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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)

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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), kit
More informations about Granzyme B, Human, 1.3_960 U_ml, ELISA Kit, includes Mab coating Ab, control, standard, Biotin secondary, HRP_Streptavidin, buffer, substrate (No plate) in Antibody-antibodies.com

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(1) IL-10 producing CD8 CD122 PD-1 regulatory T cells are expanded by dendritic cells silenced for Allograft Inflammatory Factor-1.[TOP]

Pubmed ID :30512224
Publication Date : //
Allograft Inflammatory Factor-1 (AIF1) is a cytoplasmic scaffold protein that contains Ca binding EF-hand and PDZ interaction domains important for mediating intracellular signaling complexes in immune cells. The protein plays a dominant role in both macrophage- and dendritic cell (DC)-mediated inflammatory responses. This study now reports that AIF1 expression in DC is important in directing CD8 T cell effector responses. Silencing AIF1 expression in murine CD11c DC suppressed antigen-specific CD8 T cell activation, marked by reduced CXCR3, IFNγ and Granzyme B expression, and restrained proliferation. These primed CD8 T cells had impaired cytotoxic killing of target cells in vitro. In turn, studies identified that AIF1 silencing in DC robustly expanded IL-10 producing CD8 CD122 PD-1 regulatory T cells that suppressed neighboring immune effector responses through both IL-10 and PD-1-dependent mechanisms. In vivo studies recapitulated bystander suppression of antigen-responsive CD4 T cells by the CD8 Tregs expanded from the AIF1 silenced DC. These studies further demonstrate that AIF1 expression in DC serves as a potent governor of cognate T cell responses and present a novel target for engineering tolerogenic DC-based immunotherapies.

Authors : Elizondo Diana M, Andargie Temesgen E, Haddock Naomi L, da Silva Ricardo L Louzada, de Moura Tatiana Rodrigues, Lipscomb Michael W,



(2) Immunity Against Infection: Parasite-Specific Granzyme B Induction as a Correlate of Protection.[TOP]

Pubmed ID :30483482
Publication Date : //
Zoonotic cutaneous leishmaniasis (ZCL) caused by infection is characterized by different clinical presentations which depend in part on the host factors. In attempt to investigate the impact of the host's immune response in the outcome of the disease, we conducted a prospective study of 453 individuals living in endemic foci of transmission in Central Tunisia. Several factors were assessed at the baseline including (i) the presence of typical scars of ZCL, (ii) hypersensitivity reaction to leishmanin, and (iii) the release of granzyme B (Grz B) by peripheral blood mononuclear cells (PBMC) in response to stimulation with live promastigotes. After one season of parasite's transmission, repeated clinical examinations allowed us to diagnose the new emerging ZCL cases. Heterogeneity was observed in terms of number of lesions developed by each individual as well as their size and spontaneous outcome, which led us to establish the parameter "severity of the disease." The efficacy of the presence of typical ZCL scar, the leishmanin skin test (LST) positive reactivity and the high levels of Grz B (≥2 ng/ml), in the protection against the development of ZCL were 29, 15, and 22%, respectively. However, these factors were more efficient against development of intermediate or severe forms of ZCL. Levels of Grz B >2 ng/ml showed the best efficacy of protection (equals to 72.8%) against development of these forms of ZCL. The association of such parameter with the positivity of the LST exhibited a better efficacy (equals to 83.6%). In conclusion, our results support the involvement of -specific cytotoxic cellular immune response in host protection against -infection. This factor could be of great interest in monitoring the success of vaccination against human leishmaniasis.

Authors : Boussoffara Thouraya, Chelif Sadok, Ben Ahmed Melika, Mokni Mourad, Ben Salah Afif, Dellagi Koussay, Louzir Hechmi,



(3) Increased circulating granzyme B in type 2 diabetes patients with low-grade systemic inflammation.[TOP]

Pubmed ID :30473178
Publication Date : //
In metabolic diseases, like type 2 diabetes (T2D), adipose tissue (AT) is infiltrated by macrophages and other leukocytes - which secrete many bioactive peptides leading to local and systemic low-grade chronic inflammation - and undergoes remodeling and aberrant fibrosis. Granzyme B (GrB) is a serine protease produced by some leukocytes, including cytotoxic lymphocytes and macrophages. It exerts both intracellular apoptotic function and extracellular functions, leading to tissue injury, inflammation and repair. Elevated circulating GrB levels have been found in aging- and inflammation-associated diseases and a role for GrB in the pathogenesis of several chronic inflammatory diseases has been reported. Aims of this study were to investigate circulating GrB levels in T2D patients in relation to their systemic inflammatory profile and to unravel its correlates. For this cross-sectional study, we recruited 51 consecutive T2D patients referring to our diabetes outpatient clinics (Sapienza University, Rome, Italy) for metabolic evaluations, and 29 sex, age and body mass index comparable non-diabetic subjects as control group. Study participants underwent clinical work-up; fasting blood sampling was performed for routine biochemistry and for inflammatory profile (CRP, IL-2, IL-4, IL-6, IL-8, IL-10, TNF-α, IFN-γ, GM-CSF, adiponectin, WISP1); serum GrB was measured by Human Granzyme-B Platinum Elisa kit (Affymetrix EBIO). We found that T2D patients had serum levels of GrB significantly higher than the control group (10.17 ± 12.6 vs 7.2 ± 14.1 pg/ml, p = 0.03). Moreover, in T2D patients increased GrB correlated with unfavorable inflammatory profile, as described by elevated levels of validated adipokines such as IL-6 (p = 0.04), TNF-α (p = 0.019) and WISP1 (p = 0.005). Furthermore, multivariate linear regression analysis showed that increased GrB was associated with T2D diagnosis independently from possible confounders. In conclusion, our results show that increased levels of circulating GrB are associated with T2D diagnosis and correlates with markers of AT-linked systemic inflammation, suggesting a potential role for GrB in the inflammatory and reactive processes occurring in metabolic diseases.

