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Статті в журналах з теми "GC B cell"
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Lopez-Ocasio, Maria D. "T Follicular Regulatory (TFR) Cells Regulate B Cell Responses in Both, T-cell Dependent and Independent Pathways." Journal of Immunology 200, no. 1_Supplement (May 1, 2018): 48.9. http://dx.doi.org/10.4049/jimmunol.200.supp.48.9.
Повний текст джерелаАнотація:
Abstract Production of high-affinity antibody-secreting plasma cells and memory B cells requires interaction of TFH cells with B cells in the follicle. TFR cells, a subset of Foxp3+ Tregs, localize into follicles, regulating GC responses. To elucidate the mechanisms and cellular targets used by TFR cells to suppress GC responses, we quantitated their function in vitro. In the absence of TFR cells, TFH from primed mice induce naive B cell differentiation into GC B cells and class switching in the presence of anti-CD3 alone or anti-IgM/anti-CD3 in a contact dependent manner. Addition of TFR cells from primed mice efficiently suppressed GC B cell differentiation and class switching in the anti-CD3 alone cultures, but moderately suppressed BCR-stimulated B cells. Under anti-CD3 conditions, IL-4−/− TFH cells did not promote B cell differentiation and class switching. In contrast, IL-21R−/− B cells differentiated into GC B cells with a reduced number of IgG1+ cells. When IL-4−/− TFH cells were co-cultured with IL-21R−/− B cells, both GC differentiation and class switching were reduced. Under anti-IgM/anti-CD3 conditions, IL-4−/− TFH cells promoted B cell differentiation, but class switching was reduced, while IL-21R−/− B cells differentiated normally into GC B cells, with reduced class switching. When B cells alone were stimulated in culture with either LPS or CpG, TFR cells did not block B cell proliferation, but their differentiation into plasma cells was reduced. These studies suggest that in vitro, TFR cells regulate GC responses primarily by acting on TFH cells by inhibiting cytokine production and CD40L expression, but can also directly suppress some aspects of B cell differentiation. Supported by the Intramural Research Program of the NIAID.
2
Jones, Derek, Irene Chernova, and David Allman. "B cell-intrinsic mTOR signaling regulates the generation of germinal center B cells (IRM8P.716)." Journal of Immunology 192, no. 1_Supplement (May 1, 2014): 127.17. http://dx.doi.org/10.4049/jimmunol.192.supp.127.17.
Повний текст джерелаАнотація:
Abstract Germinal centers (GCs) are sites enriched for proliferative B cells undergoing class switch, somatic hypermutation, and selection for clones expressing high-affinity antigen-specific receptors. GCs are a main source of long-lived plasma cells (PCs) and memory B cells, and many B-lineage cancers including multiple myeloma (MM), a malignancy of PCs, also originate in GCs. However, little is known about the biochemical pathways regulating GC B cells or GC-derived effectors. Thus, we sought to define the role of mammalian target of rapamycin (mTOR), a serine/threonine kinase known to regulate several biochemical pathways needed for cell growth, division, and survival, in the maintenance of GC B cells and GC-derived cells. To address the role of mTOR in GC B cell generation, we treated NP-CGG-immunized mice with rapamycin, an mTOR inhibitor. Rapamycin treatment caused a near-complete loss of NP-specific GC B cells in the spleen, and a selective reduction of newly formed bone marrow PCs. We next generated Raptorf/f x CD20-ER-Cre mice to induce B cell-specific deletion of the mTOR-requisite protein Raptor; Raptor deletion caused the ablation of antigen-specific GCs, as well as secondary antibody responses mediated by memory B cells. The data indicate that GC B cells utilize mTOR signaling to regulate metabolic pathways required for cell division and/or survival. Future studies will address the notion that malignant PCs responsible for MM must be replenished by ongoing GC responses.
3
Sewastianik, Tomasz, Juerg R. Straubhaar, Jian-Jun Zhao, Mehmet K. Samur, Keith Adler, Helen E. Tanton, Vignesh Shanmugam, et al. "miR-15a/16-1 deletion in activated B cells promotes plasma cell and mature B-cell neoplasms." Blood 137, no. 14 (April 8, 2021): 1905–19. http://dx.doi.org/10.1182/blood.2020009088.
