bluuebunny/crossref_metadata_2025_split huggingface dataset:
Immunoglobulin promotes the diversity and the function of T cells
Authors: João Cristina , Ogle Brenda M. , Geyer Susan 
Published: June 2006

AbstractIt is generally accepted in immunology that while T and B cells collaborate for the production of antibodies in response to protein antigens, T cells develop and function in the absence of B cells. However, B cell‐deficient subjects and mice have unexplained cellular immune defects. Here, we examined the contribution of B cells/Ig to the generation of diversity and function of T cells. Mice lacking B cells and Ig (JH–/–) or having oligoclonal B cells (QM) had a profoundly contracted T cell receptor (TCR) Vβ repertoire: 0.08 and 1.3% of wild type, respectively. Rejection of H‐Y‐incompatible skin grafts in QM and JH–/– mice was significantly delayed (median, 43 and 22 days, respectively) compared to wild‐type mice (median, 16 days). Furthermore, reduction of the TCR Vβ diversity by thymectomy in wild‐type mice significantly increased survival of H‐Y‐incompatible skin grafts, and reconstitution of the T cell diversity in QM mice with Ig Fab fragments significantly decreased survival of the skin grafts. These results indicate that B cells and/or Ig "help" T cells through the generation and maintenance of T cell diversity, improving T cell function. Our results may have important implications for therapy and immune reconstitution in the context of AIDS, cancer, autoimmunity and post‐myeloablative treatments.
BAFF costimulation of Toll‐like receptor‐activatedB‐1 cells
Authors: Ng Lai Guan , Ng Chee‐Hoe , Woehl Blanche , Sutherland Andrew P. R. , Huo Jianxin , Xu Shengli , Mackay Fabienne , Lam Kong‐Peng 
Published: June 2006

AbstractB cell‐activating factor belonging to the TNF family (BAFF) and its receptor BAFF‐R play critical roles in the maturation and survival of conventional peripheral B cells. However, they appeared to be dispensable for the generation and maintenance of CD5+ B‐1 cells as BAFF–/– and BAFF‐R–/– mice have normal B‐1 cell populations. Hence, it is presently unclear if B‐1 cells are responsive to BAFF and if BAFF regulates some aspects of B‐1 cell function. We show here that BAFF‐R and transmembrane activator and CAML interactor (TACI) are the major receptors expressed by B‐1 cells. Specifically, we show that BAFF treatment of B‐1 cells leads to increased NF‐κB p100 processing and CD21/CD35 expression. Interestingly, toll‐like receptor (TLR) engagement of B‐1 cells augmented the surface expression of BAFF receptors and rendered them responsive to BAFF costimulation, as evidenced by their increased proliferation, expression of cell surface activation markers and secretion of the pro‐inflammatory cytokine IL‐6 and the anti‐inflammatory cytokine IL‐10. This costimulatory effect is achieved primarily through BAFF‐R as BAFF failed to costimulate B‐1 cells obtained from A/WySnJ mice which have defective BAFF‐R signaling. Thus, as TLR are innate immune receptors and B‐1 cells are "innate‐like" lymphocytes, our data provide evidence that BAFF plays a role in innate immunity.
Coy decoy with a new ploy: Interceptor controls the levels of homeostatic chemokines
Authors: Haraldsen Guttorm , Rot Antal 
Published: June 2006

AbstractA new subfamily of chemokine receptors is emerging that do not signal along classical G‐protein‐mediated pathways. Instead, these “silent” receptors efficiently internalize their cognate chemokine ligands, hence their suggested name, “chemokine interceptors”, for internalizing receptors. Two of these interceptors, DARC and D6, possess intriguing patterns of tissue expression and are believed to be involved in controlling the local levels of proinflammatory chemokines. In this issue of the European Journal of Immunology, the biochemical properties of a third silent chemokine receptor, CCX‐CKR, have been characterized and it is suggested that it may act as a scavenger for homeostatic chemokines, pointing to a broad and significant role for this group of chemokine binding molecules in chemokine biology.See accompanying article http://www.dx.doi.org/10.1002/eji.200535716
Exposure to wood smoke, HPV infection, and genetic susceptibility for cervical neoplasia among women in Colombia
Authors: Sierra‐Torres Carlos H. , Arboleda‐Moreno Yexania Y. , Orejuela‐Aristizabal Leonora 
Published: June 2006

