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MOUSE ANTI HUMAN FOLLICULAR DENDRITIC CELLS

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[#ABS11406] MOUSE ANTI HUMAN FOLLICULAR DENDRITIC CELLS

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ABS11406 | MOUSE ANTI HUMAN FOLLICULAR DENDRITIC CELLS, 25 µg
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(1) The role of AKT and FOXO3 in preventing ovarian toxicity induced by cyclophosphamide.[TOP]

Pubmed ID :30071053
Publication Date : //
Cyclophosphamide (CTX) has immunosuppressive effects and has been wildly used as one anti-cancer drug in clinical. Significant toxicity has been noticed particularly in the reproductive system. CTX promotes the maturation of ovarian follicles, decreases follicular reserve, and ultimately lead to ovarian failure or even premature ovarian failure (POF). The placental extract (HPE) has been shown to have some beneficial impact on reproductive system; however, little is known regarding to the effect of HPE on protecting CTX-induced ovarian injury and the mechanism involved. Whether human placental extracts (HPE) has a protective effect on CTX-induced toxicity on ovarian was studied by using a CTX-induced ovarian injury animal model. The effects of HEP on histopathology, the number of atretic follicles, the weight of the ovary, serum hormone levels, and apoptosis in granulosa cells were studied in mice with CTX or control vehicle. Our results have demonstrated that HPE inhibited p-Rictor, reduced the expression of Bad, Bax and PPAR, and activated Akt and Foxo3a (increased their phosphorylation). Mice treated with HPE showed higher ovarian weight, lower number of atretic follicles, higher serum levels of the hormones E2 and progesterone, and lower apoptosis and serum levels of LH and FSH in granulosa cells, than that in the control animal group. Our data show that ovarian injury can be attenuated by HPE. HPE likely protects follicular granulosa cells from undergoing significant apoptosis and reduce atresia follicle formation, therefore, alleviates CTX-induced ovarian injury.

Authors : Zhang Bao-Fang, Hu YaXin, Liu Xinyan, Cheng Zhuo, Lei Yu, Liu YongMei, Zhao Xueke, Mu Mao, Yu Lei, Cheng Ming-Liang,



(2) Identification of Human B-1 Helper T Cells With a Th1-Like Memory Phenotype and High Integrin CD49d Expression.[TOP]

Pubmed ID :30061889
Publication Date : //
Human B-1 cells have been proposed to be CD20CD27CD43CD1c B cells found in the umbilical cord and adult peripheral blood, but their regulatory mechanisms have not been well elucidated. Previously, we reported that mouse CD49d CD4 T cells could enhance the secretion of natural antibodies by B-1 cells. In this study, we aimed to investigate the presence and helper functions of the human equivalents of murine CD49d CD4 T cells. Here, we showed that human CD49d CD4 T cells found in the peritoneal cavity (PEC), spleen, and peripheral blood can enhance the production of IgM antibodies by B-1 cells. As revealed in mouse, CD49d CD4 T cells were more abundant in the PEC and showed a higher tendency to form conjugates with B cells than CD49d CD4 T cells. Moreover, CD49d CD4 T cells showed a Th1-like memory phenotype, characterized by high expression of CD44 and CXCR3; low expression of CD62L and CCR7; rapid production of IFN-γ, tumor necrosis factor-α, and IL-2 upon stimulation with phorbol myristate acetate and ionomycin; and rapid proliferation upon stimulation with anti-CD3 and anti-CD28 antibodies. These cells also expressed high levels of PD-1, ICOS, and CD5, suggesting that they are undergoing chronic stimulation. Remarkably, CD49d CD4 T cells specifically helped B-1 cells, but not follicular memory B cells (CD27 CD43CD1c) or marginal zone B cells (CD27CD43CD1c), produce IgM and IgG antibodies. In parallel, the titer of human anti-blood group A IgM was positively correlated with the frequency of CD49d CD4 T cells. In conclusion, we identified human CD49d CD4 T cells with a Th1-like memory phenotype that secrete Th1 proinflammatory cytokines and help B-1 cells secrete antibodies, thereby aiding in primary defense. We suggest that these CD49d CD4 T cells are a unique type of B-cell helper T cells distinct from follicular helper T cells.

