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JCI - Clinical and immunological responses after CD30-specific chimeric antigen receptor-redirected lymphocytes
Clinical and immunological responses after CD30-specific chimeric antigen receptor-redirected lymphocytes. ... Clinical and immunological responses after CD30-specific chimeric antigen receptor-redirected lymphocytes. ... Targeting CD30 with T cells expressing a CD30-specific chimeric antigen receptor (CAR) may reduce the side effects and augment ...https://j8k9.com.www.mobile.jci.org/articles/view/94306/pdf
Reactive lymphocyte - Wikipedia
Reactive lymphocytes or variant lymphocytes are cytotoxic (CD8+) lymphocytes that become large as a result of antigen ... Reactive lymphocytes are usually associated with viral illnesses, but they can also be present as a result of drug reactions ( ...https://en.wikipedia.org/wiki/Reactive_lymphocyte
Patent US5419904 - Human B-lymphoblastoid cell line secreting anti-ganglioside antibody - Google Patents
A human B-lymphoblastoid cell line which is identified as L612. The L612 cell line is an Epstein-Barr virus transformed cell line which secretes a human monoclonal antibody (L612) which is reactive with glycoconjugates having an epitope of terminal NeuAc α2-3 Galactose residue such as GM3 and GM4 present on a variety of human tumor tissues. The L612 antibody is useful in treating patients with the epitope containing tumors and is also useful in raising anti-id antibodies for use as surrogate antigens and diagnostic reagents.http://www.google.com/patents/US5419904?dq=7,013,345/
Analysis of the Heavy Chain Repertoire of Human Peripheral B Cells Using Single-Cell Polymerase Chain Reaction
Brezinschek, H.P., Brezinschek, R.I. & Lipsky, P.E., 1995, "Analysis of the Heavy Chain Repertoire of Human Peripheral B Cells Using Single-Cell Polymerase Chain Reaction", Journal of Immunology, 155:191-202 ...http://www.returntickettonature.co.uk/faaaaaah.htm
Epstein-Barr virus transformation induces B lymphocytes to produce human interleukin 10. | JEM
Interleukin 10 (IL-10) is a pleiotropic factor that enhances proliferation of activated human B lymphocytes and induces them to secrete high amounts of immunoglobulins. Here we show that several human B cell lines were able to constitutively secrete human (h)IL-10. Whereas none of the pre-B nor the plasmocytic cell lines tested produced hIL-10, 25 of the 36 tested mature B cell lines (lymphoblastoid and Burkitt lymphoma cell lines) secreted hIL-10. Moreover, 24 of these 25 hIL-10-producing B cell lines contained the Epstein-Barr virus (EBV) genome, suggesting a relationship between hIL-10 production by human B cell lines and EBV expression. Accordingly, whereas polyclonal activation via triggering of surface immunoglobulins or CD40 antigen induced highly purified normal human B lymphocytes to produce only low (0.3-0.4 ng/ml) but significant amounts of hIL-10, EBV infection induced them to secrete high amounts of hIL-10 (4-9 ng/ml). Furthermore, addition of ...http://jem.rupress.org/content/177/2/295
CD137 Promotes Proliferation and Survival of Human B Cells | The Journal of Immunology
In this study, we demonstrated that, despite the reported absence of CD137 on murine B cells, CD137 is expressed on human B cells. Our studies revealed that CD137 is expressed on activated B cells following BCR stimulation. Cognate help from T cells through CD40-CD40L interaction and/or cytokines are important for the regulation of CD137 expression on human B cells. Among the cytokines tested, only the Th1 cytokine IFN-γ enhanced CD137 expression, whereas IL-4, -10, and -21 inhibited CD137 expression. Importantly, neither anti-CD40 stimulation nor cytokine alone were capable of inducing B cell expression of CD137 in the absence of BCR stimulation. In addition, polyclonal stimulation of human B cells with CpG, which stimulates TLR9-mediated B cell proliferation and differentiation in the absence of Ag, failed to upregulate CD137 (data not shown). These data suggest that CD137 expression on human B cells is tightly controlled and strictly dependent upon Ag encounter and the BCR serves as the ...http://www.jimmunol.org/content/184/2/787.long
B cell tumors that grow well in vivo and in vitro
We have been trying to get some MAIDS B cell tumors to grow in B6 mice. The tumors originally came from B6 mice but have been grown in tissue culture for several years. In the event we can not readapt them to grow in vivo we are in need of other tumors. If anyone has a B cell tumor, preferably before the plasma cell stage, and after the immature B cell stage that they have grown in B6 mice we would appreciate hearing about it. If it also grows in tissue culture, while being readly passed back into mice that would be a bonus. Please repond to this service or my email address:wiliam.wade at dartmouth.edu Thanks for your attention and help in this matter. Sincerely, William F. Wade, Ph.D. Assistant Professor of Microbiology Dartmouth Medical School ...http://www.bio.net/bionet/mm/immuno/1995-July/004766.html
"Antigen-initiated b lymphocyte differentiation. V. Electrophoretic se" by R A. Schlegel, H Von boehmer et al.
