Naive B cell

About: Naive B cell is a research topic. Over the lifetime, 4204 publications have been published within this topic receiving 266815 citations.

Complementary DNA for a novel human interleukin (BSF-2) that induces B lymphocytes to produce immunoglobulin

Abstract: When stimulated with antigen, B cells are influenced by T cells to proliferate and differentiate into antibody-forming cells. Since it was reported that soluble factors could replace certain functions of helper T cells in the antibody response, several different kinds of lymphokines and monokines have been reported in B-cell growth and differentiation. Among these, human B-cell differentiation factor (BCDF or BSF-2) has been shown to induce the final maturation of B cells into immunoglobulin-secreting cells. BSF-2 was purified to homogeneity and its partial NH2-terminal amino-acid sequence was determined. These studies indicated that BSF-2 is functionally and structurally unlike other known proteins. Here, we report the molecular cloning, structural analysis and functional expression of the cDNA encoding human BSF-2. The primary sequence of BSF-2 deduced from the cDNA reveals that BSF-2 is a novel interleukin consisting of 184 amino acids.

Human hepatocellular carcinoma cell lines secrete the major plasma proteins and hepatitis B surface antigen.

Abstract: Analysis of the cell culture fluid from two new human hepatoma-derived cell lines reveals that 17 of the major human plasma proteins are synthesized and secreted by these cells. One of these cell lines, Hep 3B, also produces the two major polypeptides of the hepatitis B virus surface antigen. When Hep 3B in injected into athymic mice, metastatic hepatocellular carcinomas appear. These cell lines provide experimental models for investigation of plasma protein biosynthesis and the relation of the hepatitis B viru genome to tumorigenicity.

B cells regulate autoimmunity by provision of IL-10.

Abstract: To assess the importance of B cell control of T cell differentiation, we analyzed the course of the T helper type 1 (TH1)-driven disease experimental autoimmune encephalomyelitis in mice with an altered B cell compartment. We found that recovery was dependent on the presence of autoantigen-reactive B cells. B cells from recovered mice produced interleukin 10 (IL-10) in response to autoantigen. With a bone marrow chimeric system, we generated mice in which IL-10 deficiency was restricted to B cells but not T cells. In the absence of IL-10 production by B cells, the pro-inflammatory type 1 immune response persisted and mice did not recover. These data show that B cell–derived IL-10 plays a key role in controlling autoimmunity.

Early Lymphocyte Expansion Is Severely Impaired in Interleukin 7 Receptor-deficient Mice By Jacques J. Peschon, Philip J. Morrissey, Kenneth H. Grabstein,

Abstract: Summary Interleukin 7 (IL-7) stimulates the proliferation of B cell progenitors, thymocytes, and mature T cells through an interaction with a high affinity receptor (IL-7R) belonging to the hematopoietin receptor superfamily. We have further addressed the role of IL-7 and its receptor during B and T cell development by generating mice genetically deficient in IL-7R. Mutant mice display a profound reduction in thymic and peripheral lymphoid cellularity. Analyses of lymphoid progenitor populations in IL-7R-deficient mice define precisely those developmental stages affected by the mutation and reveal a critical role for IL-7R during early lymphoid development. Significantly, these studies indicate that the phase of thymocyte expansion occurring before the onset of T cell receptor gene rearrangement is critically dependent upon, and mediated by the high affinity receptor for IL-7. T he development of lymphoid cells from muhipotential progenitors is dependent upon growth, survival, and differentiation factors produced by various stromal cells. Long- term cultures supporting the growth of murine B lineage cells from uncommitted precursors can be established from adult bone marrow and have been instrumental in defining factors that influence B cell development (1, 2). IL-7 was identified and cloned based upon its ability to induce short- term proliferation of B cell progenitors in the absence of stromal cells (3). The requirement for IL-7 in the prolifera- tion of B cell precursors has been clearly established in that stromal cell variants that no longer express IL-7 are incapable of efficiently supporting B ceU progenitor growth, and neu- tralizing antibodies to IL-7 or IL-7R severely inhibit B cell development in vitro and in vivo (4-6). Evidence suggests that the IL-7-responsive B lineage popu- lation displays an early/late pro-B cell phenotype character- ized by the expression of B220, heat stable antigen (HSA), and leukosialin (CD43), the presence of D-J and V-D-J rear- rangements and the absence of surface IgM (7). Less mature B lineage cells do not proliferate or differentiate in response to IL-7 in vitro, although they do express IL-7R (8). IL-7R expression is lost after productive light chain rearrangement in pre-B ceils, and thus subsequent stages of B cell matura- tion are likely to be directly IL-7 independent (9). The role of IL-7 in T cell development is less well defined. IL-7 is expressed in the thymus and has been shown to stimu- late the growth of immature CD4-/CD8- adult and fetal thymocytes (10, 11) and promote rearrangement of T cell receptor 3 and 3, chains in fetal thymus and fetal liver culture systems (12, 13). Additionally, treatment of mice with neu- tralizing antibodies to IL-7 or IL-7R results in thymic hypoplasia (5, 6), and overexpression of IL-7 in transgenic mice perturbs thymocyte cellularity (14). However, it is not known to what extent T cell development within the thymus is IL-7 dependent and which of the thymic subpopulations have specific requirements for IL-7-induced proliferation and survival in vivo. We have taken a genetic approach to further elucidate the role of IL-7 and its high affinity receptor in the proliferation and maturation of B and T lineage cells in vivo by analyzing lymphoid development in mice lacking the high affinity IL- 7R. Results obtained from these analyses implicate IL-7R as a critical signaling molecule in the proliferation of early B cell progenitors undergoing heavy chain rearrangements and in early thymocyte expansion prior to the acquisition of rearranged T cell receptor genes.