- 同
- B lymphocyte receptor:BLC:MCP-4＆CXCL13
- 同
- B lymphocyte receptor:BLC:MCP-4＆CXCL13
WordNet
- the 2nd letter of the Roman alphabet (同)b
- the blood group whose red cells carry the B antigen (同)type_B, group B
- a cellular structure that is postulated to exist in order to mediate between a chemical agent that acts on nervous tissue and the physiological response
- an agranulocytic leukocyte that normally makes up a quarter of the white blood cell count but increases in the presence of infection (同)lymph cell
PrepTutorEJDIC
- =sense organ / 受信装置
UpToDate Contents
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English Journal
- Disruption of tumor necrosis factor receptor associated factor 5 exacerbates pressure overload cardiac hypertrophy and fibrosis.
- Bian Z, Dai J, Hiroyasu N, Guan H, Yuan Y, Gan L, Zhou H, Zong J, Zhang Y, Li F, Yan L, Shen D, Li H, Tang Q.Author information Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, 430060, PR China; Cardiovascular Research Institute of Wuhan University, Wuhan, 430060, PR China.AbstractThe cytoplasmic signaling protein tumor necrosis factor (TNF) receptor-associated factor 5 (TRAF5), which was identified as a signal transducer for members of the TNF receptor super-family, has been implicated in several biological functions in T/B lymphocytes and the innate immune response against viral infection. However, the role of TRAF5 in cardiac hypertrophy has not been reported. In the present study, we investigated the effect of TRAF5 on the development of pathological cardiac hypertrophy induced by transthoracic aorta constriction (TAC) and further explored the underlying molecular mechanisms. Cardiac hypertrophy and function were evaluated with echocardiography, hemodynamic measurements, pathological and molecular analyses. For the first time, we found that TRAF5 deficiency substantially aggravated cardiac hypertrophy, cardiac dysfunction and fibrosis in response to pressure overload after 4 weeks of TAC compared to wild-type (WT) mice. Moreover, the mitogen-activated protein/extracellular signal-regulated kinase kinase (MEK)-extracellular signal-regulated kinases 1/2 (ERK1/2) signaling pathway was more activated in TRAF5-deficient mice than WT mice. In conclusion, our results suggest that as an intrinsic cardioprotective factor, TRAF5 plays a crucial role in the development of cardiac hypertrophy through the negative regulation of the MEK-ERK1/2 pathway. J. Cell. Biochem. 115: 349-358, 2014. © 2013 Wiley Periodicals, Inc.
- Journal of cellular biochemistry.J Cell Biochem.2014 Feb;115(2):349-58. doi: 10.1002/jcb.24669.
- The cytoplasmic signaling protein tumor necrosis factor (TNF) receptor-associated factor 5 (TRAF5), which was identified as a signal transducer for members of the TNF receptor super-family, has been implicated in several biological functions in T/B lymphocytes and the innate immune response against
- PMID 24038435
- Comparison of the glycosylation of in vitro generated polyclonal human IgG and therapeutic immunoglobulins.
- Ritamo I, Cloutier M, Valmu L, Néron S, Räbinä J.Author information Advanced Therapies and Product Development, Finnish Red Cross Blood Service, Kivihaantie 7, FI-00310 Helsinki, Finland. Electronic address: ilja.ritamo@thermofisher.com.AbstractWe have recently developed an in vitro culture model enabling the large-scale expansion of switched-memory B lymphocytes, producing a polyclonal human IgG repertoire. Given the importance of glycosylation for the functions of immunoglobulins, we analyzed the N-glycosylation profiles of the immunoglobulin G (IgG) in this model. Switched-memory B cells were cultured for 38 days and, using liquid chromatography-mass spectrometry, we analyzed IgGs' glycosylation profiles which were then compared to the glycosylation patterns of commercial intravenous immunoglobulin (IVIG). We observed a reproducible proliferation rate, high viability through the cultures as well as a good maintenance of the switched-memory B cells repertoire. The glycosylation pattern analyses revealed a variety of the typical biantennary N-glycan structures with diverse terminal monosaccharides. While many similarities were detected in comparison to the glycosylation profile of IVIG, in vitro-produced polyclonal IgGs were bearing higher levels of bisecting GlcNAc known to affect the effector functions of therapeutic antibodies. This data highlights the need for monitoring of the glycoform distribution in antibodies produced in vitro.