Повний текст джерелаАнотація:
Abstract Chromosome 13q deletion [del(13q)], harboring the miR-15a/16-1 cluster, is one of the most common genetic alterations in mature B-cell malignancies, which originate from germinal center (GC) and post-GC B cells. Moreover, miR-15a/16 expression is frequently reduced in lymphoma and multiple myeloma (MM) cells without del(13q), suggesting important tumor-suppressor activity. However, the role of miR-15a/16-1 in B-cell activation and initiation of mature B-cell neoplasms remains to be determined. We show that conditional deletion of the miR-15a/16-1 cluster in murine GC B cells induces moderate but widespread molecular and functional changes including an increased number of GC B cells, percentage of dark zone B cells, and maturation into plasma cells. With time, this leads to development of mature B-cell neoplasms resembling human extramedullary plasmacytoma (EP) as well as follicular and diffuse large B-cell lymphomas. The indolent nature and lack of bone marrow involvement of EP in our murine model resembles human primary EP rather than MM that has progressed to extramedullary disease. We corroborate human primary EP having low levels of miR-15a/16 expression, with del(13q) being the most common genetic loss. Additionally, we show that, although the mutational profile of human EP is similar to MM, there are some exceptions such as the low frequency of hyperdiploidy in EP, which could account for different disease presentation. Taken together, our studies highlight the significant role of the miR-15a/16-1 cluster in the regulation of the GC reaction and its fundamental context-dependent tumor-suppression function in plasma cell and B-cell malignancies.
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Lopez-Ocasio, Maria D., and Ethan M. Shevach. "T Follicular Regulatory (TFR) Cells Regulate B Cell Responses By Targeting TF Helper (TFH) Cells." Journal of Immunology 198, no. 1_Supplement (May 1, 2017): 223.11. http://dx.doi.org/10.4049/jimmunol.198.supp.223.11.
Повний текст джерелаАнотація:
Abstract Interaction of TFH cells with B cells not only helps TFH to fully commit to this lineage, but also provides B cells with survival and differentiation cues. A GC response is critical for the development of an immune response against pathogens, but a dysregulated response could lead to autoantibody production. TFR cells, a subset of Foxp3+ Tregs, localize into follicles to regulate GC responses. To elucidate the mechanism (s) and cellular target (s) utilized by TFR cells to suppress GC responses, we quantitated TFR function in vitro. In the absence of TFR cells, TFH from primed mice induce both naive B cell differentiation into GC B cells and class switching in the presence of anti-CD3 alone or anti-IgM/anti-CD3 in a contact dependent manner. Addition of TFR cells from primed mice efficiently suppressed GC B cell proliferation, differentiation and class switching in the anti-CD3 alone cultures, but only moderately suppressed BCR-stimulated B cells. Under anti-CD3 conditions, IL-4-deficient TFH cells did not promote B cell differentiation and class switching. In contrast, IL-21R-deficient B cells differentiated into GC B cells with a reduced number of IgG1+ cells. When IL-4 deficient TFH cells were co-cultured with IL-21R-deficient B cells, both GC differentiation and class switching were reduced. Under anti-IgM/anti-CD3 conditions, IL-4-deficient TFH cells promoted B cell differentiation, but class switching was reduced, while IL-21R-deficient B cells differentiated normally into GC B cells, but class switching was reduced. These studies suggest that at least in vitro, TFR cells regulate the GC responses by acting directly on TFH cells most likely by inhibiting cytokine production.
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Ding, Chuanlin, and Jun Yan. "Pivotal role of STAT3 signaling in germinal center B cell and T follicular helper cell differentiation (IRC3P.458)." Journal of Immunology 192, no. 1_Supplement (May 1, 2014): 59.1. http://dx.doi.org/10.4049/jimmunol.192.supp.59.1.
Повний текст джерелаАнотація:
Abstract Germinal center (GC) B cells and T follicular helper (Tfh) cells are critical for long-lived plasma cell differentiation and high-affinity antibody production in response to T cell-dependent antigens. Previous studies demonstrated that GC formation was intact in the absence of STAT3 in B cells at day 12. However, emerging evidence suggests that IL-21/STAT3 signaling is a potent regulator for B cell differentiation. To better understand the role of STAT3 in the kinetics of GC formation and GC B cell response, we assessed GC B cells at consecutive time points following immunization with antigen OVA. In B cell conditional STAT3-dificient mice, fewer GC and GC B cells were generated upon immunization in the late phase (day 21) but not on day 14 compared with that of control mice. Increased cell death and decreased cell proliferation were found in the STAT3 deficient GC B cells. Consequently, plasma cell differentiation and antibody production were impaired in B cell STAT3-deficient mice. In addition, the Tfh cell response was correlated with the magnitude of the GC B cell response and significantly decreased in B cell STAT3-deficient mice. Furthermore, GC B cells and autoantibody production were also significantly decreased in autoreactive B cell STAT3-deficient mice after apoptotic cell immunization. These data provide new insights into the GC and Tfh differentiation and the function of STAT3 in humoral immune responses.
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Benet, Zachary, Rita Wu, Matangi Marthi, Jackson Turner, and Irina Grigorova. "B cell-intrinsic production of CCL3/4 promotes direct sampling of Germinal Center B cells by T follicular regulatory cells and limits non-foreign antigen specific B cell response." Journal of Immunology 196, no. 1_Supplement (May 1, 2016): 195.13. http://dx.doi.org/10.4049/jimmunol.196.supp.195.13.