Authors : Lee Jae-Ghi, Jang Joon Young, Fang Taishi, Xu Yixuan, Yan Ji-Jing, Ryu Jung-Hwa, Jeon Hee Jung, Koo Tai Yeon, Kim Dong Ki, Oh Kook-Hwan, Kim Tae Jin, Yang Jaeseok,



(3) Xenotransplantation of pre-pubertal ovarian cortex and prevention of follicle depletion with anti-Müllerian hormone (AMH).[TOP]

Pubmed ID :30043336
Publication Date : //
To determine whether recombinant AMH (rAMH) could prevent post-transplant follicular depletion by acting on the stemness markers Oct-4, Sox2, and NANOG.

Authors : Detti Laura, Fletcher Nicole M, Saed Ghassan M, Sweatman Trevor W, Uhlmann Rebecca A, Pappo Alberto, Peregrin-Alvarez Irene,



(4) Act1 is a negative regulator in T and B cells via direct inhibition of STAT3.[TOP]

Pubmed ID :30013031
Publication Date : //
Although Act1 (adaptor for IL-17 receptors) is necessary for IL-17-mediated inflammatory responses, Act1- (but not Il17ra-, Il17rc-, or Il17rb-) deficient mice develop spontaneous SLE- and Sjögren's-like diseases. Here, we show that Act1 functions as a negative regulator in T and B cells via direct inhibition of STAT3. Mass spectrometry analysis detected an Act1-STAT3 complex, deficiency of Act1 (but not Il17ra-, Il17rc-, or Il17rb) results in hyper IL-23- and IL-21-induced STAT3 activation in T and B cells, respectively. IL-23R deletion or blockade of IL-21 ameliorates SLE- and Sjögren's-like diseases in Act1 mice. Act1 deficiency results in hyperactivated follicular Th17 cells with elevated IL-21 expression, which promotes T-B cell interaction for B cell expansion and antibody production. Moreover, anti-IL-21 ameliorates the SLE- and Sjögren's-like diseases in Act1-deficient mice. Thus, IL-21 blocking antibody might be an effective therapy for treating SLE- and Sjögren's-like syndrome in patients containing Act1 mutation.

Authors : Zhang Cun-Jin, Wang Chenhui, Jiang Meiling, Gu Chunfang, Xiao Jianxin, Chen Xing, Martin Bradley N, Tang Fangqiang, Yamamoto Erin, Xian Yibo, Wang Han, Li Fengling, Sartor R Balfour, Smith Howard, Husni M Elaine, Shi Fu-Dong, Gao Ji, Carman Julie, Dongre Ashok, McKarns Susan C, Coppieters Ken, Jørgensen Trine N, Leonard Warren J, Li Xiaoxia,



(5) LDL-Reactive T Cells Regulate Plasma Cholesterol Levels and Development of Atherosclerosis in Humanized Hypercholesterolemic Mice.[TOP]

Pubmed ID :29997115
Publication Date : //
-Atherosclerotic cardiovascular disease is a chronic inflammatory process initiated when cholesterol-carrying low-density lipoprotein (LDL) is retained in the arterial wall. CD4 T cells, some of which recognize peptide components of LDL as antigen, are recruited to the forming lesion, resulting in T-cell activation. Although these T cells are thought to be proatherogenic, LDL immunization reduces disease in experimental animals. These seemingly contradictory findings have hampered the development of immune-based cardiovascular therapy. The present study was designed to clarify how activation of LDL-reactive T cells impacts on metabolism and vascular pathobiology. -We have developed a T-cell receptor(TCR)-transgenic mouse model to characterize the effects of immune reactions against LDL. Through adoptive cell transfers and cross-breeding to hypercholesterolemic mice expressing the antigenic human LDL protein ApoB100, we evaluate the effects on atherosclerosis. -A subpopulation of LDL-reactive T cells survived clonal selection in the thymus, developed into T follicular helper cells in lympoid tissues upon antigen recognition, and promoted B-cell activation. This led to production of anti-LDL immunoglobulin G (IgG) antibodies that enhanced LDL clearance through immune complex formation. Furthermore, the cellular immune response to LDL was associated with increased cholesterol excretion in faeces and with reduced vascular inflammation. -These data show that anti-LDL immunoreactivity evokes three atheroprotective mechanisms, namely antibody-dependent LDL clearance, increased cholesterol excretion, and reduced vascular inflammation.

