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MOUSE ANTI HUMAN CD100 Low Endotoxin

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[#ABS10425] MOUSE ANTI HUMAN CD100 Low Endotoxin


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(1) Semaphorin 4D inhibits neutrophil activation and is involved in the pathogenesis of neutrophil-mediated autoimmune vasculitis.[TOP]

Pubmed ID :28416516
Publication Date : //
Inappropriate activation of neutrophils plays a pathological role in antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV). The aim of this study was to investigate the functions of semaphorin 4D (SEMA4D) in regulation of neutrophil activation, and its involvement in AAV pathogenesis.

Authors : Nishide Masayuki, Nojima Satoshi, Ito Daisuke, Takamatsu Hyota, Koyama Shohei, Kang Sujin, Kimura Tetsuya, Morimoto Keiko, Hosokawa Takashi, Hayama Yoshitomo, Kinehara Yuhei, Kato Yasuhiro, Nakatani Takeshi, Nakanishi Yoshimitsu, Tsuda Takeshi, Park Jeong Hoon, Hirano Toru, Shima Yoshihito, Narazaki Masashi, Morii Eiichi, Kumanogoh Atsushi,

(2) Possible pathogenic engagement of soluble Semaphorin 4D produced by γδT cells in medication-related osteonecrosis of the jaw (MRONJ).[TOP]

Pubmed ID :27720716
Publication Date : //
Prior consensus held that medication-related osteonecrosis of the jaw (MRONJ) lesion was composed of necrotic bone; however, more recent studies have identified inflammatory infiltrates in the lesion. Herein, we report that remarkably elevated infiltrating γδT cells (90% of lymphocytes) express Semaphorin 4D (Sema4D) in human patient with MRONJ lesion, whereas γδT cells only account for 2-5% of lymphocytes in blood. Importantly, Sema4D is implicated in the pathogenesis of T cell-mediated inflammatory diseases, such as rheumatoid arthritis and multiple sclerosis. Indeed, in a mouse model of MRONJ, an elevated number of γδT, but not αβT, cells infiltrating in the MRONJ-like lesion was observed. Both elevated soluble Sema4D (sSema4D) production accompanied by pro-inflammatory cytokines, including TNF-α IFN-γ and IL-1β, and Sema4D-expressing γδT cells were detected in mouse MRONJ-like lesion. Activated γδT cells produced sSema4D in vitro, which could promote TNF-α production from macrophages. Meanwhile, γδT cell-KO mice were resistant to the induction of MRONJ and, hence, showed no elevation of local productions of Sema4D and TNF-α. Finally, systemic administration of anti-Sema4D neutralizing mAb suppressed the onset of MRONJ in wild-type mice in conjunction with diminished level of TNF-α. These results suggested a critical pathogenic engagement of Sema4D produced by γδT cells in the development of MRONJ.

Authors : Movila Alexandru, Mawardi Hani, Nishimura Kazuaki, Kiyama Tomomi, Egashira Kenji, Kim Jae-Young, Villa Alessandro, Sasaki Hajime, Woo Sook-Bin, Kawai Toshihisa,

(3) Semaphorin 4D Contributes to Rheumatoid Arthritis by Inducing Inflammatory Cytokine Production: Pathogenic and Therapeutic Implications.[TOP]

Pubmed ID :25707877
Publication Date : //
Semaphorin 4D (Sema4D)/CD100 has pleiotropic roles in immune activation, angiogenesis, bone metabolism, and neural development. We undertook this study to investigate the role of Sema4D in rheumatoid arthritis (RA).

Authors : Yoshida Yuji, Ogata Atsushi, Kang Sujin, Ebina Kousuke, Shi Kenrin, Nojima Satoshi, Kimura Tetsuya, Ito Daisuke, Morimoto Keiko, Nishide Masayuki, Hosokawa Takashi, Hirano Toru, Shima Yoshihito, Narazaki Masashi, Tsuboi Hideki, Saeki Yukihiko, Tomita Tetsuya, Tanaka Toshio, Kumanogoh Atsushi,

(4) Antibody Blockade of Semaphorin 4D Promotes Immune Infiltration into Tumor and Enhances Response to Other Immunomodulatory Therapies.[TOP]