Повний текст джерелаАнотація:
Abstract A hallmark of adaptive humoral immunity is the germinal center (GC) reaction. GCs are the primary site of antigen-dependent clonal expansion, immunoglobulin diversification, and affinity maturation and give rise to memory cells and long-lived plasma cells that secrete high-affinity antibodies. These coordinated processes in GCs are highly dependent on cognate follicular T cells. Previous studies and our findings suggest increased expression of proinflammatory chemokines CCL3/4 in GC centrocytes. However, the role of CCL3/4 for centrocyte interactions with follicular T cells and regulation of humoral immunity is poorly understood. We found that B cell intrinsic production of CCL3/4 is required for control of B cell expansion within GCs and restrict the development of class-switched anti-nuclear antibodies following immunization with foreign antigen. We determined that follicular regulatory T cells (Tfr) respond to CCL3/4 chemokines ex vivo and interact more frequently with WT compared to CCL3-deficient GC B cells in vivo using two photon microscopy. Finally, we have identified a subpopulation of GC centrocytes that have significantly increased expression levels of CCL3/4. These data suggests that CCL3/4 secreted by a subset of GC B cells promotes their direct interactions with Tfr cells and plays a role in the elimination of potentially self-reactive B cell clones within GCs.
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Rea, I. Maeve. "Activated P13Kδ disrupts germinal center GC T(fh)/GC B cell cross talk and B cell antibody coding". Cellular & Molecular Immunology 16, № 11 (8 жовтня 2019): 848–50. http://dx.doi.org/10.1038/s41423-019-0295-0.
Повний текст джерела
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Grigorova, Irina, and Jackson S. Turner. "Dissecting the contribution of antigen-dependent B cell receptor engagement and T cell help to Germinal Center B cell selection and differentiation." Journal of Immunology 200, no. 1_Supplement (May 1, 2018): 107.9. http://dx.doi.org/10.4049/jimmunol.200.supp.107.9.
Повний текст джерелаАнотація:
Abstract Proper selection of somatically hyper mutated B cells in the Germinal Centers (GCs) and their differentiation into long-lived plasma cells is key for the development of high-affinity long-term humoral immunity. However, relative contribution towards GC B cell selection by the two key factors: antigen-driven B cell receptor (BCR) signaling and T cell help, remains an open question. We have addressed this long-standing question in the field using an experimental model that enables independent manipulation of both antigen-driven BCR engagement and antigenic peptide presentation in GC B cells. Our studies suggest that in the absence of antigen-driven BCR engagement, T cell help is sufficient for robust selection of GC B cells and their differentiation into plasmablasts. In contrast, neither is induced by antigen-dependent BCR crosslinking in the absence of T cell help. Interestingly, when the levels of MHCII/peptide presentation by GC B cells are suboptimal, antigen-dependent BCR engagement can synergize with T cell help to promote selection of GC B cells and their differentiation into plasmablasts. Our findings reconcile somewhat contradictory data reported in previous studies and point towards the importance of the two signal model in the GC response.
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Saniee, Avva, Kihyuck Kwak, Nicolas Quizon, Haewon Sohn, Javier Manzella-Lapeira, Prasida Holla, Jinghua Lu, et al. "Human germinal center B cells are intrinsically able to discriminate antigen affinity and with T cell help express plasma cell transcription factors." Journal of Immunology 200, no. 1_Supplement (May 1, 2018): 107.17. http://dx.doi.org/10.4049/jimmunol.200.supp.107.17.
Повний текст джерелаАнотація:
Abstract The selection of GC B cells that express high affinity B cell receptors (BCRs) is driven by the ability of B cells to both signal through the BCR and to extract antigen and present it to follicular helper T cells (T FH cells). Using anti-kappa antibodies of low (KD=3.9×10 −7 ) versus high (KD=2.4×10 −9 ) affinities attached to membranes as surrogate antigens, we show that LZ GC B cells are able to discriminate between these and responded only to the high affinity antigen. In contrast, naïve B cells responded to both high and low affinity antigens. LZ GC B cells engaged membrane associated surrogate antigens through highly dynamic F-actin and ezrin-rich pod-like structures that concentrated BCRs at their contact points. Using DNA-based mechanical force nano-sensors we observed robust pulling forces localized to the contact sites of the pods with the membrane. In contrast, naïve B cells formed flat stable contacts with the membranes and showed only defuse weak pulling forces. GC B cells optimally express transcription factors that drive plasma cell differentiation, namely IRF-4 and PRDM-1, in response to antigen in combination with T FH help while naïve B cells increased IRF-4 and PRDM-1 transcription in response to T FH alone and less so to antigen alone. Thus, LZ GC B cells appear to be intrinsically capable of antigen affinity discrimination and with the acquisition of T FH help BCR-activated LZ GC B cells differentiate into plasma cells.
