B cell-activating factor enhances interleukin-6 and interleukin-10 production by ODN-activated human B cells.

We aim to investigate the additive value of B cell-activating factor (BAFF) when added to oligodeoxynucleotides (ODN)-activated B cells with respect to TLR-9, CD69, MHC-II expression, IL-6 and IL-10 secretion and B cell cycling. Therefore, B cells from healthy individuals were incubated under the following conditions: (1) B cells with medium, (2) B cells with ODN 0.5 µm, (3) B cells with BAFF 20 µm and (4) B cells with both ODN 0.5 µm and BAFF 20 µm. We found that addition of BAFF did not enhance the expression of TLR-9, CD69 and MHC-II in ODN-activated B cells. Incubation of B cells with BAFF and ODN together leads to a marked elevation of IL-6 and IL-10 levels compared to ODN alone. Synthesis and mitosis were higher in B cells stimulated by BAFF than in B cells stimulated by ODN. These findings suggest that both BAFF and TLR-9 contribute independently to B cell function.

Looking into the eyes of patients with antiphospholipid syndrome.

Diagnosis of antiphospholipid syndrome (APS) should be considered in all patients with recurrent systemic or ocular thrombosis in the absence of known risk factors. Because of the frequent ocular involvement in APS patients (as many as 80%), an ophthalmologic assessment should become a routine part of the clinical work-up of all patients in whom APS is highly suspected. The presence of isolated ocular thrombosis with persistently increased titers of antiphospholipid antibodies should be considered as definite APS. Ocular involvement in APS is frequently associated with other manifestations of the central nervous system (CNS), such as transient ischemic attack or cerebral vascular events. Diagnostic tools are needed to better establish a diagnosis of retinal vascular thrombosis. The treatment of isolated ocular APS should be based on the same principles as in all patients with systemic APS. Anticoagulation is aimed to prevent recurrent ocular or cerebral thromboses.

Increased susceptibility of cord blood B lymphocytes to undergo spontaneous apoptosis.

In this study, we compared the rate of spontaneous apoptosis of B cells from umbilical cord blood with adult B cells and assessed the role of Bcl-2, CD5, interleukin (IL)-4 and B cell-activating factor in B cell spontaneous apoptosis. We found that spontaneous apoptosis of cultured B cells, as assessed by utilizing annexin-V binding, was significantly higher in cord blood than in healthy adult individuals (77.5; 95 CI, 73.5-81.5 versus 59.2; 95 CI, 54-64, respectively, P < 0.0001) and further confirmed by 4' 6-diamidino-2-phenylindole, dihydrochloride (DAPI) staining. Whereas the expression of B cell-activating factor from the tumour necrosis factor family (BAFF) receptor mRNA was similar in B cells from adults and cord blood, we detected lower levels of circulating BAFF in the serum of cord blood (0.68 +/- 0.13 ng versus 1.83 +/- 0.54 ng, P = 0.01). The latter may explain, in part, our observation of lower levels of mean fluorescence intensity of Bcl-2 in cord B cells compared with adults (1.6 +/- 0.9 versus 2.85 +/- 1.3, P = 0.033). CD19(+) CD5(+) B cells from cord blood underwent a lower rate of apoptosis in comparison to CD19(+) CD5(-) B cells (25.1 +/- 9.3%versus 58.5 +/- 12.5%, P < 0.0001). This pattern of sensitivity was comparable in adult blood (15 +/- 5.5%versus 22.7 +/- 9.3%, P = 0.01). Nevertheless, the rate of apoptosis was higher in CD19(+) CD5(+) from cord blood compared to CD19(+) CD5(+) from adults (25.1 +/- 9.3%versus 15 +/- 5.5%, P = 0.0013). The addition of rIL-4 (10 u/ml) to cultured cells decreased B cell apoptosis in a similar fashion in both cord and adults blood. This rescue was strengthened when BAFF (100 microg/ml) was further added. Thus, alterations in Bcl-2 or serum BAFF level may explain the increased rate of cord blood B cell apoptosis.

The autoimmune characteristics of progressive or sudden sensorineural hearing loss.

Autoimmune sensorineural hearing loss (ASNHL) is a clinical syndrome that typically produces a bilateral rapidly progressive hearing loss. Autoantibodies and autoreactive T cells have been implicated in the etiopathogenesis of ASNHL. However, the identity of a specific or highly relevant inner-ear self-antigen is still required. In recent years, a role for antiphospholipid antibodies has been also suggested, assuming sudden/progressive hearing loss to be part of the primary antiphospholipid syndrome (APS). In this review, we address the need for specific diagnostic tools in order to establish an autoimmune origin for hearing loss. Moreover, the decision of whether anti-inflammatory drugs or anti-coagulation should be given is also discussed.