Pubmed ID :25614511
Publication Date : //
Semaphorin 4D (SEMA4D, CD100) and its receptor plexin-B1 (PLXNB1) are broadly expressed in murine and human tumors, and their expression has been shown to correlate with invasive disease in several human tumors. SEMA4D normally functions to regulate the motility and differentiation of multiple cell types, including those of the immune, vascular, and nervous systems. In the setting of cancer, SEMA4D-PLXNB1 interactions have been reported to affect vascular stabilization and transactivation of ERBB2, but effects on immune-cell trafficking in the tumor microenvironment (TME) have not been investigated. We describe a novel immunomodulatory function of SEMA4D, whereby strong expression of SEMA4D at the invasive margins of actively growing tumors influences the infiltration and distribution of leukocytes in the TME. Antibody neutralization of SEMA4D disrupts this gradient of expression, enhances recruitment of activated monocytes and lymphocytes into the tumor, and shifts the balance of cells and cytokines toward a proinflammatory and antitumor milieu within the TME. This orchestrated change in the tumor architecture was associated with durable tumor rejection in murine Colon26 and ERBB2(+) mammary carcinoma models. The immunomodulatory activity of anti-SEMA4D antibody can be enhanced by combination with other immunotherapies, including immune checkpoint inhibition and chemotherapy. Strikingly, the combination of anti-SEMA4D antibody with antibody to CTLA-4 acts synergistically to promote complete tumor rejection and survival. Inhibition of SEMA4D represents a novel mechanism and therapeutic strategy to promote functional immune infiltration into the TME and inhibit tumor progression.

Authors : Evans Elizabeth E, Jonason Alan S, Bussler Holm, Torno Sebold, Veeraraghavan Janaki, Reilly Christine, Doherty Michael A, Seils Jennifer, Winter Laurie A, Mallow Crystal, Kirk Renee, Howell Alan, Giralico Susan, Scrivens Maria, Klimatcheva Katya, Fisher Terrence L, Bowers William J, Paris Mark, Smith Ernest S, Zauderer Maurice,

(5) Lycorine hydrochloride selectively inhibits human ovarian cancer cell proliferation and tumor neovascularization with very low toxicity.[TOP]

Pubmed ID :23376478
Publication Date : //
Uncontrolled tumor cell proliferation and robust neovascularization are prominent features of aggressive ovarian cancers. Although great efforts in anti-ovarian cancer therapy have been made in the past 4 decades, the 5-year survival rates for ovarian cancer patients are still poor, and effective drugs to cure ovarian cancer patients are absent. In this study, we evaluated the anti-cancer effects of lycorine hydrochloride (LH), a novel anti-ovarian cancer agent, using the highly-invasive ovarian cancer cell line, Hey1B, as a model. Our data showed that LH effectively inhibited mitotic proliferation of Hey1B cells (half maximal inhibitory concentration=1.2μM) with very low toxicity, resulting in cell cycle arrest at the G2/M transition through enhanced expression of the cell cycle inhibitor p21 and marked down-regulation of cyclin D3 expression. Moreover, LH suppressed both the formation of capillary-like tubes by Hey1B cells cultured in vitro and the ovarian cancer cell-dominant neovascularization in vivo when administered to Hey1B-xenotransplanted mice. LH also suppressed the expression of several key angiogenic genes, including VE-cadherin, vascular endothelial growth factor, and Sema4D, and reduced Akt phosphorylation in Hey1B cells. These results suggest that LH selectively inhibits ovarian cancer cell proliferation and neovascularization and is a potential drug candidate for anti-ovarian cancer therapy.