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De La Pena Enterina, Jhon Ralph, Susmita Sarkar, and Matthew Macauley. "Glycan Remodelling Controls Germinal Centre B cell Responses." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 71.3. http://dx.doi.org/10.4049/jimmunol.204.supp.71.3.
Повний текст джерелаАнотація:
Abstract Germinal centre (GC) B cells are routinely identified through distinct changes on their surface carbohydrates, called glycans; yet, whether these modifications play an essential role in GC reaction remain unknown. One striking change relates to the monosaccharide sialic acid. In mice, this change is mediated through downregulation of an enzyme called Cmah. As a consequence, GC B cells lose the preferred ligand for CD22, a member of the sialic acid-binding immunoglobulin-type lectins (Siglecs) and a co-inhibitory receptor of the B cell antigen receptor. Since CD22 regulates B cell function, we hypothesize that this specific glycan remodelling on B cells control the GC reaction by modulating the activity of CD22. To test our hypothesis, we developed a mouse model that constitutively expresses Cmah in B cells. Following immunization, we find that sustained expression of Cmah in B cells results in impaired generation of antigen-specific GC B cells. More significantly, this observed defect is dependent on CD22, highlighting that coordinated loss of preferred ligands for CD22 on B cells plays a critical function in the GC. Furthermore, antibody affinity maturation is significantly impaired in immunized mice harbouring B cells which lack either CD22 or its cis glycan ligands, further supporting the role of CD22 and its glycan ligands in the GC. Ongoing efforts are focused on defining the GC-specific nature of these observations and examining potential mechanism related to BCR signalling, GC B cell survival and exit to plasma cells, and B-T cell interactions.
Дисертації з теми "GC B cell"
1
Boyden, Alexander Wiser. "Influenza A virus induces regulated T cell-driven B cell responses." Diss., University of Iowa, 2012. https://ir.uiowa.edu/etd/3432.
Повний текст джерелаАнотація:
Protection from influenza A virus (IAV) challenge requires switched, high affinity Abs derived from long-lived memory B cells and plasma cells. These subsets are generated in germinal centers (GCs), hallmark structures of T helper cell-driven B cell immunity. A full understanding of the acute and persistent GC B cell reaction following respiratory IAV infection is lacking, as is the characterization of IAV-induced T follicular helper (TFH) cells that support GCs. Additionally, it remains unclear as to whether IAV-induced GC B cells are subject to control by regulatory T cells (Tregs). To address this, GC B cell and TFH cell responses were analyzed in mice following pulmonary challenge with IAV. Studies demonstrated that marked GC reactions were induced in lung-draining lymph nodes (dLNs), lung, spleen and nasal-associated lymphoid tissue (NALT), although the magnitude, kinetics, and isotype switching patterns of the response was site-specific, and largely depended on the magnitude of IAV-induced TFH cell populations. TFH cell magnitude peaked prior to that of GC B cells in all tissues, and TFH cells purified from dLNs generated IL-21 and IFN-gamma upon activation, although CD4+CXCR5- T effector cells produced higher levels of all cytokines. IgA+ GC B cells were infrequent in most sites, but composed a significant subset of the switched GC population in NALT. Further, splenectomized mice withstood a lethal recall challenge, suggesting the spleen to be unnecessary for long-term protection. Additionally, GC B cell populations were analyzed at distal time points to assess the understudied, persistent GC B cell response after IAV infection. Our analysis demonstrated that persistent GC B cell populations in mouse lungs directly correlated with infectious dose, pathogenicity of the virus, as well as the presence of long-term CD4+ T cell help. Finally, experiments showed that Tregs contribute to the control of GCs induced in the spleen by IAV challenge. This was demonstrated by a marked increase in the number of total and switched GC B cell numbers when Tregs were either depleted or disrupted in vivo proximal to IAV exposure.
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Mühle, Kerstin. "Interaction of CD8+CD40L+ T cells with B cells." Doctoral thesis, Humboldt-Universität zu Berlin, 2018. http://dx.doi.org/10.18452/19127.
