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MHC Class II, Mab anti_Cat; Clone PF6J_6D, ELISA,flow,WB

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[#YSRTMCA2723] MHC Class II, Mab anti_Cat; Clone PF6J_6D, ELISA,flow,WB

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YSRTMCA2723 | MHC Class II, Mab anti_Cat; Clone PF6J_6D, ELISA,flow,WB, 0.25 mg.
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(1) Generation of Fcabs targeting human and murine LAG-3 as building blocks for novel bispecific antibody therapeutics.[TOP]

Pubmed ID :30208333
Publication Date : //
The immunoglobulin superfamily protein lymphocyte-activation gene 3 (LAG-3) participates in immune suppression and has been identified as a suitable target for cancer therapies. In order to generate bispecific antibodies targeting LAG-3, Fcabs (Fc-region with antigen binding) targeting human and murine LAG-3 were generated from phage libraries. These Fcabs bind to LAG-3, inhibiting its interaction with MHC class II, and induce IL-2 production in a T cell assay. Bispecific antibodies, known as mAb, were produced by replacing the Fc region of a monoclonal antibody with Fcab sequences in the CH3 domain. mAb containing anti-LAG-3 Fcabs have mAb-like biophysical characteristics and retain LAG-3 binding and functional activity. mAb can thus be generated using multiple Fabs to investigate bispecific parings and develop novel therapeutics.

Authors : Everett Katy L, Kraman Matthew, Wollerton Francisca P G, Zimarino Carlo, Kmiecik Katarzyna, Gaspar Miguel, Pechouckova Sarka, Allen Natalie L, Doody Jacqueline F, Tuna Mihriban,



(2) Ligation of Na, K ATPase β3 subunit on monocytes by a specific monoclonal antibody mediates T cell hypofunction.[TOP]

Pubmed ID :29940031
Publication Date : //
T cells play a crucial role in orchestrating body immune responses. T cell hyperfunction, however, leads to inflammation and induction of autoimmune diseases. Understanding of T cell regulation mechanisms and successful modulation of T cell responses is beneficial in treatment of disease associated to T cell hyperresponsiveness. Our previous study indicated that monoclonal antibody (mAb) P-3E10, a mAb to Na, K ATPase β3 subunit, inhibited anti-CD3-induced PBMC proliferation. In the current study, we further investigated the mechanism of mAb P-3E10 in the induction of T cell hypofunction. We demonstrated that mAb P-3E10 decreased T cell proliferation and Th1, Th2 and Th17 cytokine production. Monocytes were the cells playing a key role in mediation of mAb P-3E10 induced T cell hypofunction. The inhibition of T cell activation by mAb P-3E10 required cell contact between monocytes and T cells. The mAb P-3E10 induced the down-expression level of MHC class II and CD86 and increased IL-6, IL-10 and TNF-α production of monocytes. We concluded that ligation of the Na, K ATPase β3 subunit on monocytes by mAb P-3E10 arbitrated T cell hypofunction. This mAb might be a promising novel immunotherapeutic antibody for the treatment of hyperresponsive T cell associated diseases.

Authors : Takheaw Nuchjira, Laopajon Witida, Surinkaew Sirirat, Khummuang Saichit, Pata Supansa, Kasinrerk Watchara,



(3) SslE (YghJ), a Cell-Associated and Secreted Lipoprotein of Neonatal Septicemic Escherichia coli, Induces Toll-Like Receptor 2-Dependent Macrophage Activation and Proinflammation through NF-κB and MAP Kinase Signaling.[TOP]

Pubmed ID :29891541
Publication Date : //
SslE (YghJ), a cell surface-associated and secreted lipoprotein, was identified as a potential vaccine candidate for extraintestinal pathogenic , providing nearly complete protection from sepsis in a mouse model. We earlier found that SslE from neonatal septicemic could trigger the secretion of various proinflammatory cytokines in murine macrophages, the signaling pathway of which is still obscure. In this study, we showed that SslE specifically binds to Toll-like receptor 2 (TLR2)/TLR1 heterodimers and recruits downstream adaptors MyD88, TIRAP, and TRAF6. In addition, SslE stimulates nuclear translocation of NF-κB and activates different mitogen-activated protein (MAP) kinase signaling cascades specific to the secretion of each cytokine in murine macrophages, which becomes impaired in TLR2 small interfering RNA (siRNA)-transfected cells and in cells blocked with a monoclonal antibody (MAb) against TLR2, suggesting the involvement of TLR2 in NF-κB and MAP kinase activation and subsequent cytokine secretion. Furthermore, our study is the first to show that SslE can stimulate TLR2-dependent production of other proinflammatory hallmarks, such as reactive nitrogen and oxygen species as well as type 1 chemokines, which contribute to the anti-infection immune response of the host. Also, the overexpression of major histocompatibility complex class II (MHC II) and other costimulatory molecules (CD80 and CD86) in macrophages essentially indicates that SslE promotes macrophage activation and M1 polarization, which are crucial in framing the host's innate immune response to this protein, and hence, SslE could be a potent immunotherapeutic target against sepsis.

