SOCS1 Regulates the Immunomodulatory Roles of MSCs on B Cells

Background and Objectives@#The effective use of MSCs for the treatment of some B cell-mediated immune diseases is quite limited. The main reason is that the immunomodulatory effects of mesenchymal stem cells (MSCs) on B cells are unclear, and their underlying mechanisms have not been fully explored. @*Methods@#and Results: By co-culturing B cells with MSCs without (MSC/CTLsh) or with suppressor of cytokine signaling 1 (SOCS1) knockdown (MSC/SOCS1sh), we found that MSCs inhibited B cell proliferation, activation and terminal differentiation. Remarkably, the highest inhibition of B cell proliferation was observed in MSC/SOCS1sh co-culture. Besides, MSC/SOCS1sh reversed the inhibitory effect of MSCs in the last stage of B cell differentiation. However, MSC/SOCS1sh had no effect on inhibiting B cell activation by MSCs. We also showed that IgA+ B cell production was significantly higher in MSC/SOCS1sh than in MSC/CTLsh, although no difference was observed when both MSCs co-cultures were compared to isolated B cells. In addition, MSCs increased PGE2 production after TNF-α/IFN-γ stimulation, with the highest increase observed in MSC/SOCS1sh co-culture. @*Conclusions@#Our results highlighted the role of SOCS1 as an important new mediator in the regulation of B cell function by MSCs. Therefore, these data may help to develop new treatments for B cell-mediated immune diseases.

Analysis on mutations of GJB2 gene in Chinese population / 中华医学遗传学杂志

<p><b>OBJECTIVE</b>To determine the prevalence and types of GJB2 mutations and to investigate the genetic mechanism in Chinese autosomal recessive deafness.</p><p><b>METHODS</b>The subjects were four Chinese pedigrees (39 individuals) and 50 normal adults. GJB2 was amplified by PCR. The products were digested with restriction enzyme Apa I, then sequenced.</p><p><b>RESULTS</b>Homozygous deletion C at position 232-235 of GJB2 (235delC),which resulted in frameshift mutation, was found in four affected individuals of two pedigrees; the compound heterozygous deletions (235delC/232G to A) were found in two affected individuals in one pedigree. One carrier with 235delC was found in normal controls (1% allele). Two kinds of polymorphisms 79G to A(V27I) and 3 41A to G(E114G) were found in both affected and normal controls. The frequencies of allele for 79G to A and 341A to G in normal controls were 30%, 21%, respectively.</p><p><b>CONCLUSION</b>235delC mutation of GJB2 was related with Chinese autosomal recessive deafness, and the 232G to A(Ala78Thr) missense mutation was found to be a novel mutation.</p>