Повний текст джерелаАнотація:
ZTLs vermitteln die Eliminierung von infizierten und entarteten Zellen durch Apoptose. Neuste Erkenntnisse unserer Gruppe haben gezeigt, dass eine Subpopulation der CD8+ T-Zellen, anstelle der zytotoxischen Marker das Oberflächenmolekül CD40L exprimiert. Die Expression von CD40L ist bislang als Schlüsselmolekül für die CD4+ T-Zell vermittelte Hilfe bekannt, welche durch Bindung an den CD40 Rezeptor auf anderen Immunzellen induziert wird. Das von den CD4+ T–Zellen ausgehende CD40L Signal ist besonders für die T-Zell abhängige B-Zell Aktivierung und die Bildung von Keimzentren essentiell, in denen B-Zellen heranreifen und hochaffine Antikörper produzieren um den Organismus vor eindringenden Erregern zu schützen. Aufgrund der CD40L-assoziierten Helferfunktion sollte in dieser Arbeit untersucht werden, welche Auswirkungen die Interaktion von CD8+CD40L+ T-Zellen mit B Zellen hat. In in vitro Studien konnte gezeigt werden, dass 50% der antigen-spezifischen CD8+ T-Zellen nach Aktivierung durch B-Zellen CD40L hochregulieren. Sowohl auf RNA- als auch auf Proteinebene induzierten CD8+CD40L+ T-Zellen einen B-Zell Phänotyp, der stark dem von CD4+ T-Zellen stimulierten B-Zellen ähnelte. In Infektionsversuchen mit dem B-Zell-trophen Virus MHV-68 konnte gezeigt werden, dass transgene Mäuse mit CD40L defizienten CD8+ T-Zellen im Vergleich zu Kontrolltieren eine signifikante Reduktion der Keimzentrums-B-Zellen in den Lymphknoten der oberen Halsregion aufweisen. Eine genauere Betrachtung des B-Zell Repertoires von IgG Gedächtniszellen ergab jedoch, dass die Sequenzen der IGHJ3 Genfamilie bevorzugt für die Modifikation der CDR3 Region in Mäusen mit CD40L defizienten CD8+ T-Zellen verwendet wird, die eine entscheidende Rolle bei der Antigenerkennung spielt. Zusammengefasst kann mit dieser Arbeit zum ersten Mal gezeigt werden, dass CD8+CD40L+ T-Zellen Helferfunktionen durch Unterstützung der B-Zell Aktivierung und Bildung von Keimzentren übernehmen können.CTLs are important for the elimination of infected and degenerated cells by inducing apoptosis of the target cells. Recently our group identified a sub-population of CD8+ T cells expressing CD40L instead of common CTL markers. To that date, transient CD40L expression on T cells has been only described as a function of activated CD4+ T cells, which displays this key molecule for CD4+ T cell mediated help by binding to the CD40 receptor on other immune cells. Particularly, CD40L signaling provided by CD4+ T cells is indispensable for T cell dependent B cell activation and GC responses, which generate B cells secreting high affinity antibodies that protect the host from invading pathogens. Due to its associated helper functions, this thesis aimed to dissect whether CD40L positive CD8+ T cells are restricted to cytotoxic killing or if this sub-population possesses similar properties as CD4+ T cells when interacting with B cells. In vitro co-culture experiments showed that 50% of murine antigen specific CD8+ T cells up-regulated CD40L upon activation by antigen presenting B cells. When compared to CD40L deficient CD8+ T cells, the interaction of CD8+ CD40L+ T cells induced remarkable changes in B cells on the RNA and protein level and triggered a B cell phenotype resembling that of B cells primed by CD4+ T cells. By the infection of mice with the B cell trophic virus MHV-68, it was found that E8IcrexCD40Lflox transgenic mice lacking CD40L only on matured CD8+ T cells, exhibited a significant decrease of GC B cells in superficial cervical lymph nodes at the acute state of infection compared to WT mice. A closer look into the memory B cell repertoire revealed a preferred usage of the murine IGHJ3 gene family that modifies the CDR3 and thus the recognition groove of the B cell antibody in E8IcrexCD40Lflox mice. In summary, this work provides sufficient evidence that CD8+ CD40L+ T cells adopt helper-like functions by supporting B cell activation and subsequent GC formation.
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Weisenburger, Thomas [Verfasser], Thomas H. [Akademischer Betreuer] Winkler, Thomas H. [Gutachter] Winkler, and David [Gutachter] Vöhringer. "The role of Fas (CD95) for positive selection of GC B cells / Thomas Weisenburger ; Gutachter: Thomas H. Winkler, David Vöhringer ; Betreuer: Thomas H. Winkler." Erlangen : Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), 2020. http://d-nb.info/1216704309/34.
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Pratama, Alvin. "Post-transcriptional control of T follicular helper cells." Phd thesis, 2015. http://hdl.handle.net/1885/13828.
Повний текст джерелаАнотація:
Antibody production is a key feature of the adaptive immune response. High affinity
antibodies neutralise and clear invading pathogens, thereby protecting the host
against microbial infections. It is now well-established that T follicular helper (Tfh)
cells – a distinct subset of CD4+ T helper cells – are essential in providing cognate
help to B cells in the germinal centre (GC) to differentiate into memory and long-lived
plasma cells that secrete high affinity antibodies. However, stringent control of Tfh
cell numbers is crucial to produce optimally affinity-matured antibody responses that
are devoid of self-reactivity. Indeed, excessive number of Tfh cells has been
associated with autoimmunity. However, our understanding of the molecular
mechanisms controlling Tfh cell differentiation is still incomplete. This thesis focuses
on characterising novel post-transcriptional mechanisms that limit Tfh cell numbers.