Schlegel, R A.; Von boehmer, H; and Shortman, K, "Antigen-initiated b lymphocyte differentiation. V. Electrophoretic separation of different subpopulations of afc progenitors for unprimed igm and memory igg responses to the nip determinant." (1975). Subject Strain Bibliography 1975. 1320 ...https://mouseion.jax.org/ssbb1975/1320/
A human B-lymphoblastoid cell clone, L55-81, that produces human monoclonal antibody (MAb) to ganglioside GM2 was established from peripheral blood B lymphocytes of a melanoma patient. L55-81 secretes IgMκ light chain antibody in a serum-free medium. GM2 specificity of the antibody was tested by immune adherence assay, TLC immunostaining, and ELISA. Anti-GM2 antibody was shown to have the ability to kill the GM2-rich human melanoma cell line M14 in the presence of human or rabbit complement. A purified L55-81 MAb (,99.5% purity in protein concentration) was biotinylated and tested for its reactivity to various histological-type biopsied tumor and normal tissues in an avidin-biotin detection system. L55-81 MAb (20 µg/ml) reacted with several types of tumor tissues such as melanoma (7 of 10), colon carcinoma (4 of 5), ovary carcinoma (4 of 5), breast carcinoma (1 of 5), kidney carcinoma (1 of 5), and prostate carcinoma (1 of 5). None of the normal tissues derived from 24 different organs and ...http://cancerres.aacrjournals.org/content/56/24/5666
CD21 Positive B Cell: A Novel Target For Treatment Of Multiple Sclerosis | 19699
Etiologic-based therapy is an ideal pharmacological option to treat or prevent diseases. There is no known etiology for multiple sclerosis (MS); however, envir...https://www.omicsonline.org/proceedings/cd21-positive-b-cell-a-novel-target-for-treatment-of-multiple-sclerosis-19699.html
"The expression of lyb-2.1 On murine b lymphocytes. Abstr." by L D. Brown, F W. Shen et al.
Brown, L D.; Shen, F W.; Uhr, J W.; and Vitetta, E S., "The expression of lyb-2.1 On murine b lymphocytes. Abstr." (1978). Subject Strain Bibliography 1978. 1222 ...https://mouseion.jax.org/ssbb1978/1222/
Cultured human endothelial cells expressing HIV-1 Vpu and Tat support the expansion of malignant B cells from primary central...
Intraocular lymphoma is an aggressive non-Hodgkin B cell lymphoma involving the posterior eye. Basic research on this tumour has been hindered by an inability to expand the malignant B cell population. We developed a cell culture system, in which endothelial cell monolayers were infected with adenoviral vectors encoding HIV-1 proteins, Vpu and Tat. These monolayers permitted adhesion and proliferation of CD20-positive B cells from specimens of cerebrospinal fluid obtained from patients with intracranial tumor. The system provides a method for expansion of the malignant B cell population present in small volumes of fluid that are available for research use. ...http://bjo.bmj.com/content/92/2/297
B-1b Cells Secrete Atheroprotective IgM and Attenuate AtherosclerosisNovelty and Significance | Circulation Research
Results of the present study are the first to demonstrate that B-1b cells produce IgM to OSE and attenuate diet-induced atherosclerosis. B-1b cells are developmentally and functionally unique when compared with B-1a and B-2 cells.36,37 B-1a cells produce IgM natural antibodies in an antigen-independent manner, whereas B-1b cells respond to T-cell-independent antigens providing them the capacity to form memory.12,38 The work of Haas et al33 and Alugupalli et al39 established B-1b cells as the source of T-cell-independent memory and support B-1b cells as targets of T-cell-independent antigen-directed vaccination, which has been discussed as a novel therapeutic against atherosclerosis.18,19,30,40 As such, understanding the impact of B-1b cells on atherosclerosis and elucidating factors that regulate their activity is of clear importance.. Studies presented here provide novel evidence that B-1b cells produce atheroprotective IgM antibodies. The finding that ...http://circres.ahajournals.org/content/117/3/e28
北京大学医学部机构知识库(IR@PKUHSC): Toll-like receptor 4-mediated signaling regulates IL-7-driven proliferation and differentiation of B...