AbstractCervical cancer is the second leading cause of death from cancer among women in Colombia (16/100,000). Infection with high‐risk human papillomavirus (HPV) plays a major role in the etiology of high‐grade squamous intraepithelial lesions (HSILs). Exposure to chemical agents may be a cofactor for tumor induction, and individual genetic differences in the metabolism of these chemical agents may affect the susceptibility of individuals towards the development of HSIL. In this case–control study, a total of 91 cases with HSIL and 92 healthy controls, frequency‐matched by age and place of origin, were recruited, and their frequencies of CYP2E1, GSTM1, and GSTT1 polymorphism were determined. We then evaluated the association of these polymorphisms, by themselves and in combination with wood smoke exposure and HPV‐infection status, with the risk of HSIL. The results indicate that GSTM1 and GSTT1 polymorphism were not associated with HSIL, although a small increase in risk was observed for individuals who were GSTT1 null (OR = 1.4, 95% CI = 0.57–3.44). Contrary to other investigations, the c2/c2 variant of the CYP2E1 gene was associated with a significant increase in risk after adjusting for wood smoke exposure (OR = 6.3, 95% CI = 1.10–36.38) or wood smoke exposure and HPV‐infection status (OR = 10.7, 95% CI = 1.76–65.58). Wood smoke exposure also increased the risk of HSIL among CYP2E1 c2/c2 HPV‐positive women (OR = 3.3, CI = 0.50–22.50); however, the increase did not achieve statistical significance. Our study provides tantalizing evidence that genetic differences in the metabolism of wood smoke carcinogens, particularly metabolism by CYP2E1, may confer susceptibility for HSIL development. Further investigations with larger populations will be needed to confirm this association, which may provide important information for improving cervical cancer prevention programs. Environ. Mol. Mutagen., 2006. © 2006 Wiley‐Liss, Inc.
Evaluation of micronucleus frequencies and DNA damage in glass workers exposed to arsenic
Authors: Vuyyuri Saleha B. , Ishaq Mohamed , Kuppala Danadevi , Grover Paramjit , Ahuja Y.R. 
Published: June 2006

AbstractArsenic (As) is a known human carcinogen; however, very little is known about the health consequences of occupational exposure to As. In the present study, we assessed the genotoxic damage in the blood cells and in the buccal cells of south Indian glass factory workers who are occupationally exposed to As. The As content in the whole blood of 200 workers and 165 controls was evaluated with inductively coupled plasma mass spectrometry. Blood leukocytes from the subjects were monitored for the level of DNA damage using the Comet assay (mean comet tail length); buccal cells were used to determine the frequency of micronuclei (MN). The mean As concentration was significantly higher in the workers (56.76 μg/L) than in the controls (11.74 μg/L) (P < 0.001). The workers also had increased frequencies of MN in the buccal cells and increased levels of DNA damage in leukocytes compared to the controls (P < 0.001). There were significant correlations between the genotoxicity endpoints that were evaluated and blood As concentration, smoking, age, and the duration of working in the factory. Also, a significant correlation was observed between the frequency of MN and comet tail‐length for the worker samples. Our findings indicate that chronic occupational exposure to As is genotoxic and that the Comet assay and micronucleus test are useful assays for evaluating genotoxicity in humans occupationally exposed to As. Environ. Mol. Mutagen., 2006. © 2006 Wiley‐Liss, Inc.
Innate immune response to human bone marrow fibroblastic cell implantation in CB17 scid/beige mice
Authors: Xia Zhidao , Taylor Philip R. , Locklin Rachel M. , Gordon Siamon , Cui Zhanfeng , Triffitt James T. 
Published: June 2006