The data presented in this thesis show that RNA-binding proteins, Roquin and its
paralogue Roquin-2, cooperate to repress Icos, a key Tfh cell molecule, and limit GC
reactions. Mutations in the RING or ROQ domain of Roquin disrupted Icos mRNA
regulation, but, unlike the ROQ mutant that still occupied mRNA-regulating stress
granules, RING-deficient Roquin failed to localise to stress granules and allowed
Roquin-2 to compensate in the repression of ICOS. In addition, the data presented
here show that microRNA-146a is highly expressed in human and mouse Tfh cells
and its peak expression marks the decline of the Tfh cell response. Loss of miR-146a
caused cell-autonomous, spontaneous accumulation of Tfh and GC B cells.
Mechanistically, miR-146a acted in both Tfh and GC B cells to control ICOS-ICOSL
interactions and limit Tfh and GC B cell numbers. Collectively, Roquin family proteins
and miR-146a emerge as novel post-transcriptional brakes on ICOS expression, thus
limiting Tfh cell numbers and GC responses.
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März, Sabine. "Regulation of fungal polar tip extension through NDR kinase signalling." Doctoral thesis, 2009. http://hdl.handle.net/11858/00-1735-0000-0006-ADB2-B.
Повний текст джерелаЧастини книг з теми "GC B cell"
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Chu, Van Trung, Robin Graf, and Klaus Rajewsky. "CRISPR/Cas9-Mediated In Vitro Mutagenesis in GC-Like B Cells." In Methods in Molecular Biology, 135–45. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7095-7_12.
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"GC/Post-GC Type B-Cell Tumors." In Encyclopedia of Cancer, 1515. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_2345.
Повний текст джерелаТези доповідей конференцій з теми "GC B cell"
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Ishii, Hiroyuki, Yoshihisa Kishiyama, and Hideaki Takahashi. "A novel architecture for LTE-B :C-plane/U-plane split and Phantom Cell concept." In 2012 IEEE Globecom Workshops (GC Wkshps). IEEE, 2012. http://dx.doi.org/10.1109/glocomw.2012.6477646.
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Ruiz-Justiz, Armando J., Mona Yazdani, Xin Sun, Lili Chen, Michael Wang, John Le, Haiping Guo, et al. "Characterization of T/B cell antigen specific-engineered tumors for studying T cell and GC B cell function in a murine model of NSCLC." In Leading Edge of Cancer Research Symposium. The University of Texas at MD Anderson Cancer Center, 2022. http://dx.doi.org/10.52519/00080.
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Zhang, Jiyuan, David Dominguez-Sola, Shafinaz Hussein, Ji-Eun Lee, Antony B. Holmes, Mukesh Bansal, Sofija Vlasevska, et al. "Abstract B25: Disruption of KMT2D-dependent histone methylation perturbs GC B cell development and cooperates with BCL2 deregulation in lymphomagenesis." In Abstracts: AACR Special Conference: Chromatin and Epigenetics in Cancer; September 24-27, 2015; Atlanta, GA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.chromepi15-b25.
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Chen, Kok Hao, and Jong Hyun Choi. "Nanoparticle-Aptamer: An Effective Growth Inhibitor for Human Cancer Cells." In ASME 2009 International Mechanical Engineering Congress and Exposition. ASMEDC, 2009. http://dx.doi.org/10.1115/imece2009-11966.
