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Granzyme B, Human, 1.3_960 U_ml, ELISA Kit, includes Mab coating Ab, control, standard, Biotin secondary, HRP_Streptavidin, buffer, substrate (No plate)

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[#CLBM1936] Granzyme B, Human, 1.3_960 U_ml, ELISA Kit, includes Mab coating Ab, control, standard, Biotin secondary, HRP_Streptavidin, buffer, substrate (No plate)


CLBM1936 | Granzyme B, Human, 1.3_960 U_ml, ELISA Kit, includes Mab coating Ab, control, standard, Biotin secondary, HRP_Streptavidin, buffer, substrate (No plate), kit
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(1) Immune system-mediated atherosclerosis caused by deficiency of long noncoding RNA MALAT1 in ApoE-/- mice.[TOP]

Pubmed ID :30101304
Publication Date : //
The immune system is considered a key driver of atherosclerosis, and beyond proteins and microRNAs (miRs), long noncoding RNAs (lncRNAs) are implicated in immune control. We previously described that lncRNA MALAT1 is involved in cardiac innate immunity in a myocarditis model. Here, we investigated the impact of MALAT1 deficiency upon atherosclerosis development.

Authors : Gast Martina, Rauch Bernhard H, Nakagawa Shinichi, Haghikia Arash, Jasina Andrzej, Haas Jan, Nath Neetika, Jensen Lars, Stroux Andrea, Böhm Andreas, Friebel Julian, Rauch Ursula, Skurk Carsten, Blankenberg Stefan, Zeller Tanja, Prasanth Kannanganattu V, Meder Benjamin, Kuss Andreas, Landmesser Ulf, Poller Wolfgang,

(2) Human CD8 T cell activation in acute and chronic Chikungunya infection.[TOP]

Pubmed ID :30099739
Publication Date : //
There is a need for more detailed elucidation of T cell immunity in Chikungunya infection. CD8 T cells are one of main actors against viruses. Here, we analyzed CD8 T lymphocytes from patients in the acute and chronic phases of the illness (CHIKD). Our results demonstrate that CD8 T cells expressed higher ex vivo Granzyme B, Perforin and CD107A expression in patients in the acute phase of CHIKD compared with healthy individuals and higher ex vivo expression of CD69, IL17A, IL10, CD95L and coexpression of CD95/CD95L. These results elucidate the importance of these lymphocytes, demonstrating immune mechanisms mediated in human chikungunya infection. This article is protected by copyright. All rights reserved.

Authors : de Sousa Dias Cinthia Nóbrega, Gois Bruna Macêdo, Lima Viviane Silva, Guerra-Gomes Isabel Cristina, Araújo Josélio Maria Galvão, de Assis Silva Gomes Juliana, de Araújo Demétrius Antônio Machado, de Medeiros Isac Almeida, de Lourdes Assunção Araújo de Azevedo Fátima, Veras Robson Cavalcanti, Janebro Daniele Idalino, do Amaral Ian Porto Gurgel, Keesen Tatjana Souza Lima,

(3) Human CD49a Lung Natural Killer Cell Cytotoxicity in Response to Influenza A Virus.[TOP]

Pubmed ID :30079068
Publication Date : //
Influenza A virus (IAV) is a major global public health burden due to its routine evasion of immunization strategies. Natural killer (NK) cells are innate cytotoxic cells with important antiviral activity in the human body, yet the function of these cells in the control of IAV infection is unclear. The aim of this study was to determine the role of lung NK cell cytotoxic responses to IAV. Human lung explants were infected with IAV, and lung NK cell activation was analyzed by flow cytometry. Cytotoxic responses of NK cell subsets against IAV-infected macrophages were measured by flow cytometry and ELISA. Despite reports of hypofunctionality in the pulmonary environment, human lung-associated NK cells responded rapidly to IAV infection, with upregulation of surface CD107a 24 h post-infection. The lung NK cell phenotype is similar in maturity and differentiation to NK cells of the peripheral blood but a unique CD56CD49aCD103CD69 NK cell population was identified in the lung, indicating NK cell residency within this organ. In response to IAV infection a greater proportion of resident CD56CD49a NK cells expressed surface CD107a compared with CD56CD49a NK cells, suggesting a hyperfunctional NK cell population may be present within human lung tissue and could be the result of innate immunological training. Furthermore, NK cells provided significant antiviral, cytotoxic activity following contact with influenza-infected cells, including the production and release of IFN-γ and granzyme-B resulting in macrophage cell death. These results suggest that a resident, trained NK cell population are present in the human lung and may provide early and important control of viral infection. A greater understanding of this resident mucosal population may provide further insight into the role of these cells in controlling viral infection and generating appropriate adaptive immunity to IAV.