Authors : Cimini Flavia Agata, D'Eliseo Donatella, Barchetta Ilaria, Bertoccini Laura, Velotti Francesca, Cavallo Maria Gisella,



(4) Immune response and evasion mechanisms in lip carcinogenesis: An immunohistochemical study.[TOP]

Pubmed ID :30468994
Publication Date : //
Programmed death ligand-1 (PD-L1) and human leukocyte antigen-G (HLA-G) are considered immune checkpoint molecules that inhibit T-cell effectiveness, contributing to tumor immune escape. This study investigated PD-L1, HLA-G, CD8, and granzyme B (GrB) expression at different stages of lip carcinogenesis.

Authors : Lopes Maria Luiza Diniz de Sousa, Gonzaga Amanda Katarinny Goes, Mosconi Carla, Palomino Gustavo Martelli, Mendonça Elismauro Francisco, Batista Aline Carvalho, Silveira Éricka Janine Dantas da,



(5) Resistance to anti-PD-1-based immunotherapy in basal cell carcinoma: a case report and review of the literature.[TOP]

Pubmed ID :30458852
Publication Date : //
Immunotherapy with immune checkpoint inhibitors has radically changed the management of a broad spectrum of tumors. In contrast, only very limited information is available about the efficacy of these therapies in non-melanoma skin cancers, especially in basal cell carcinoma. The latter malignancy is often associated with both an impairment of the host immune response and a high mutation burden, suggesting that immune checkpoint inhibitor-based immunotherapy may be effective in the treatment of this tumor.

Authors : Sabbatino Francesco, Marra Antonio, Liguori Luigi, Scognamiglio Giosuè, Fusciello Celeste, Botti Gerardo, Ferrone Soldano, Pepe Stefano,



(6) The injectable contraceptive medroxyprogesterone acetate attenuates Mycobacterium tuberculosis-specific host immunity through the glucocorticoid receptor.[TOP]

Pubmed ID :30452655
Publication Date : //
The effects of the widely used progestin-only injectable contraceptives, medroxyprogesterone acetate (MPA) and norethisterone acetate (NET-A), on host susceptibility to Mycobacterium tuberculosis (M.tb) are unknown.

Authors : Tomasicchio Michele, Davids Malika, Pooran Anil, Theron Grant, Smith Liezel, Semple Lynn, Meldau Richard, Hapgood Janet Patricia, Dheda Keertan,



(7) Deficiency of the T cell regulator Casitas B-cell lymphoma-B aggravates atherosclerosis by inducing CD8+ T cell-mediated macrophage death.[TOP]

Pubmed ID :30452556
Publication Date : //
The E3-ligase CBL-B (Casitas B-cell lymphoma-B) is an important negative regulator of T cell activation that is also expressed in macrophages. T cells and macrophages mediate atherosclerosis, but their regulation in this disease remains largely unknown; thus, we studied the function of CBL-B in atherogenesis.

Authors : Seijkens Tom T P, Poels Kikkie, Meiler Svenja, van Tiel Claudia M, Kusters Pascal J H, Reiche Myrthe, Atzler Dorothee, Winkels Holger, Tjwa Marc, Poelman Hessel, Slütter Bram, Kuiper Johan, Gijbels Marion, Kuivenhoven Jan Albert, Matic Ljubica Perisic, Paulsson-Berne Gabrielle, Hedin Ulf, Hansson Göran K, Nicolaes Gerry A F, Daemen Mat J A P, Weber Christian, Gerdes Norbert, de Winther Menno P J, Lutgens Esther,



(8) Role of Natural Killer T (NKT) Cells in Type II Diabetes-Induced Vascular Injuries.[TOP]