Authors : Gisterå Anton, Klement Maria L, Polyzos Konstantinos A, Mailer Reiner K, Duhlin Amanda, Karlsson Mikael C I, Ketelhuth Daniel F J, Hansson Göran K,



(6) Past, Present, and Future of Rituximab-The World's First Oncology Monoclonal Antibody Therapy.[TOP]

Pubmed ID :29915719
Publication Date : //
Rituximab is a chimeric mouse/human monoclonal antibody (mAb) therapy with binding specificity to CD20. It was the first therapeutic antibody approved for oncology patients and was the top-selling oncology drug for nearly a decade with sales reaching $8.58 billion in 2016. Since its initial approval in 1997, it has improved outcomes in all B-cell malignancies, including diffuse large B-cell lymphoma, follicular lymphoma, and chronic lymphocytic leukemia. Despite widespread use, most mechanistic data have been gathered from studies while the roles of the various response mechanisms in humans are still largely undetermined. Polymorphisms in Fc gamma receptor and complement protein genes have been implicated as potential predictors of differential response to rituximab, but have not yet shown sufficient influence to impact clinical decisions. Unlike most targeted therapies developed today, no known biomarkers to indicate target engagement/tumor response have been identified, aside from reduced tumor burden. The lack of companion biomarkers beyond CD20 itself has made it difficult to predict which patients will respond to any given anti-CD20 antibody. In the past decade, two new anti-CD20 antibodies have been approved: ofatumumab, which binds a distinct epitope of CD20, and obinutuzumab, a mAb derived from rituximab with modifications to the Fc portion and to its glycosylation. Both are fully humanized and have biological activity that is distinct from that of rituximab. In addition to these new anti-CD20 antibodies, another imminent change in targeted lymphoma treatment is the multitude of biosimilars that are becoming available as rituximab's patent expires. While the widespread use of rituximab itself will likely continue, its biosimilars will increase global access to the therapy. This review discusses current research into mechanisms and potential biomarkers of rituximab response, as well as its biosimilars and the newer CD20 binding mAb therapies. Increased ability to assess the effectiveness of rituximab in an individual patient, along with the availability of alternative anti-CD20 antibodies will likely lead to dramatic changes in how we use CD20 antibodies going forward.

Authors : Pierpont Timothy M, Limper Candice B, Richards Kristy L,



(7) Non-conventional Inhibitory CD4Foxp3PD-1 T Cells as a Biomarker of Immune Checkpoint Blockade Activity.[TOP]

Pubmed ID :29894689
Publication Date : //
A significant proportion of cancer patients do not respond to immune checkpoint blockade. To better understand the molecular mechanisms underlying these treatments, we explored the role of CD4Foxp3 T cells expressing PD-1 (4PD1) and observed that 4PD1 accumulate intratumorally as a function of tumor burden. Interestingly, CTLA-4 blockade promotes intratumoral and peripheral 4PD1 increases in a dose-dependent manner, while combination with PD-1 blockade mitigates this effect and improves anti-tumor activity. We found that lack of effective 4PD1 reduction after anti-PD-1 correlates with poor prognosis. Mechanistically, we provide evidence that mouse and human circulating and intra-tumor 4PD1 inhibit T cell functions in a PD-1/PD-L1 dependent fashion and resemble follicular helper T cell (T)-like cells. Accordingly, anti-CTLA-4 activity is improved in T deficient mice.