Повний текст джерелаАнотація:
Semiconductor nanocrystals have unique optical properties due to quantum confinement effects, and a variety of promising approaches have been devised to interface the nanomaterials with biomolecules for bioimaging and therapeutic applications. Such bio-interface can be facilitated via a DNA template for nanoparticles as oligonucleotides can mediate the aqueous-phase nucleation and capping of semiconductor nanocrystals.[1,2] Here, we report a novel scheme of synthesizing fluorescent nanocrystal quantum dots (NQDs) using DNA aptamers and the use of this biotic/abiotic nanoparticle system for growth inhibition of MCF-7 human breast cancer cells for the first time. Particularly, we used two DNA sequences for this purpose, which have been developed as anti-cancer agents: 5-GGT GGT GGT GGT TGT GGT GGT GGT GG-3 (also called, AGRO) and 5-(GT)15-3.[3–5] This study may ultimately form the basis of unique nanoparticle-based therapeutics with the additional ability to optically report molecular recognition. Figure 1a shows the photoluminescence (PL) spectra of GT- and AGRO-passivated PbS QD that fluoresce in the near IR, centered at approximately 980 nm. A typical synthesis procedure involves rapid addition of sodium sulfide in the mixture solution of DNA and Pb acetate at a molar ratio of 2:4:1. The resulting nanocrystals are washed to remove unreacted DNA and ions by adding mixture solution of NaCl and isopropanol, followed by centrifugation. The precipitated nanocrystals are collected and re-suspended in aqueous solution by mild sonication. Optical absorption measurements reveal that approximately 90 and 77% of GT and AGRO DNA is removed after the washing process. The particle size distribution in Figure 1b suggests that the GT sequence-capped PbS particles are primarily in 3–5 nm diameter range. These nanocrystals can be easily incorporated with mammalian cells and remain highly fluorescent in sub-cellular environments. Figure 1c serially presents an optical image of a MCF-7 cell and a PL image of the AGRO-capped QD incorporated with the cell. Figure 1. (a) Normalized fluorescence spectra of PbS QD synthesized with GT and AGRO sequences, which were previously developed as anti-cancer agents. The DNA-capped QD fluoresce in the near IR centered at ∼980 nm. (b) TEM image of GT-templated nanocrystals ranging 3–5 nm in diameter. (c) Optical image of an MCF-7 human breast cancer cell after a 12-hour exposure to aptamer-capped QD. (d) PL image of AGRO-QD incorporated with the cell, indicating that these nanocrystals remain highly fluorescent in sub-cellular environments. One immediate concern for interfacing inorganic nanocrystals with cells and tissue for labeling or therapeutics is their cytotoxicity. The nanoparticle cytotoxicity is primarily determined by material composition and surface chemistry, and QD are potentially toxic by generating reactive oxygen species or by leaching heavy metal ions when decomposed.[6] We examined the toxicity of aptamer-passivated nanocrystals with NIH-3T3 mouse fibroblast cells. The cells were exposed to PbS nanocrystals for 2 days before a standard MTT assay as shown in Figure 2, where there is no apparent cytotoxicity at these doses. In contrast, Pb acetate exerts statistically significant toxicity. This observation suggests a stable surface passivation by the DNA aptamers and the absence of appreciable Pb2+ leaching. Figure 2. Viability of 3T3 mouse fibroblast cells after a 2-day exposure to DNA aptamer-capped nanocrystals. There is no apparent dose-dependent toxicity, whereas a statistically significant reduction in cell viability is observed with Pb ions. Note that Pb acetate at 133 μM is equivalent to the Pb2+ amount that was used for PbS nanocrystal synthesis at maximum concentration. Error bars are standard deviations of independent experiments. *Statistically different from control (p<0.005). Finally, we examined if these cyto-compatible nanoparticle-aptamers remained therapeutically active for cancer cell growth inhibition. The MTT assay results in Figure 3a show significantly decreased growth of breast cancer cells incorporated with AGRO, GT, and the corresponding templated nanocrystals, as anticipated. In contrast, 5-(GC)15-3 and the QDs synthesized with the same sequence, which were used as negative controls along with zero-dose control cells, did not alter cell viability significantly. Here, we define the growth inhibition efficacy as (100 − cell viability) per DNA of a sample, because the DNA concentration is significantly decreased during the particle washing. The nanoparticle-aptamers demonstrate 3–4 times greater therapeutic activities compared to the corresponding aptamer drugs (Figure 3b). We speculate that when a nanoparticle-aptamer is internalized by the cancer cells, it forms an intracellular complex with nucleolin and nuclear factor-κB (NF-κB) essential modulator, thereby inhibiting NF-κB activation that would cause transcription of proliferation and anti-apoptotic genes.[7] The nanoparticle-aptamers may more effectively block the pathways for creating anti-apoptotic genes or facilitate the cellular delivery of aptamers via nanoparticle uptake. Our additional investigation indicates that the same DNA capping chemistry can be utilized to produce aptamer-mediated Fe3O4 nanocrystals, which may be potentially useful in MRI and therapeutics, considering their magnetic properties and biocompatibility. In summary, the nanoparticle-based therapeutic schemes developed here should be valuable in developing a multifunctional drug delivery and imaging agent for biological systems. Figure 3. Anti-proliferation of MCF-7 human breast cancer cells with aptamer-passivated nanocrystals. (a) Viability of MCF-7 cells exposed to AGRO and GT sequences, and AGRO-/GT-capped QD for 7 days. The DNA concentration was 10 uM, while the particles were incubated with cells at 75 nM. (b) Growth inhibition efficacy is defined as (100 − cell viability) per DNA to correct the DNA concentration after particle washing.
