anti-CD20 monoclonal antibody rituximab has been less successful in treating chronic lymphocytic leukemia (CLL) than lymphoma, possibly due to the lower density of CD20 on B lymphocytes from CLL patients than on those from lymphoma patients. This lowering may result from insufficiency of one of the transcription factors of cd20. Of these, purine-rich box-1 (PU.1) is poorly expressed in CLL. To estimate its weight in CD20 expression, pu.1 cDNA was transfected into CLL B cells and shown to raise the membrane expression of CD20 and to improve the rituximabinduced lysis of transfected cells. Granulocyte macrophage colony-stimulating factor and all-trans-retinoic acids were not involved in the defective expression of PU.1 or the excessive methylation of the pu.1 gene, because 6 of 14 CLL samples tested were normally methylated. This was confirmed by the failure of DNA methyltransferase inhibitors to restore pu.1 transcription in hypermethylated CLL, and, in fact, the expression of PU.1 was down-regulated by excessive expression of the FMS proto-oncogene-like tyrosine kinase 3 (Flt3) receptor. This abnormality is consistent with our finding of elevated levels of Flt3 ligand (FL) in 20 of 23 CLL sera tested. We propose that FL-dependent increased Flt3 signaling prevents the expression of PU.1, which down-regulates that of CD20, and accounts for resistance of leukemic B cells to rituximab-induced lysis.

Objectives:To evaluate the outcome of our experience in the treatment of salivary gland disorders in children undergoing sialendoscopy and to assess the evolution of the technique. Results: Pediatric sialendoscopy was performed on the parotid gland in 23 patients (61%) and on the submandibular gland in 15 patients (39%). The most frequent indication for sialendoscopy was recurrent salivary gland swelling. Thirty-two of 38 procedures (84%) were performed endoscopically, whereas a combined intervention was necessary for 3 patients and a submandibular gland excision for another 3 patients. Sialendoscopy allowed the diagnosis of 12 patients with salivary duct lithiasis, 21 with salivary duct stenosis, and 2 with both submandibular lithiasis and stenosis, and findings from 3 sialendoscopies were normal. Preoperative ultrasonographic results were confirmed by sialendoscopy in only 7 patients. Of the 10 patients with lithiasis found using sialendoscopy, only 4 had been detected using preoperative ultrasonography.Conclusions: Sialendoscopy is a pertinent technique for the diagnosis and treatment of salivary gland disorders in children. It also allows the most conservative treatment of sialolithiasis and juvenile recurrent parotitis.

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