Authors : Cooper Grace E, Ostridge Kristoffer, Khakoo Salim I, Wilkinson Tom M A, Staples Karl J,

(4) Checkpoint Blockade Rescues the Repressive Effect of Histone Deacetylases Inhibitors on γδ T Cell Function.[TOP]

Pubmed ID :30072989
Publication Date : //
Histone deacetylases (HDAC) are one of the key epigenetic modifiers that control chromatin accessibility and gene expression. Their role in tumorigenesis is well established and HDAC inhibitors have emerged as an effective treatment modality. HDAC inhibitors have been investigated for their specific antitumor activities and also clinically evaluated in treatment of various malignancies. In the present study, we have investigated the effect of HDAC inhibitors on the effector functions of human γδ T cells. HDAC inhibitors inhibit the antigen-specific proliferative response of γδ T cells and cell cycle progression. In antigen-activated γδ T cells, the expression of transcription factors (Eomes and Tbet) and effector molecules (perforin and granzyme B) were decreased upon treatment with HDAC inhibitors. Treatment with HDAC inhibitors attenuated the antitumor cytotoxic potential of γδ T cells, which correlated with the enhanced expression of immune checkpoints programmed death-1 (PD-1) and programmed death ligand-1 in γδ T cells. Interestingly, PD-1 blockade improves the antitumor effector functions of HDAC inhibitor-treated γδ T cells, which is reflected in the increased expression of Granzyme B and Lamp-1. This study provides a rationale for designing HDAC inhibitor and immune check point blockade as a combinatorial treatment modality for cancer.

Authors : Bhat Sajad A, Vedpathak Disha Mohan, Chiplunkar Shubhada V,

(5) Blimp-1 induces and Hobit maintains the cytotoxic mediator granzyme B in CD8 T cells.[TOP]

Pubmed ID :30051906
Publication Date : //
CD8 T cells acquire cytotoxic molecules including granzyme B during effector differentiation. Both tissue-resident memory CD8 T cells (Trm) and circulating CD45RA+ effector-type T cells (Temra) cells have the ability to retain granzyme B protein expression into the memory phase, but it is unclear how this persistence of cytolytic activity is regulated during steady state. Previously, we have described that the transcriptional regulators Hobit and Blimp-1 have overlapping target genes that include granzyme B, but their impact on the regulation of cytotoxicity in Trm and Temra cells during homeostasis has remained unclear. We examined the expression regulation of Hobit and Blimp-1 in murine and human CD8 T-cells to determine their timeframe of activity. While Blimp-1 mRNA was expressed throughout effector and memory T cells, Blimp-1 protein, was only transiently expressed during the effector stage. In contrast, Hobit mRNA and protein expression was stably maintained during quiescence, but downregulated after activation. Notably, Blimp-1 was required for expression of granzyme B in murine effector T cells and Trm, while Hobit specifically regulated granzyme B in murine Trm during the memory phase. These findings suggest that Blimp-1 initiates cytotoxic effector function and that Hobit maintains cytotoxicity in a deployment-ready modus in Trm. This article is protected by copyright. All rights reserved.

Authors : Kragten Natasja A M, Behr Felix M, Vieira Braga Felipe A, Remmerswaal Ester B M, Wesselink Thomas H, Oja Anna E, Hombrink Pleun, Kallies Axel, van Lier Rene A W, Stark Regina, van Gisbergen Klaas P J M,

(6) Antigen-Specific CD4CD8 Double-Positive T Cells Are Increased in the Blood and Spleen During Infection in the Canine Host.[TOP]

Pubmed ID :30050533
Publication Date : //
is an obligate intracellular bacterium belonging to the order, Rickettsiales and is a frequent cause of severe and fatal tick-borne infection in people in North America. The reservoir host for is the white-tailed deer, while humans and dogs are regarded as common incidental hosts. In dogs, we and others have shown that establishes a chronic infection that persists for several weeks to months, while promoting the development of Th1 and Th17 cellular responses and pathogen-specific humoral immunity. We demonstrate here that vaccination with a live, attenuated clone of bearing a targeted mutation in the Ech_0230 gene neither promotes the development of long-lived cellular or humoral immunity, nor confers protection against secondary wild-type challenge. In dogs, a population of mature CD4CD8 double-positive (DP) T cells exists in the periphery that shares similarities with the DP T cell populations that have been described in humans and swine. Little is known about the function of these cells, particularly in the context of infectious diseases. Here, we demonstrate that canine DP T cells expand significantly in response to infection. Using antigen recall assays, we further demonstrate that canine DP T cells undergo clonal expansion, produce IFNγ and IL-17, and upregulate expression of granzyme B and granulysin. Together, our results demonstrate that DP T cells accumulate in the host during infection, and suggest that alternative lymphocyte populations may participate in the immune response to tick-borne infections in the incidental host.