AbstractImmunocompromised mouse models have been extensively used to assess human cell implantation for evaluation of cytotherapy, gene therapy and tissue engineering strategies, as these mice are deficient in T and B lymphoid cells. However, the innate immune response and its effect on human cell xenotransplantation in these mouse models are mainly unknown. The aim of this study is to characterise the myeloid populations in the spleen and blood of CB17 scid beige (CB17 sb) mice, and to study the inflammatory cell responses to xenogeneic implantation of enhanced green fluorescent protein (GFP)‐labelled human bone marrow fibroblastic (HBMF) cells into CB17 sb mice. The results indicate that even though CB17 sb mice are deficient in B‐ and T‐cells, they exhibit some increases in their monocyte (Mo), macrophage (MΦ) and neutrophil (Neu) populations. NK cell and eosinophil populations show no differences compared with wild‐type Balb/C mice. An innate immune response, identified by CR3 (CD11b/CD18)‐positive myeloid inflammatory cells and F4/80‐positive macrophages, was evident in the tissues where HBMF cells were implanted. As a consequence, the majority of implanted HBMF cells were eliminated by 4 weeks after implantation. Interestingly, the mineralised matrix formed by osteogenic HBMF cells was also eroded by multinuclear MΦ‐like giant cells. We conclude that CB17 sb mice retain active innate immune cells, which respond to HBMF cell xenotransplantation. This study highlights the importance of the innate immune cells in the anti‐xenograft response and suggests that strategies to block the activities of these cells may ameliorate the progressive long‐term elimination of xenotransplants. J. Cell. Biochem. 98: 966–980, 2006. © 2006 Wiley‐Liss, Inc.
TGF‐β2 stimulates cranial suture closure through activation of the Erk‐MAPK pathway
Authors: Lee Sang‐Won , Choi Kang‐Young , Cho Je‐Yoel , Jung Sung‐Hwa , Song Kun‐Bae , Park Eui‐Kyun , Choi Je‐Yong , Shin Hong‐In , Kim Shin‐Yoon , Woo Kyung‐Mi , Baek Jeong‐Hwa , Nam Soon‐Hyeun , Kim Young‐Jin , Kim Hyun‐Jung , Ryoo Hyun‐Mo 
Published: June 2006

AbstractCranial sutures are important growth sites of the skull. During suture closure, the dura mater is one of the most important sources of various positive and negative regulatory signals. Previous results indicate that TGF‐β2 from dura mater strongly accelerates suture closure, however, its exact regulatory mechanism is still unclear. In this study, we confirmed that removal of dura mater in calvarial organ culture strongly accelerates sagittal suture closure and that this effect is further enhanced by TGF‐β2 treatment. TGF‐β2 stimulated cell proliferation in the MC3T3‐E1 cell line. Similarly, it stimulated the proliferation of cells in the sutural space in calvarial organ culture. Furthermore, TGF‐β2‐mediated enhanced cell proliferation and suture closure were almost completely inhibited by an Erk‐MAPK blocker, PD98059. These results indicate that TGF‐β2‐induced activation of Erk‐MAPK is an important signaling component that stimulates cell proliferation to enrich osteoprogenitor cells, thereby promoting their differentiation into osteoblasts to achieve a rapid calvarial bone expansion. J. Cell. Biochem. 98: 981–991, 2006. © 2006 Wiley‐Liss, Inc.
Osteogenic growth peptide effects on primary human osteoblast cultures: Potential relevance for the treatment of glucocorticoid‐induced osteoporosis
Authors: Spreafico Adriano , Frediani Bruno , Capperucci Caterina , Leonini Alessandra , Gambera Dario , Ferrata Paolo , Rosini Sergio , Di Stefano Anna , Galeazzi Mauro , Marcolongo Roberto 
Published: June 2006

