Rabbit Anti-Human IL7 Polyclonal Antibody

The present study describes our efforts to induce the proliferation of human B cell precursors (BCP). Committed BCP (CD10+, slgM-) isolated from fetal bone marrow (18-25 weeks) were induced to proliferate at low levels in the presence of IL7. IL3 potentiated this effect of IL7 on BCP, while IL4 partially inhibited this proliferation. However, neither of these cytokines allowed the emergence of mature B cells. The growth of BCP was strongly potentiated by the presence of an adherent fibroblastic bone marrow stromal layer devoid of cells of hematopoietic origin. Addition of IL7 to such cocultures further increased BCP proliferation. BCP were shown to proliferate as stroma-adherent and non adherent cells. Total cell numbers expanded during 3 weeks, as much as 8 fold in the presence of IL7 when compared with input BCP numbers. Finally, BCP remained slgM- in stroma dependent cultures, and only a subpopulation of cells became CD20+ in the presence of IL7. Our present study demonstrates the feasibility of human BCP expansion in vitro. However, the signals required for the transition of BCP to mature B cells remain to be determined.

Background: Peripheral gene expression of several molecular pathways has been studied in major depressive disorder (MDD) with promising results. We sought to investigate some of these genes in a treatment-free Latino sample of Mexican descent. Material and Methods: The sample consisted of 50 MDD treatment-free cases and 50 sex and age-matched controls. Gene expression of candidate genes of neuroplasticity (BDNF, p11, and VGF), inflammation (IL1A, IL1B, IL4, IL6, IL7, IL8, IL10, MIF, and TNFA), the canonical Wnt signaling pathway (TCF7L2, APC, and GSK3B), and mTOR, was compared in cases and controls. RNA was obtained from blood samples. We used bivariate analyses to compare subjects versus control mean mRNA quantification of target genes and lineal regression modelling to test for effects of age and body mass index on gene expression. Results: Most subjects were female (66%) with a mean age of 26.7 (SD 7.9) years. Only GSK3B was differentially expressed between cases and controls at a statistically significant level (p = 0.048). TCF7L-2 showed the highest number of correlations with MDD-related traits, yet these were modest in size. Discussion: GSK3B encodes a moderator of the canonical Wnt signaling pathway. It has a role in neuroplasticity, neuroprotection, depression, and other psychiatric phenotypes. We found that adding population diversity has the potential to elicit distinct peripheral gene expression markers in MDD and MDD-related traits. However, our results should only be considered as hypothesis-generating research that merits further replication in larger cohorts of similar ancestry.