Authors : McGill Jodi L, Wang Ying, Ganta Chanran K, Boorgula Gunavanthi D Y, Ganta Roman R,

(7) Cytotoxic CD8 T cells recognize and kill Plasmodium vivax-infected reticulocytes.[TOP]

Pubmed ID :30038217
Publication Date : //
Plasmodium vivax causes approximately 100 million clinical malaria cases yearly. The basis of protective immunity is poorly understood and thought to be mediated by antibodies. Cytotoxic CD8 T cells protect against other intracellular parasites by detecting parasite peptides presented by human leukocyte antigen class I on host cells. Cytotoxic CD8 T cells kill parasite-infected mammalian cells and intracellular parasites by releasing their cytotoxic granules. Perforin delivers the antimicrobial peptide granulysin and death-inducing granzymes into the host cell, and granulysin then delivers granzymes into the parasite. Cytotoxic CD8 T cells were thought to have no role against Plasmodium spp. blood stages because red blood cells generally do not express human leukocyte antigen class I. However, P. vivax infects reticulocytes that retain the protein translation machinery. Here we show that P. vivax-infected reticulocytes express human leukocyte antigen class I. Infected patient circulating CD8 T cells highly express cytotoxic proteins and recognize and form immunological synapses with P. vivax-infected reticulocytes in a human leukocyte antigen-dependent manner, releasing their cytotoxic granules to kill both host cell and intracellular parasite, preventing reinvasion. P. vivax-infected reticulocytes and parasite killing is perforin independent, but depends on granulysin, which generally efficiently forms pores only in microbial membranes. We find that P. vivax depletes cholesterol from the P. vivax-infected reticulocyte cell membrane, rendering it granulysin-susceptible. This unexpected T cell defense might be mobilized to improve P. vivax vaccine efficacy.

Authors : Junqueira Caroline, Barbosa Camila R R, Costa Pedro A C, Teixeira-Carvalho Andréa, Castro Guilherme, Sen Santara Sumit, Barbosa Rafael P, Dotiwala Farokh, Pereira Dhelio B, Antonelli Lis R, Lieberman Judy, Gazzinelli Ricardo T,

(8) Skin resident memory CD8 T cells are phenotypically and functionally distinct from circulating populations and lack immediate cytotoxic function.[TOP]

Pubmed ID :30030847
Publication Date : //
The in depth understanding of skin resident memory CD8 T lymphocytes (T ) may help uncover strategies for their manipulation during disease. We investigated isolated T from healthy human skin, which expressed the residence marker CD69, and compared them to circulating CD8 T cell populations from the same donors. There were significantly increased proportions of CD8 CD45RA CD27 T cells in the skin that expressed low levels KLRG1, CD57, perforin and granzyme B. The CD8 T in skin were therefore phenotypically distinct from circulating CD8 CD45RA CD27 T cells that expressed high levels of all these molecules. Nevertheless the activation of CD8 T with TCR/CD28 or IL-2 or IL-15 in vitro induced the expression of granzyme B. Blocking signaling through the inhibitory receptor PD-1 further boosted granzyme B expression. A unique feature of some CD8 T cells was their ability to secrete high levels of TNF-α and IL-2, a cytokine combination that was not frequently seen in circulating CD8 T cells. The cutaneous CD8 T are therefore diverse and appear to be phenotypically and functionally distinct from circulating cells. Indeed, the surface receptors used to distinguish differentiation stages of blood T cells cannot be applied to T cells in the skin. Furthermore the function of cutaneous T appears to be stringently controlled by environmental signals in situ. This article is protected by copyright. All rights reserved.

Authors : Seidel J A, Vukmanovic-Stejic M, Muller-Durovic B, Patel N, Fuentes-Duclan J, Henson S M, Krueger J G, Rustin M H A, Nestle F O, Lacy K E, Akbar A N,

(9) Early effector maturation of naïve human CD8 T cells requires mitochondrial biogenesis.[TOP]

Pubmed ID :30028501
Publication Date : //
The role of mitochondrial biogenesis during naïve to effector differentiation of CD8 T cells remains ill explored. In this study, we describe a critical role for early mitochondrial biogenesis in supporting cytokine production of nascent activated human naïve CD8 T cells. Specifically, we found that prior to the first round of cell division activated naïve CD8 T cells rapidly increase mitochondrial mass, mitochondrial respiration, and mitochondrial reactive oxygen species (mROS) generation, which were all inter-linked and important for CD8 T cell effector maturation. Inhibition of early mitochondrial biogenesis diminished mROS dependent IL-2 production - as well as subsequent IL-2 dependent TNF, IFN-γ, perforin, and granzyme B production. Together, these findings point to the importance of mitochondrial biogenesis during early effector maturation of CD8 T cells.

Authors : Fischer Marco, Bantug Glenn R, Dimeloe Sarah, Gubser Patrick M, Burgener Anne-Valérie, Grählert Jasmin, Balmer Maria L, Develioglu Leyla, Steiner Rebekah, Unterstab Gunhild, Sauder Ursula, Hoenger Gideon, Hess Christoph,

(10) Deep Profiling of the CD8+ T cell Compartment identifies Activated cell subsets and Multifunctional Responses Associated with Control of Cytomegalovirus Viremia.[TOP]

Pubmed ID :30028417
Publication Date : //
Human cytomegalovirus (HCMV) is a common opportunistic pathogen in transplant recipients. Patterns of viremia and reactivation are influenced by the host immune response, including CD8 T cells. However, the cellular deficits or phenotypic differences that account for differential outcomes during HCMV viremia are incompletely understood.

Authors : Ferreira Victor H, Kumar Deepali, Humar Atul,