AbstractThe osteogenic growth peptide (OGP) is a naturally occurring tetradecapeptide that has attracted considerable clinical interest as a bone anabolic agent and hematopoietic stimulator. In vivo studies on animals have demonstrated that the synthetic peptide OGP (10–14), reproducing the OGP C‐terminal active portion [H‐Tyr‐Gly‐Phe‐Gly‐Gly‐OH] increases bone formation, trabecular bone density and fracture healing. In vitro studies performed on cellular systems based on osteoblastic‐like cell lines or mouse stromal cells, have demonstrated that OGP (10–14) increases osteoblast proliferation, alkaline phosphatase (ALKP) activity and matrix synthesis and mineralization. In view of a potential application of OGP (10–14) in clinical therapy, we have tested different concentrations of OGP (10–14) on primary human osteoblast (hOB) cultures. We have observed significant increases of hOB proliferation (+35%), ALKP activity (+60%), osteocalcin secretion (+50%), and mineralized nodules formation (+49%). Our experimental model based on mature hOBs was used to investigate if OGP (10–14) could prevent the effects on bone loss induced by sustained glucocorticoid (GC) treatments. A strong decrease in bone formation has been attributed to the effects of GCs on osteoblastogenesis and osteocyte apoptosis, while an increase in bone resorption was due to a transient osteoblastic stimulation, mediated by the OPG/RANKL/RANK system, of osteoclasts recruitment and activation. Moreover, GCs act on hOBs decreasing the release of osteoprotegerin (OPG) a regulator of the RANKL/RANK interaction. Here, we provide evidences that OGP (10–14) inhibits hOB apoptosis induced by an excess of dexamethasone (−48% of apoptotic cells). Furthermore, we show that OGP (10–14) can increase OPG secretion (+20%) and can restore the altered expression of OPG induced by GCs to physiological levels. Our results support the employment of OGP (10–14) in clinical trials addressed to the treatment of different bone remodeling alterations including the GC‐induced osteoporosis. J. Cell. Biochem. 98: 1007–1020, 2006. © 2006 Wiley‐Liss, Inc.
Effects of PPARγ agonists on cell survival and focal adhesions in a Chinese thyroid carcinoma cell line
Authors: Chen Ying , Wang Seu‐Mei , Wu Jiahn‐Chun , Huang Shih‐Horng 
Published: June 2006

AbstractPeroxisome proliferator‐activated receptor γ (PPARγ) agonists cause cell death in several types of cancer cells. The aim of this study was to examine the effects of two PPARγ agonists, ciglitazone and 15‐deoxy‐Δ12,14‐prostaglandin J2 (15dPGJ2), on the survival of thyroid carcinoma CGTH W‐2 cells. Both ciglitazone and 15dPGJ2 decreased cell viability in a time‐ and dose‐dependent manner. Cell death was mainly due to apoptosis, with a minor contribution from necrosis. Increased levels of active caspase 3, cleaved poly (ADP‐ribose) polymerase (PARP), and cytosolic cytochrome‐cwere noted. In addition, ciglitazone and 15dPGJ2 induced detachment of CGTH W‐2 cells from the culture substratum. Both the protein levels and immunostaining signals of focal adhesion (FA) proteins, including vinculin, integrin β1, focal adhesion kinase (FAK), and paxillin were decreased after PPARγ agonist treatment. Meanwhile, reduced phosphorylation of FAK and paxillin was noted. Furthermore, PPARγ agonists induced expression of protein tyrosine phosphatase‐PEST (PTP‐PEST), and of phosphatase and tensin homologue deleted on chromosome ten (PTEN). The upregulation of these phosphatases might contribute to the dephosphorylation of FAK and paxillin, since pre‐treatment with orthovanadate prevented PPARγ agonist‐induced dephosphorylation of FAK and paxillin. Perturbation of CGTH W‐2 cells with anti‐integrin β1 antibodies induced FA disruption and apoptosis in the same cells, thus the downregulation of integrin β1 by PPARγ agonists resulted in FA disassembly and might induce apoptosis via anoikis. Our results suggested the presence of crosstalk between apoptosis and integrin‐FA signaling. Moreover, upregulation and activation of PTEN was correlated with reduced phosphorylation of Akt, and this consequence disfavored cell survival. In conclusion, PPARγ agonists induced apoptosis of thyroid carcinoma cells via the cytochrome‐ccaspase 3 and PTEN‐Akt pathways, and induced necrosis via the PARP pathway. J. Cell. Biochem. 98: 1021–1035, 2006. © 2006 Wiley‐Liss, Inc.
Okadaic acid induces phosphorylation of p65NF‐κB on serine 536 and activates NF‐κB transcriptional activity in human osteoblastic MG63 cells
Authors: Ozaki Akiko , Morimoto Hiroyuki , Tanaka Hiroaki , Okamura Hirohiko , Yoshida Kaya , Amorim Bruna Rabelo , Haneji Tatsuji 
Published: June 2006