Authors : Tapader Rima, Bose Dipro, Dutta Pujarini, Das Santasabuj, Pal Amit,



(4) Aire is not essential for regulating neuroinflammatory disease in mice transgenic for human autoimmune-diseases associated MHC class II genes HLA-DR2b and HLA-DR4.[TOP]

Pubmed ID :29789121
Publication Date : //
The human autoimmune disease-associated HLA alleles HLA-DR2b (DRB1*1501) and HLA-DR4 (DRB1*0401) are strongly linked to increased susceptibility for multiple sclerosis (MS) and rheumatoid arthritis (RA), respectively. The underlying mechanisms are not fully understood, but these MHC alleles may shape the repertoire of pathogenic T cells via central tolerance. The transcription factor autoimmune regulator (AIRE) promotes central T cell tolerance via ectopic expression of tissue-specific antigens (TSAs). Aire deficiency in humans causes autoimmune polyendocrinopathy syndrome type 1 (APS1), and Aire knockout mice (Aire) develop spontaneous autoimmune pathology characterized by multi-organ lymphocytic infiltrates. Here, we asked whether impaired TSAs gene expression in the absence of Aire promoted spontaneous MS- or RA-like autoimmune pathology in the context of human HLA alleles in HLA-DR2b or HLA-DR4 transgenic (tg) mice. The results show that reduced TSAs gene expression in the thymus of Aire-deficient HLA-DR2b or HLA-DR4 tg mice corresponded to mild spontaneous inflammatory infiltrates in salivary glands, liver, and pancreas. Moreover, Aire-deficiency modestly enhanced experimental autoimmune encephalomyelitis (EAE) in HLA-DR tg mice, but the animals did not show signs of spontaneous neuroinflammation or arthritis. No significant changes were observed in CD4 T cell numbers, T cell receptor (TCR) distribution, regulatory T cells (Treg), or antigen-induced cytokine production. Abrogating Treg function by treatment with anti-CTLA-4 or anti-CD25 mAb in Aire-deficient HLA-DR tg mice did not trigger EAE or other autoimmune pathology. Our results suggest a redundant role for Aire in maintaining immune tolerance in the context of autoimmune disease-associated human HLA alleles.

Authors : Nalawade Saisha A, Ji Niannian, Raphael Itay, Pratt Andrew, Kraig Ellen, Forsthuber Thomas G,



(5) High macrophage PD-L1 expression not responsible for T cell suppression.[TOP]

Pubmed ID :29305065
Publication Date : //
Tumors are often comprised of microenvironments (TMEs) with a high proportion of cells and molecules that regulate immunity. Peritoneal cavity (PerC) cell culture reproduces key features of TMEs as lymphocyte proliferation is suppressed by PerC macrophages (Mϕs). We monitored the expression of T cell stimulatory (Class II MHC, B7) and inhibitory (PD-L1) molecules by PerC APCs before and after culture and report here that IFNγ-driven PD-L1 expression increased markedly on PerC Mϕs after TCR ligation, even more so than seen with direct APC activation by LPS. Considering the high APC composition of and pronounced PD-L1 expression by PerC cells, it was surprising that blocking PD-1/PD-L1 interaction by mAb neutralization or genetic ablation did not relieve suppression. This result parallels TME challenges observed in the clinic and validates the need for further study of this culture model to inform strategies to promote anti-tumor immunity.

Authors : Goldman Naomi, Lomakova Yelizavet D, Londregan Jennifer, Bucknum Amanda, DePierri Kelley, Somerville John, Riggs James E,



(6) Surface LAMP-2 Is an Endocytic Receptor That Diverts Antigen Internalized by Human Dendritic Cells into Highly Immunogenic Exosomes.[TOP]