- Molecular immunology.Mol Immunol.2014 Feb;57(2):255-62. doi: 10.1016/j.molimm.2013.10.005. Epub 2013 Nov 1.
- We have recently developed an in vitro culture model enabling the large-scale expansion of switched-memory B lymphocytes, producing a polyclonal human IgG repertoire. Given the importance of glycosylation for the functions of immunoglobulins, we analyzed the N-glycosylation profiles of the immunoglo
- PMID 24184880
- Contribution of humoral immune responses to the antitumor effects mediated by anthracyclines.
- Hannani D, Locher C, Yamazaki T, Colin-Minard V, Vetizou M, Aymeric L, Viaud S, Sanchez D, Smyth MJ, Bruhns P, Kroemer G, Zitvogel L.Author information 1] INSERM U1015, Equipe labellisée Ligue contre le Cancer, Villejuif, France [2] Institut de Cancérologie Gustave Roussy, Villejuif, France [3] University of Paris Sud XI, Villejuif, France.AbstractImmunogenic cell death induced by cytotoxic compounds contributes to the success of selected chemotherapies by eliciting a protective anticancer immune response, which is mediated by CD4(+) and CD8(+) T cells producing interferon-γ. In many instances, cancer progression is associated with high titers of tumor-specific antibodies, which become detectable in the serum, but whose functional relevance is elusive. Here, we explored the role of humoral immune responses in the anticancer efficacy of anthracyclines. Chemotherapy reduced the number of tumor-infiltrating B cells, and failed to promote humoral responses against immunodominant tumor antigens. Although anthracycline-based anticancer chemotherapies failed in T cell-deficient mice, they successfully reduced the growth of cancers developing in mice lacking B lymphocytes (due to the injection of a B-cell-depleting anti-CD20 antibody), immunoglobulins (Igs) or Ig receptors (Fc receptor) due to genetic manipulations. These results suggest that the humoral arm of antitumor immunity is dispensable for the immune-dependent therapeutic effect of anthracyclines against mouse sarcoma. In addition, we show here that the titers of IgA and IgG antibodies directed against an autoantigen appearing at the cell surface of tumor cells post chemotherapy (calreticulin, CRT) did not significantly increase in patients treated with anthracyclines, and that anti-CRT antibodies had no prognostic or predictive significance. Collectively, our data indicate that humoral anticancer immune responses differ from cellular responses in, thus far, that they do not contribute to the success of anthracycline-mediated anticancer therapies in human breast cancers and mouse sarcomas.
- Cell death and differentiation.Cell Death Differ.2014 Jan;21(1):50-8. doi: 10.1038/cdd.2013.60. Epub 2013 Jun 7.
- Immunogenic cell death induced by cytotoxic compounds contributes to the success of selected chemotherapies by eliciting a protective anticancer immune response, which is mediated by CD4(+) and CD8(+) T cells producing interferon-γ. In many instances, cancer progression is associated with high tite
- PMID 23744294
Japanese Journal
- Reduced T-Cell Thymic Export Reflected by sj-TREC in Patients with Coronary Artery Disease
- Mucosal-Associated Invariant T Cell Is a Potential Marker to Distinguish Fibromyalgia Syndrome from Arthritis
Related Links
- 1. J Immunol. 1987 Mar 15;138(6):1845-51. Characterization of a monoclonal antibody directed against the murine B lymphocyte receptor for IgE. Rao M, Lee WT, Conrad DH. A rat hybridoma producing a high-affinity IgG2a monoclonal ...
- 1. Adv Immunol. 2005;88:1-50. CD22: a multifunctional receptor that regulates B lymphocyte survival and signal transduction. Tedder TF(1), Poe JC, Haas KM. Author information: (1)Department of Immunology, Duke ...
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- Mg2+存在下でC3, B, Dが反応してC3bBbとなり、これがC3転換酵素(C3bBb)あるいはC5転換酵素(C3bBb3b)を形成する。これらはP(properdin)と結合して活性化し、それぞれC3、C5を活性化する
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リンパ球
- 同
- lymphocytes＆development