AbstractNuclear factor‐kappa B (NF‐κB) is an essential transcription factor in the control of expression of genes involved in cell growth, differentiation, inflammation, and neoplastic transformation. Previously, we reported that okadaic acid (OA), which is a specific inhibitor of serine/threonine protein phosphatases, induced apoptosis in cells of human osteosarcoma cell line MG63. However, to date, it is not clear whether the phosphorylation status of NF‐κB could be affected by the treatment with OA. In this report, we demonstrate that treatment of MG63 cells with OA enhanced the phosphorylation level of NF‐κB, as judged from the results of Western blot analysis and a λ protein phosphatase dephosphorylation assay. The phosphorylation level of NF‐κB was enhanced in both time‐ and dose‐dependent manners. In the cells treated with 100 nM OA for 3 h, consequential translocation of NF‐κB from the cytosol to the nucleus occurred. Western blotting experiments with an anti‐phospho‐p65NF‐κB antibody disclosed that the NF‐κB was phosphorylated on serine 536. Furthermore, OA stimulated the transcriptional activity of NF‐κB in MG63 cells, as judged from the results of a luciferase assay. Our findings indicate that OA elicit phosphorylation of NF‐κB on serine 536 in MG63 cells, resulting in the translocation of phospho‐NF‐κB to the nucleus, thereby promoting transcriptional activity of genes. J. Cell. Biochem. 99: 1275–1284, 2006. © 2006 Wiley‐Liss, Inc.
Biologic properties of mesenchymal stem cells derived from bone marrow and adipose tissue
Authors: Izadpanah Reza , Trygg Cynthia , Patel Bindiya , Kriedt Christopher , Dufour Jason , Gimble Jeffery M. , Bunnell Bruce A. 
Published: June 2006

AbstractThe biologic characteristics of mesenchymal stem cells (MSCs) isolated from two distinct tissues, bone marrow and adipose tissue were evaluated in these studies. MSCs derived from human and non‐human primate (rhesus monkey) tissue sources were compared. The data indicate that MSCs isolated from rhesus bone marrow (rBMSCs) and human adipose tissue (hASCs) had more similar biologic properties than MSCs of rhesus adipose tissue (rASCs) and human bone marrow MSCs (hBMSCs). Analyses of in vitro growth kinetics revealed shorter doubling time for rBMSCs and hASCs. rBMSCs and hASCs underwent significantly more population doublings than the other MSCs. MSCs from all sources showed a marked decrease in telomerase activity over extended culture; however, they maintained their mean telomere length. All of the MSCs expressed embryonic stem cell markers, Oct‐4, Rex‐1, and Sox‐2 for at least 10 passages. Early populations of MSCs types showed similar multilineage differentiation capability. However, only the rBMSCs and hASCs retain greater differentiation efficiency at higher passages. Overall in vitro characterization of MSCs from these two species and tissue sources revealed a high level of common biologic properties. However, the results demonstrate clear biologic distinctions, as well. J. Cell. Biochem. 99: 1285–1297, 2006. © 2006 Wiley‐Liss, Inc.
A limited number of genes are involved in the differentiation of germinal center B cells
Authors: Nakayama Yasuhiro , Stabach Paul , Maher Stephen E. , Mahajan Milind C. , Masiar Peter , Liao Cheng , Zhang Xueqing , Ye Zhi‐jia , Tuck David , Bothwell Alfred L.M. , Newburger Peter E. , Weissman Sherman M. 
Published: June 2006