Pubmed ID :28607115
Publication Date : //
The lysosome-associated membrane protein (LAMP) family includes the dendritic cell endocytic receptors DC-LAMP and CD68, as well as LAMP-1 and LAMP-2. In this study we identify LAMP-1 (CD107a) and LAMP-2 (CD107b) on the surface of human monocyte-derived dendritic cells (MoDC) and show only LAMP-2 is internalized after ligation by specific Abs, including H4B4, and traffics rapidly but transiently to the MHC class II loading compartment, as does Ag conjugated to H4B4. However, pulsing MoDC with conjugates of primary (keyhole limpet hemocyanin; KLH) and recall (Bet v 1) Ags (H4B4*KLH and H4B4*Bet v 1) induced significantly less CD4 cell proliferation than pulsing with native Ag or Ag conjugated to control mAb (ISO*KLH and ISO*Bet v 1). In H4B4*KLH-pulsed MoDC, the duration of KLH residence in MHC class II loading compartments was significantly reduced, as were surface HLA-DR and DR-bound KLH-derived peptides. Paradoxically, MoDC pulsed with H4B4*KLH, but not the other KLH preparations, induced robust proliferation of CD4 cells separated from them by a transwell membrane, indicating factors in the supernatant were responsible. Furthermore, extracellular vesicles from supernatants of H4B4*KLH-pulsed MoDC contained significantly more HLA-DR and KLH than those purified from control MoDC, and KLH was concentrated specifically in exosomes that were a uniquely effective source of Ag in standard T cell proliferation assays. In summary, we identify LAMP-2 as an endocytic receptor on human MoDC that routes cargo into unusual Ag processing pathways, which reduces surface expression of Ag-derived peptides while selectively enriching Ag within immunogenic exosomes. This novel pathway has implications for the initiation of immune responses both locally and at distant sites.

Authors : Leone Dario Armando, Peschel Andrea, Brown Markus, Schachner Helga, Ball Miriam J, Gyuraszova Marianna, Salzer-Muhar Ulrike, Fukuda Minoru, Vizzardelli Caterina, Bohle Barbara, Rees Andrew J, Kain Renate,



(7) Comparison of 6B11 mAb and α-GalCer-loaded CD1d dextramers for detection of iNKT cells by flow cytometry.[TOP]

Pubmed ID :28365328
Publication Date : //
Invariant natural killer T (iNKT) cells are a small population of thymus-derived T cells that are restricted by non-classical MHC class I molecule CD1d and express an evolutionary conserved TCR with an invariant α-chain. The frequency of iNKT cells in peripheral blood is very low, thus, accurate methods to identify and enumerate iNKT cells are needed. The aim of the study was to compare 6B11 mAb or α-GalCer-loaded CD1d dextramers usage in iNKT cell detection. The frequency of CD3CD56 lymphocytes is much higher, with statistical significance (p<0,001), than real iNKT cells detected by 6B11 mAb or α-GalCer-loaded CD1d dextramers. The frequency of iNKT cells, recognized by 6B11 mAb or α-GalCer-loaded CD1d dextramers, was in a similar range. Nonetheless, when we compared whether 6B11 and α-GalCer-loaded CD1d dextramers are the same populations, it turned out that by this approach we were able to identify three distinct subsets of iNKT cells: i) 6B11/α-GalCer-loaded dextramer cells, ii) 6B11/α-GalCer-loaded dextramer cells, and iii) 6B11/α-GalCer-loaded dextramer. Thus, although 6B11 mAb and α-GalCer-loaded dextramers may identify not exactly the same cells, application of these methods seems to give similar results of iNKT cell frequency in peripheral blood. It seems that both approaches for iNKT detection can be used for precise identification of these cells. Moreover, our results indicate that CD3CD56 lymphocytes are a heterogeneous population of T cells, expressing activation markers of both NK and T lymphocytes, yet with not well characterized properties.

Authors : Lenart Marzena, Gruca Anna, Mueck Anna, Rutkowska-Zapała Magdalena, Surman Marta, Szaflarska Anna, Kobylarz Krzysztof, Baran Jarosław, Siedlar Maciej,



(8) Intratumoral administration of cGAMP transiently accumulates potent macrophages for anti-tumor immunity at a mouse tumor site.[TOP]

Pubmed ID :28243692
Publication Date : //
Stimulator of IFN genes (STING) spontaneously contributes to anti-tumor immunity by inducing type I interferons (IFNs) following sensing of tumor-derived genomic DNAs in the tumor-bearing host. Although direct injection of STING ligands such as cyclic diguanylate monophosphate (c-di-GMP) and cyclic [G(2',5')pA(3',5')p] (cGAMP) into the tumor microenvironment exerts anti-tumor effects through strong induction of type I IFNs and activation of innate and adaptive immunity, the precise events caused by STING in the tumor microenvironment remain to be elucidated. We describe here our finding that a CD45 CD11b Ly6C cell subset transiently accumulated in mouse tumor microenvironment of 4T1 breast cancer, squamous cell carcinomas, CT26 colon cancer, or B16F10 melanoma tissue after intratumoral injection of cGAMP. The accumulated cells displayed a macrophage (M ) phenotype since the cells were positive for F4/80 and MHC class II and negative for Ly6G. Intratumoral cGAMP treatment did not induce Mφ accumulation in STING-deficient mice. Depletion of CD8 T cell using anti-CD8 mAb impaired the anti-tumor effects of cGAMP treatment. Depletion of the Mφ using clodronate liposomes impaired the anti-tumor effects of cGAMP treatment. Functional analysis indicated that the STING-triggered tumor-migrating Mφ exhibited phagocytic activity, production of tumor necrosis factor alpha TNFα), and high expression levels of T cell-recruiting chemokines, Cxcl10 and Cxcl11, IFN-induced molecules, MX dynamin-like GTPase 1 (Mx1) and 2'-5' oligoadenylate synthetase-like 1 (Oasl1), nitric oxide synthase 2 (Nos2), and interferon beta 1 (Ifnb1). These results indicate that the STING-triggered tumor-migrating Mφ participate in the anti-tumor effects of STING-activating compounds.