Lipopolysaccharide (LPS) is known to be a potent activator of mature B cells by signaling through Toll-like receptor 4 (TLR4). Its impact on early B-cell development, however, is not well defined. When comparing to C3H/HeN mice, TLR4-mutant C3H/HeJ mice showed an increase in the number of pro-B and pre-B cells in the bone marrow. When cultured in the presence of IL-7, the proliferation of pro-B and large pre-B cells was significantly inhibited by LPS, possibly due to reduced IL-7 receptor-alpha (IL-7R alpha) expression. Meanwhile, the generation of IgM(+)/IgD(+) B cells was greatly enhanced in IL-7 cultures of pro-B and pre-B cells. Consistent with these results, treatment with LPS facilitated the progression of adoptively transferred B220(+)IgM(-)IgD(-) precursors into IgD(+) cells. Overall, these data suggest that LPS has a profound influence on early B-cell development, which may contribute to the deregulated B-cell development under physiological and pathological conditions such as bacterial ...http://ir.bjmu.edu.cn/handle/400002259/52747
CD40, but not lipopolysaccharide and anti-IgM stimulation of primary B lymphocytes, leads to a persistent nuclear accumulation...
In this study we analyzed the effect of CD40 stimulation on the activity and nuclear appearance of Rel/nuclear factor kappaB (NF-kappaB) factors in primary murine B lymphocytes. We show that triggering of CD40 signaling pathway(s) by CD40 ligands expressed on L cells led to strong activation of an NF-kappaB-controlled beta-globin reporter gene in primary B lymphocytes from transgenic mice. Analyses of nuclear translocation of individual members of Rel proteins after CD40 induction of primary B cells showed a strong and long-lasting accumulation of RelB and, less pronounced, of c-Rel. LPS stimulation did not give rise to a persistent nuclear accumulation of RelB and c-Rel, whereas nuclear c-Rel, but not RelB, accumulated after B cell receptor stimulation. CD40 induced not only nuclear translocation but also de novo synthesis of RelB RNA and protein. S107 plasmacytoma cells, which express CD40 but are defective for the nuclear appearance of p50/p65-NF-kappaB, do not express ...https://www.semanticscholar.org/paper/CD40-but-not-lipopolysaccharide-and-anti-IgM-stimu-Neumann-Wohlleben/534630a6ab5b9ba8c9cc37c4296ec66400a643e6
"Lyb antigens and their role in b lymphocyte activation." by B Subbarao and D E. Mosier
Subbarao, B and Mosier, D E., "Lyb antigens and their role in b lymphocyte activation." (1982). Subject Strain Bibliography 1982. 1201 ...https://mouseion.jax.org/ssbb1982/1201/
CD19 and BAFF‐R can signal to promote B‐cell survival in the absence of Syk | The EMBO Journal
We show here that approximately 25% of the mature peripheral B cells can survive in the mouse for at least 2 months without Syk, in a manner that requires BAFF‐R and CD19 signaling. In contrast, deletion of the Syk gene in early B cells results in the appearance of a small number of immature IgM+ B cells, which, however, fail to give rise to any mature B cells in the periphery (Cheng et al, 1995). Thus, pre‐B and mature B cells have different requirements for Syk. Indeed, the pre‐BCR is an autonomously signaling receptor that continuously engages Syk, whereas the BCR forms an autoinhibited oligomer on mature B cells that is not in contact with Syk. This notion is supported by a proximity ligation analysis showing that Syk is localized near the BCR only after BCR activation (Infantino et al, 2010; Klasener et al, 2014).. The presence of large amounts of Syk‐negative mature B cells in the induced mb1‐CreERT2;Sykfl/fl mice allowed us to analyze the in vivo role of this kinase in the ...http://emboj.embopress.org/content/34/7/925
CD19 and BAFF‐R can signal to promote B‐cell survival in the absence of Syk | The EMBO Journal
We show here that approximately 25% of the mature peripheral B cells can survive in the mouse for at least 2 months without Syk, in a manner that requires BAFF‐R and CD19 signaling. In contrast, deletion of the Syk gene in early B cells results in the appearance of a small number of immature IgM+ B cells, which, however, fail to give rise to any mature B cells in the periphery (Cheng et al, 1995). Thus, pre‐B and mature B cells have different requirements for Syk. Indeed, the pre‐BCR is an autonomously signaling receptor that continuously engages Syk, whereas the BCR forms an autoinhibited oligomer on mature B cells that is not in contact with Syk. This notion is supported by a proximity ligation analysis showing that Syk is localized near the BCR only after BCR activation (Infantino et al, 2010; Klasener et al, 2014).. The presence of large amounts of Syk‐negative mature B cells in the induced mb1‐CreERT2;Sykfl/fl mice allowed us to analyze the in vivo role of this kinase in the ...http://emboj.embopress.org/content/early/2015/01/25/embj.201489732