Authors : Zappasodi Roberta, Budhu Sadna, Hellmann Matthew D, Postow Michael A, Senbabaoglu Yasin, Manne Sasikanth, Gasmi Billel, Liu Cailian, Zhong Hong, Li Yanyun, Huang Alexander C, Hirschhorn-Cymerman Daniel, Panageas Katherine S, Wherry E John, Merghoub Taha, Wolchok Jedd D,



(8) Co-transplantation of Human Ovarian Tissue with Engineered Endothelial Cells: A Cell-based Strategy Combining Accelerated Perfusion with Direct Paracrine Delivery.[TOP]

Pubmed ID :29863664
Publication Date : //
Infertility is a frequent side effect of chemotherapy and/or radiotherapy and for some patients, cryopreservation of oocytes or embryos is not an option. As an alternative, an increasing number of these patients are choosing to cryopreserve ovarian tissue for autograft following recovery and remission. Despite improvements in outcomes among patients undergoing auto-transplantation of cryopreserved ovarian tissue, efficient revascularization of grafted tissue remains a major obstacle. To mitigate ischemia and thus improve outcomes in patients undergoing auto-transplantation, we developed a vascular cell-based strategy for accelerating perfusion of ovarian tissue. We describe a method for co-transplantation of exogenous endothelial cells (ExECs) with cryopreserved ovarian tissue in a mouse xenograft model. We extend this approach to employ ExECs that have been engineered to constitutively express Anti-Mullerian hormone (AMH), thus enabling sustained paracrine signaling input to ovarian grafts. Co-transplantation with ExECs increased follicular volume and improved antral follicle development, and AMH-expressing ExECs promoted retention of quiescent primordial follicles. This combined strategy may be a useful tool for mitigating ischemia and modulating follicular activation in the context of fertility preservation and/or infertility at large.

Authors : Man Limor, Park Laura, Bodine Richard, Ginsberg Michael, Zaninovic Nikica, Schattman Glenn, Schwartz Robert E, Rosenwaks Zev, James Daylon,



(9) Lipopolysaccharide Preconditioning Increased the Level of Regulatory B cells in the Spleen after Acute Ischaemia/Reperfusion in Mice.[TOP]

Pubmed ID :29803621
Publication Date : //
The inflammatory reaction of the spleen is an important component in the pathophysiology of cerebral ischaemia (CI). Regulatory B cells (Bregs) derived from the spleen can inhibit the expansion of inflammation and reduce the damage caused by CI.

Authors : Wang Zhe, Zhou Yu, Yu Yan, He Ke, Cheng La-Mei,



(10) T Cell-Derived Lymphotoxin Is Essential for the Anti-Herpes Simplex Virus 1 Humoral Immune Response.[TOP]

Pubmed ID :29743364
Publication Date : //
B cell-derived lymphotoxin (LT) is required for the development of follicular dendritic cell clusters for the formation of primary and secondary lymphoid follicles, but the role of T cell-derived LT in antibody response has not been well demonstrated. We observed that lymphotoxin β-receptor (LTβR) signaling is essential for optimal humoral immune response and protection against an acute herpes simplex virus 1 (HSV-1) infection. Blocking the LTβR pathway caused poor maintenance of germinal center B (GC-B) cells and follicular helper T (Tfh) cells. Using bone marrow chimeric mice and adoptive transplantation, we determined that T cell-derived LT played an indispensable role in the humoral immune response to HSV-1. Upregulation of gamma interferon by the LTβR-Ig blockade impairs the sustainability of Tfh-like cells, leading to an impaired humoral immune response. Our findings have identified a novel role of T cell-derived LT in the humoral immune response against HSV-1 infection. Immunocompromised people are susceptible to HSV-1 infection and lethal recurrence, which could be inhibited by anti-HSV-1 humoral immune response in the host. This study sought to explore the role of T cell-derived LT in the anti-HSV-1 humoral immune response using LT-LTβR signaling-deficient mice and the LTβR-Ig blockade. The data indicate that the T cell-derived LT may play an essential role in sustaining Tfh-like cells and ensure Tfh-like cells' migration into primary or secondary follicles for further maturation. This study provides insights for vaccine development against infectious diseases.

Authors : Yang Kaiting, Liang Yong, Sun Zhichen, Xue Diyuan, Xu Hairong, Zhu Mingzhao, Fu Yang-Xin, Peng Hua,