Authors : Cao Zhifei, Yu Di, Fu Shilong, Zhang Gaochuan, Pan Yanyan, Bao Meimei, Tu Jian, Shang Bingxue, Guo Pengda, Yang Ping, Zhou Quansheng,

(6) The hypoxia-inducible factor-responsive proteins semaphorin 4D and vascular endothelial growth factor promote tumor growth and angiogenesis in oral squamous cell carcinoma.[TOP]

Pubmed ID :22652457
Publication Date : //
Growth and metastasis of solid tumors requires induction of angiogenesis to ensure the delivery of oxygen, nutrients and growth factors to rapidly dividing transformed cells. Through either mutations, hypoxia generated by cytoreductive therapies, or when a malignancy outgrows its blood supply, tumor cells undergo a change from an avascular to a neovascular phenotype, a transition mediated by the hypoxia-inducible factor (HIF) family of transcriptional regulators. Vascular endothelial growth factor (VEGF) is one example of a gene whose transcription is stimulated by HIF. VEGF plays a crucial role in promoting tumor growth and survival by stimulating new blood vessel growth in response to such stresses as chemotherapy or radiotherapy-induced hypoxia, and it therefore has become a tempting target for neutralizing antibodies in the treatment of advanced neoplasms. Emerging evidence has shown that the semaphorins, proteins originally associated with control of axonal growth and immunity, are regulated by changes in oxygen tension as well and may play a role in tumor-induced angiogenesis. Through the use of RNA interference, in vitro and in vivo angiogenesis assays and tumor xenograft experiments, we demonstrate that expression of semaphorin 4D (SEMA4D), which is under the control of the HIF-family of transcription factors, cooperates with VEGF to promote tumor growth and vascularity in oral squamous cell carcinoma (OSCC). We use blocking antibodies to show that targeting SEMA4D function along with VEGF could represent a novel anti-angiogenic therapeutic strategy for the treatment of OSCC and other solid tumors.

Authors : Zhou Hua, Yang Ying-Hua, Binmadi Nada O, Proia Patrizia, Basile John R,

(7) Plexin-B1 activates NF-κB and IL-8 to promote a pro-angiogenic response in endothelial cells.[TOP]

Pubmed ID :22028792
Publication Date : //
The semaphorins and their receptors, the plexins, are proteins related to c-Met and the scatter factors that have been implicated in an expanding signal transduction network involving co-receptors, RhoA and Ras activation and deactivation, and phosphorylation events. Our previous work has demonstrated that Semaphorin 4D (Sema4D) acts through its receptor, Plexin-B1, on endothelial cells to promote angiogenesis in a RhoA and Akt-dependent manner. Since NF-κB has been linked to promotion of angiogenesis and can be activated by Akt in some contexts, we wanted to examine NF-κB in Sema4D treated cells to determine if there was biological significance for the pro-angiogenic phenotype observed in endothelium.

Authors : Yang Ying-Hua, Zhou Hua, Binmadi Nada O, Proia Patrizia, Basile John R,

(8) Involvement of CD100, a lymphocyte semaphorin, in the activation of the human immune system via CD72: implications for the regulation of immune and inflammatory responses.[TOP]

Pubmed ID :12882840
Publication Date : //
CD100/Sema4D belongs to the semaphorin family, factors known to act as repulsive cues for axons during neuronal development. Mouse CD100 plays a crucial role in both humoral and cellular immunity through ligation of the lymphocyte receptor, CD72. It remains controversial, however, whether human CD100 can function through human CD72 in a manner similar to mouse CD100. To determine the function of human CD100, we generated a recombinant soluble human CD100 protein comprised of the extracellular region of human CD100 fused to the human IgG1 Fc region (hCD100-Fc). hCD100-Fc specifically binds to cells expressing human CD72. As observed previously in the mouse, hCD100-Fc induces the tyrosine dephosphorylation of human CD72, leading to the dissociation of SHP-1 from the CD72 cytoplasmic tail. Consistent with findings for mouse CD100, hCD100-Fc exerts a co-stimulatory effect on B cells and dendritic cells that are stimulated with anti-CD40 mAb. Furthermore, both hCD100-Fc and anti-human CD72 agonistic mAb induce the production of the pro-inflammatory cytokines tumor necrosis factor-alpha, IL-6 and IL-8, even in the absence of anti-CD40 mAb. Collectively, our findings not only demonstrate that human CD100, interacting with human CD72, can function as a ligand in a manner similar to mouse CD100, but also suggest the involvement of human CD100 in inflammatory responses.

Authors : Ishida Isao, Kumanogoh Atsushi, Suzuki Kazuhiro, Akahani Shiro, Noda Kazuhiro, Kikutani Hitoshi,