Differentiation-associated redox-regulation in human B cell lines from stem cell/pro-B to plasma cell
Redox-regulation of receptors and transcription factors are important for lymphocyte activation, differentiation and apoptosis. Thioredoxin (Trx) is a key redox-regulating protein and oxidative stress sensor operating in synergy with Trx-reductase and protein disulfide isomerase (PDI). The expression of Trx, PDI, and the Trx-regulated transcription-factor Pax5 were analyzed in a panel of human B cell lines and were compared with that of the Bcl-2 family proteins, also redox-controlled. The panel included representative cells from various stages: FLEB14-4 (pro-B), REH and NALM-6 (pre-B), Rael and Daudi (small mature B), U-698 and NC0467.3 (B-blasts), LP-1, U-1996, and U-266 (plasma cells). We found a significant congruence and co-variation of Trx and Bcl-2 levels in the B-lineage, with high expression levels in early stages (pro-B and pre-B) and in the late stage representing terminally-differentiated plasma cells, whereas mid-stage small resting B cells showed a very low expression. PDI ...http://liu.diva-portal.org/smash/record.jsf?pid=diva2:244529
"A distinct role for B1b lymphocytes in T cell-independent immunity" by Kishore R. Alugupalli
Pathogenesis of infectious disease is not only determined by the virulence of the microbe but also by the immune status of the host. Vaccination is the most effective means to control infectious diseases. A hallmark of the adaptive immune system is the generation of B cell memory, which provides a long-lasting protective antibody response that is central to the concept of vaccination. Recent studies revealed a distinct function for B1b lymphocytes, a minor subset of mature B cells that closely resembles that of memory B cells in a number of aspects. In contrast to the development of conventional B cell memory, which requires the formation of germinal centers and T cells, the development of B1b cell-mediated long-lasting antibody responses occurs independent of T cell help. T cell-independent (TI) antigens are important virulence factors expressed by a number of bacterial pathogens, including those associated with biological threats. TI antigens cannot be ...http://jdc.jefferson.edu/mifp/3/
the relationship between surface immunoglobulin isotype and immune function of murine B lymphocytes. III. Expression of a...
We determined whether primed and unprimed B cells in the spleen of (BALB/c × C57BL/Ka)F(1) mice contain subpopulations that express a predominant surface Ig isotype. Spleen cells were stained for surface isotypes and sorted on the fluorescence-activated cell sorter (FACS) in order to obtain B cells bearing predominantly IgM (μp cells), IgD (δp cells), or IgG (γp cells). Each population was assayed for its capacity to restore the adoptive primary and secondary anti-bovine serum albumin (BSA) antibody response in irradiated syngeneic recipients. In addition, the adoptive response restored by isotype-predominant cells was compared to that restored by isotype- positive cells (B cells bearing a given surface isotype alone or in combination with others). The experimental results show that μp cells restore the adoptive primary and secondary IgM and IgG responses to BSA, and γP cells restore only the primary and secondary IgG response. Δp Cells restored the adoptive secondary IgG response, but ...http://jem.rupress.org/content/147/5/1374
Control of B cell development and malignant transformation by microRNA-142 | The Journal of Immunology
MicroRNA-142 (miR-142) is a versatile posttranscriptional regulator that plays a crucial role in the regulation of both innate and adaptive immune responses. Abrogation of miR-142 expression in mice results in a profound immunodeficiency that is characterized by hypoimmunoglobulinemia and failure to mount robust humoral immune responses to soluble antigen challenges. Paradoxically, miR-142−/− mice display a significant expansion of the B cell compartment due to the accumulation of immature and mature B lymphocytes. To better understand the role of miR-142 in B cell ontogenesis, we examined the early B cell development in miR-142−/− mice using the Hardy fraction analysis. We found that miR-142 deletion results in a significant increase in the frequency of the pro-B and large pre-B cells (Fractions B and C), while the pre-pro-B cell population (Fraction A) decreased. In contrast, miR-142 ablation had little effect on the frequency of small pre-B cell and immature B cell ...http://www.jimmunol.org/content/198/1_Supplement/202.21
CD24, a signal-transducing molecule expressed on human B lymphocytes, is a marker for human regenerating muscle | SpringerLink