5
Levels, MJ, CM Fehres, NOP Van Uden, AQ Bakker, H. Spits, DL Baeten, and NG Yeremenko. "P035 The transcriptional co-activator bob.1 prevents terminal differentiation and induces costimulatory capacity of B cells in GC-like environment." In 38th European Workshop for Rheumatology Research, 22–24 February 2018, Geneva, Switzerland. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-ewrr2018.57.
Повний текст джерела
6
Mazumdar, Darshana. "Association of organochlorine pesticides and risk of epithelial ovarian cancer: A case control study." In 16th Annual International Conference RGCON. Thieme Medical and Scientific Publishers Private Ltd., 2016. http://dx.doi.org/10.1055/s-0039-1685303.
Повний текст джерелаАнотація:
Background: Organochlorine pesticides (OCPs) belongs to the class of hydrocarbons characterized by its cyclic structure. Due to their persistent nature OCP gets accumulated in the food chain and cause possible adverse health effects specifically various hormone mediated disorders. Ovarian cancer is also one of the hormone dependant cancer and begins with the transformation of cells that comprises the ovaries including surface epithelial, germ cells, etc. It has been suggested that endocrine disruption, exposure to xenobiotic and subsequent oxidative stress may antedate ovarian cancer and contribute to its pathogenesis. However, no report regarding any association of OCP level with etiology of epithelial ovarian cancer is so far available among North Indian population. Methods: A total of 120 subjects were included in this case control study, consisting of 60 histological proven cases of epithelial ovarian cancer and 60 controls subjects. Quantification of OCP levels was done by Perkin Elmer Gas Chromatograph (GC) equipped with 63Ni selective Electron Capture Detector. Results: Levels of b-HCH, endosulfan I, p’p’-DDT, p’p’-DDE and heptachlor were found significantly high in cases of epithelial ovarian cancer as compared to control. A significant association was also observed between higher levels of b-HCH and heptachlor and EOC with odds ratio of 2.76 and 2.97 respectively. Conclusion: Results indicate the plausible role of OCPs with the pathogenesis of epithelial ovarian cancer among North Indian population. Moreover, it is one of the first report suggesting significant level of heptachlor among north Indian women population with epithelial ovarian cancer.
Звіти організацій з теми "GC B cell"
1
Yalovsky, Shaul, and Julian Schroeder. The function of protein farnesylation in early events of ABA signal transduction in stomatal guard cells of Arabidopsis. United States Department of Agriculture, January 2002. http://dx.doi.org/10.32747/2002.7695873.bard.
Повний текст джерелаАнотація:
Loss of function mutations in the farnesyltransferase β subunit gene ERA1 (enhanced response to abscisic acid), cause abscisic acid hypersensitivity in seedlings and in guard cells. This results in slowed water loss of plants in response to drought. Farnesyltransferase (PFT) catalyses the attachment of the 15-carbon isoprenoid farnesyl to conserved cysteine residues located in a conserved C-terminal domain designated CaaX box. PFT is a heterodimeric protein comprised of an a and b sununits. The a subunit is shared between PFT and geranylgeranyltransferase-I (PGGTI) which catalyses the attachemt of the 20-carbon isoprenoid geranylgeranyl to CaaX box proteins in which the last amino acid is almost always leucine and in addition have a polybasic domain proximal to the CaaL box. Preliminary data presented in the proposal showed that increased cytoplasmic Ca2+ concentration in stomal guard cells in response to non-inductive ABA treatements. The goals set in the proposal were to characterize better how PFT (ERA1) affects ABA induced Ca2+ concentrations in guard cells and to identify putative CaaX box proteins which function as negative regulators of ABA signaling and which function is compromised in era1 mutant plants. To achieve these goals we proposed to use camelion Ca2+ sensor protein, high throughput genomic to identify the guard cell transcriptome and test prenylation of candidate proteins. We also proposed to focus our efforts of RAC small GTPases which are prenylated proteins which function in signaling. Our results show that farnesyltransferaseprenylates protein/s that act between the points of ABA perception and the activation of plasma membrane calcium influx channels. A RAC protein designated AtRAC8/AtRop10 also acts in negative regulation of ABA signaling. However, we discovered that this protein is palmitoylated and not prenylated although it contains a C-terminal CXXX motif. We further discovered a unique C-terminal sequence motif required for membrane targeting of palmitoylatedRACs and showed that their function is prenylation independent. A GC/MS based method for expression in plants, purification and analysis of prenyl group was developed. This method would allow highly reliable identification of prenylated protein. Mutants in the shared α subunit of PFT and PGGT-I was identified and characterized and was shown to be ABA hypersensitive but less than era1. This suggested that PFT and PGGT-I have opposing functions in ABA signaling. Our results enhanced the understanding of the role of protein prenylation in ABA signaling and drought resistance in plants with the implications of developing drought resistant plants. The results of our studies were published 4 papers which acknowledge support from BARD.