Pubmed ID :30451213
Publication Date : //
BACKGROUND This study investigated the distribution and features of natural killer T (NKT) cells in the peripheral blood of diabetic patients, and their regulatory roles on vascular endothelial cells. MATERIAL AND METHODS Peripheral lymphocytes were isolated from diabetic patients. NKT cell distribution, proportion, and surface and intracellular markers were detected with flow cytometry. Peripheral blood-derived NKT cells were isolated and co-cultured with human umbilical vein endothelial cells (HUVECs). Proliferation and migration of HUVECs were assessed with the CCK-8 assay and the Transwell chamber assay. RESULTS The ratios of CD3-CD56+ NK and CD3+CD56+ NKT cells in the peripheral blood of patients with type II diabetes were significantly elevated. The expression levels of NKp30, NKG2D, and NKp44 on the surface were increased in the CD3+CD56+ NKT cells, while the expression levels of NKG2A and 158b were significantly downregulated. The expression level of granzymes in the peripheral blood-derived NKT cells were not changed in patients with type II diabetes, but the expression levels of IFNg and IL-4 were significantly increased. However, after co-culture with NKT cells derived from the peripheral blood of diabetic patients, the proliferation and migration of HUVECs were significantly inhibited, and was restored by treatment with IL-4 antibody. In addition, the IL-4 stimulus inhibited the proliferation and migration of HUVECs. ls were not changed in patients with type II diabetes, while the expression levels of IFNγ and IL-4 were significantly increased. However, after co-cultured with NKT cells derived from the peripheral blood of diabetic patients, the proliferation and migration of HUVECs were significantly inhibited, which could significantly restored by the treatment of IL-4 antibody. In addition, the IL-4 stimulus could down-regulate the proliferation and migration of HUVECs.  CONCLUSIONS Peripheral blood NKT cells are increased and activated in diabetes. NKT cells inhibit the proliferation and migration of HUVECs by secreting IL-4, thereby inducing vascular injuries.

Authors : Lv Xiaohong, Gao Yun, Dong Tantan, Yang Libo,



(9) Helper CD4 T cells expressing granzyme B cause glial fibrillary acidic protein fragmentation in astrocytes in an MHCII-independent manner.[TOP]

Pubmed ID :30444064
Publication Date : //
During inflammatory processes of the central nervous system, helper T cells have the capacity to cross the blood-brain barrier and injure or kill neural cells through cytotoxic mechanisms. Glial fibrillary acidic protein (GFAP) is an intermediate filament protein that is part of the astrocyte cytoskeleton that can become fragmented in neuroinflammatory conditions. The mechanism of action by which helper T cells with cytotoxic properties injure astrocytes is not completely understood. Primary human astrocytes were obtained from fetal brain tissue. Human helper (CD4 ) T cells were isolated from peripheral blood mononuclear cells and activated with the superantigen staphylococcal enterotoxin E (SEE). Granzyme B was detected by enzyme linked immunosorbent assay and intracellular flow cytometry. GFAP fragmentation was monitored by western blotting. Cell death was monitored by lactic acid dehydrogenase release and terminal biotin-dUTP nick labeling (TUNEL). Astrocyte migration was monitored by scratch assay. Adult human oligodendrocytes were cultured with sublethally injured astrocytes to determine support function. Helper T cells activated with SEE expressed granzyme B but not perforin. Helper T cells released granzyme B upon contact with astrocytes and caused GFAP fragmentation in a caspase-dependent, MHCII-independent manner. Sublethally injured astrocytes were not apoptotic; however, their processes were thin and elongated, their migration was attenuated, and their ability to support oligodendrocytes was reduced in vitro. Helper T cells can release granzyme B causing sublethal injury to astrocytes, which compromises the supportive functions of astrocytes. Blocking these pathways may lead to improved resolution of neuroinflammatory lesions.

Authors : Stopnicki Brandon, Blain Manon, Cui Qiao-Ling, Kennedy Timothy E, Antel Jack P, Healy Luke M, Darlington Peter J,



(10) Decrease in Intracellular Perforin Levels and IFN- Production in Human CD8 T Cell Line following Long-Term Exposure to Asbestos Fibers.[TOP]

Pubmed ID :30426024
Publication Date : //
Although the tumorigenicity of asbestos, which is thought to cause mesothelioma, has been clarified, its effect on antitumor immunity requires further investigation. We previously reported a decrease in the percentage of perforin cells of stimulated CD8 lymphocytes derived from patients with malignant mesothelioma. Therefore, we examined the effects of long-term exposure to asbestos on CD8 T cell functions by comparing long-term cultures of the human CD8 T cell line EBT-8 with and without exposure to chrysotile (CH) asbestos as an model. Exposure to CH asbestos at 5 g/ml or 30 g/ml did not result in a decrease in intracellular granzyme B in EBT-8 cells. In contrast, the percentage of perforin cells decreased at both doses of CH exposure. CH exposure at 30 g/ml did not suppress degranulation following stimulation with antibodies to CD3. Secreted production of IFN- stimulated via CD3 decreased by CH exposure at 30 g/ml, although the percentage of IFN- cells induced by PMA/ionomycin did not decrease. These results indicate that long-term exposure to asbestos can potentially suppress perforin levels and the production of IFN- in human CD8 T cells.

Authors : Kumagai-Takei Naoko, Nishimura Yasumitsu, Matsuzaki Hidenori, Lee Suni, Yoshitome Kei, Otsuki Takemi,