The expression of the CD24 molecule, a glycoprotein expressed at the surface of most B lymphocytes and differentiating neuroblasts, was studied in developing nerve and muscle (after 16 weeks of gestathttps://link.springer.com/article/10.1007%2FBF00304142
Defects in B Lymphocyte Maturation and T Lymphocyte Activation in Mice Lacking Jak3 | Science
Biochemical studies of signaling mediated by many cytokine and growth factor receptors have implicated members of the Jak family of tyrosine kinases in these pathways. Specifically, Jak3 has been shown to be associated with the interleukin-2 (IL-2) receptor γ chain, a component of the receptors for IL-2, IL-4, IL-7, IL-9, and IL-15. Mice lacking Jak3 showed a severe block in B cell development at the pre-B stage in the bone marrow. In contrast, although the thymuses of these mice were small, T cell maturation progressed relatively normally. In response to mitogenic signals, peripheral T cells in Jak3-deficient mice did not proliferate and secreted small amounts of IL-2. These data demonstrate that Jak3 is critical for the progression of B cell development in the bone marrow and for the functional competence of mature T cells. ...http://science.sciencemag.org/content/270/5237/794
"Characterization of antigen processing and presentation by resting B l" by Edmund J. Gosselin, Hans-Peter Tony et al.
The production of antibody to a thymus-dependent Ag requires cooperation between the B cell and an Ag-specific Th cell. MHC restriction of this interaction implies that the Th cell recognizes Ag on the B cell surface in the context of MHC molecules and that the Ag-specific B cell gets help by acting as an APC for the Th cell. However, a number of studies have suggested that normal resting B cells are ineffective as APC, implying that the B cell must leave the resting state before it can interact specifically with a Th cell. Other studies, including our own with rabbit globulin-specific mouse T cell lines and hybridomas, show that certain T cell lines can be efficiently stimulated by normal resting B cells. One possible explanation for the above contradiction is that our B cells have become activated before presentation. Here we show that presentation by size-selected small B cells is not the result of nonspecific activation signals generated by the T cells or components of the medium. Also, although LPShttp://escholarship.umassmed.edu/gsbs_sp/404/
Signaling events resulting from synchronous BCR and CD180 activation on murine B cells differ from activating CD180 or the BCR...
CD180 (RP105), expressed on dendritic cells and B cells, is a receptor closely related to TLR4. CD180 signaling does not require adaptor proteins like MyD88, instead it resembles B cell receptor (BCR) signaling, including the activation of PI3K and Akt. Recently, others and we have found αCD180 also induces the Pim-1 kinase, but much of the CD180 signaling pathway remains ill defined. We previously found that targeting antigen (Ag) to B cells via CD180, by coupling the Ag to an anti-CD180 antibody (Ag-αCD180), induces a rapid and strong Ag-specific IgG antibody (Ab) response in mice. Furthermore, IgG Ab responses were maintained in immunodeficient mice that lack mature B cells (BAFFR−/−). These studies led us to investigate the signaling events that occur within B cells upon coincident activation of the BCR and CD180. For this study we have employed B1-8hi transgenic mice, which have a BCR that binds to NP-hapten on some splenic B cells, and the K46μm17 murine B cell line, that expresses ...http://www.jimmunol.org/content/196/1_Supplement/75.22
PU.1 Regulates Ig Light Chain Transcription and Rearrangement in Pre-B Cells during B Cell Development | The Journal of...
B cell development and Ig rearrangement are governed by cell type- and developmental stage-specific transcription factors. PU.1 and Spi-B are E26-transformation-specific transcription factors that are critical for B cell differentiation. To determine whether PU.1 and Spi-B are required for B cell development in the bone marrow, Spi1 (encoding PU.1) was conditionally deleted in B cells by Cre recombinase under control of the Mb1 gene in Spib (encoding Spi-B)-deficient mice. Combined deletion of Spi1 and Spib resulted in a lack of mature B cells in the spleen and a block in B cell development in the bone marrow at the small pre-B cell stage. To determine target genes of PU.1 that could explain this block, we applied a gain-of-function approach using a PU.1/Spi-B-deficient pro-B cell line in which PU.1 can be induced by doxycycline. PU.1-induced genes were identified by integration of chromatin immunoprecipitation-sequencing and RNA-sequencing data. We found that PU.1 interacted with multiple sites ...http://www.jimmunol.org/content/198/4/1565