AbstractMature B cells, upon activation, progressively differentiate through centroblasts into centrocytes and finally to plasmacytes that express large amounts of selected immunoglobulins. A significant part of this maturation is thought to involve induction of the unfolded protein response (UPR). We have compared gene expression in normal germinal center centroblasts, centrocytes, lymphoblastoid cells undergoing induced UPR, and the CCL155 plasmacytoma cell line. In the centroblast to centrocyte transition there is a change in the expression of a relatively small number of genes. These include a limited subset of the genes upregulated by a fully activated UPR as well as a small number of other transcription factors, some disulphide isomerases, and other genes. This is consistent with a model in which this transition is mediated by changes in the levels of expression of transcription factor B‐lymphocyte‐induced maturation protein 1 (Blimp1) (PRDM1), BACH2, X‐box binding protein 1 (XBP1), interferon regulatory factor 4 (IRF4), and possibly vitamin D receptor (VDR) expression, together with post‐transcriptional changes and a limited induction of aspects of the UPR. J. Cell. Biochem. 99: 1308–1325, 2006. © 2006 Wiley‐Liss, Inc.
Chromosome organization and gene control: It is difficult to see the picture when you are inside the frame
Authors: Verschure Pernette J. 
Published: June 2006

AbstractThe organization of the genome in the nucleus is related to its function. The functional compartmentalization of the genome is described at the nuclear, chromosomal, subchromosomal, nucleosomal, and DNA sequence level. These descriptions originate from the techniques that were used for analysis. The different levels of compartmentalization are not easily reconciled, because the techniques applied to identify genome compartmentalization generally cannot be performed in combination. We have obtained a large body of information on individual “actors” and “scenes” in the nucleus regarding genome compartmentalization, but we still do not understand how and by what pieces of equipment the “actors” play their game. The next challenge is to understand the combined operation of the various levels of functional genome organization in the nucleus, that is, how do the epigenetic and genetic levels act together. In this paper, I will highlight some of the general features and observations of functional organization of the eukaryotic genome in interphase nuclei and discuss the concepts and views based on observed correlations between genome organization and function. I will reflect on what is to be expected from this field of research when the functional levels of genome compartmentalization are integrated. In this context I will draw attention to what might be needed to improve our understanding. J. Cell. Biochem. © 2006 Wiley‐Liss, Inc.
Methods for measuring rates of protein binding to insoluble scaffolds in living cells: Histone H1‐chromatin interactions
Authors: Lele Tanmay , Wagner Stefan R. , Nickerson Jeffrey A. , Ingber Donald E. 
Published: June 2006

AbstractUnderstanding of cell regulation is limited by our inability to measure molecular binding rates for proteins within the structural context of living cells, and many systems biology models are hindered because they use values obtained with molecules binding in solution. Here, we present a kinetic analysis of GFP‐histone H1 binding to chromatin within nuclei of living cells that allows both the binding rate constant kON and dissociation rate constant kOFF to be determined based on data obtained from fluorescence recovery after photobleaching (FRAP) analysis. This is accomplished by measuring the ratio of bound to free concentration of protein at steady state, and identifying the rate‐determining step during FRAP recovery experimentally, combined with mathematical modeling. We report kOFF = 0.0131/s and kON = 0.14/s for histone H1.1 binding to chromatin. This work brings clarity to the interpretation of FRAP experiments and provides a way to determine binding kinetics for nuclear proteins and other cellular molecules that interact with insoluble scaffolds within living cells. J. Cell. Biochem. 99: 1334–1342, 2006. © 2006 Wiley‐Liss, Inc.