Authors : Ohkuri Takayuki, Kosaka Akemi, Ishibashi Kei, Kumai Takumi, Hirata Yui, Ohara Kenzo, Nagato Toshihiro, Oikawa Kensuke, Aoki Naoko, Harabuchi Yasuaki, Celis Esteban, Kobayashi Hiroya,



(9) Characterization of a Broadly Reactive Anti-CD40 Agonistic Monoclonal Antibody for Potential Use as an Adjuvant.[TOP]

Pubmed ID :28107431
Publication Date : //
Lack of safe and effective adjuvants is a major hindrance to the development of efficacious vaccines. Signaling via CD40 pathway leads to enhanced antigen processing and presentation, nitric oxide expression, pro-inflammatory cytokine expression by antigen presenting cells, and stimulation of B-cells to undergo somatic hypermutation, immunoglobulin class switching, and proliferation. Agonistic anti-CD40 antibodies have shown promising adjuvant qualities in human and mouse vaccine studies. An anti-CD40 monoclonal antibody (mAb), designated 2E4E4, was identified and shown to have strong agonistic effects on primary cells from multiple livestock species. The mAb recognize swine, bovine, caprine, and ovine CD40, and evoked 25-fold or greater proliferation of peripheral blood mononuclear cells (PBMCs) from these species relative to cells incubated with an isotype control (p<0.001). In addition, the mAb induced significant nitric oxide (p<0.0001) release by bovine macrophages. Furthermore, the mAb upregulated the expression of MHC-II by PBMCs, and stimulated significant (p<0.0001) IL-1α, IL6, IL-8, and TNF-α expression by PBMCs. These results suggest that the mAb 2E4E4 can target and stimulate cells from multiple livestock species and thus, it is a potential candidate for adjuvant development. This is the first study to report an anti-swine CD40 agonistic mAb that is also broadly reactive against multiple species.

Authors : Martin Cameron, Waghela Suryakant D, Lokhandwala Shehnaz, Ambrus Andy, Bray Jocelyn, Vuong Christina, Vinodkumar Vanitha, Dominowski Paul J, Rai Sharath, Mwangi Duncan, Foss Dennis L, Mwangi Waithaka,



(10) TCR Signaling and CD28/CTLA-4 Signaling Cooperatively Modulate T Regulatory Cell Homeostasis.[TOP]

Pubmed ID :28053234
Publication Date : //
Foxp3 T regulatory cells (Tregs), conventional CD4Foxp3 T cells, and CD8 T cells represent heterogeneous populations composed of naive phenotype (NP, CD44) and memory phenotype (MP, CD44) subpopulations. NP and MP subsets differ in their activation state, contribution to immune function, and capacity to proliferate in vivo. To further understand the factors that contribute to the differential homeostasis of NP/MP subsets, we examined the differential effects of CD28 and CTLA-4 interaction with CD80/CD86, as well as MHC class II-TCR interaction within mouse Treg pools and CD4 and CD8 T cell pools. Blockade of CD80/CD86 with CTLA-4-Ig markedly reduced the cycling and absolute numbers of MP Tregs and MP CD4 T cells, with minimal effect on the NP T cell subpopulations. Blockade of MHC class II-TCR interaction led to selective expansion of MP Tregs and MP CD4 and CD8 T cells that was reversed upon cotreatment with CTLA-4-Ig. Treatment with anti-CTLA-4 mAb altered MP Treg and MP CD4 and CD8 T cell homeostasis in a manner similar to that observed with anti-MHC class II. We postulate a complex pathway in which CD28 is the primary driver of Treg proliferation and CTLA-4 functions as the main brake but is likely dependent on TCR signals and CD80/CD86. These findings have important implications for the use of biologic agents targeting such pathways to modulate autoimmune and neoplastic disease.

Authors : Holt Michael P, Punkosdy George A, Glass Deborah D, Shevach Ethan M,