Academic literature on the topic 'ST2 antibodies'
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Journal articles on the topic "ST2 antibodies"
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Miller, Ashley M., Damo Xu, Darren L. Asquith, Laura Denby, Yubin Li, Naveed Sattar, Andrew H. Baker, Iain B. McInnes, and Foo Y. Liew. "IL-33 reduces the development of atherosclerosis." Journal of Experimental Medicine 205, no. 2 (February 11, 2008): 339–46. http://dx.doi.org/10.1084/jem.20071868.
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Atherosclerosis is a chronic inflammatory disease of the vasculature commonly leading to myocardial infarction and stroke. We show that IL-33, which is a novel IL-1–like cytokine that signals via ST2, can reduce atherosclerosis development in ApoE−/− mice on a high-fat diet. IL-33 and ST2 are present in the normal and atherosclerotic vasculature of mice and humans. Although control PBS-treated mice developed severe and inflamed atherosclerotic plaques in the aortic sinus, lesion development was profoundly reduced in IL-33–treated animals. IL-33 also markedly increased levels of IL-4, -5, and -13, but decreased levels of IFNγ in serum and lymph node cells. IL-33 treatment also elevated levels of total serum IgA, IgE, and IgG1, but decreased IgG2a, which is consistent with a Th1-to-Th2 switch. IL-33–treated mice also produced significantly elevated antioxidized low-density lipoprotein (ox-LDL) antibodies. Conversely, mice treated with soluble ST2, a decoy receptor that neutralizes IL-33, developed significantly larger atherosclerotic plaques in the aortic sinus of the ApoE−/− mice compared with control IgG-treated mice. Furthermore, coadministration of an anti–IL-5 mAb with IL-33 prevented the reduction in plaque size and reduced the amount of ox-LDL antibodies induced by IL-33. In conclusion, IL-33 may play a protective role in the development of atherosclerosis via the induction of IL-5 and ox-LDL antibodies.
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Liu, Boyi, Yan Tai, Satyanarayana Achanta, Melanie M. Kaelberer, Ana I. Caceres, Xiaomei Shao, Jianqiao Fang, and Sven-Eric Jordt. "IL-33/ST2 signaling excites sensory neurons and mediates itch response in a mouse model of poison ivy contact allergy." Proceedings of the National Academy of Sciences 113, no. 47 (November 7, 2016): E7572—E7579. http://dx.doi.org/10.1073/pnas.1606608113.
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Poison ivy-induced allergic contact dermatitis (ACD) is the most common environmental allergic condition in the United States. Case numbers of poison ivy ACD are increasing due to growing biomass and geographical expansion of poison ivy and increasing content of the allergen, urushiol, likely attributable to rising atmospheric CO2. Severe and treatment-resistant itch is the major complaint of affected patients. However, because of limited clinical data and poorly characterized models, the pruritic mechanisms in poison ivy ACD remain unknown. Here, we aim to identify the mechanisms of itch in a mouse model of poison ivy ACD by transcriptomics, neuronal imaging, and behavioral analysis. Using transcriptome microarray analysis, we identified IL-33 as a key cytokine up-regulated in the inflamed skin of urushiol-challenged mice. We further found that the IL-33 receptor, ST2, is expressed in small to medium-sized dorsal root ganglion (DRG) neurons, including neurons that innervate the skin. IL-33 induces Ca2+ influx into a subset of DRG neurons through neuronal ST2. Neutralizing antibodies against IL-33 or ST2 reduced scratching behavior and skin inflammation in urushiol-challenged mice. Injection of IL-33 into urushiol-challenged skin rapidly exacerbated itch-related scratching via ST2, in a histamine-independent manner. Targeted silencing of neuronal ST2 expression by intrathecal ST2 siRNA delivery significantly attenuated pruritic responses caused by urushiol-induced ACD. These results indicate that IL-33/ST2 signaling is functionally present in primary sensory neurons and contributes to pruritus in poison ivy ACD. Blocking IL-33/ST2 signaling may represent a therapeutic approach to ameliorate itch and skin inflammation related to poison ivy ACD.
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YOSHIDA, KAZUKO, TAKAO ARAI, TAKASHI YOKOTA, NORIO KOMATSU, YASUSADA MIURA, KEN YANAGISAWA, TSUNAO TETSUKA, and SHIN-ICHI TOMINAGA. "Studies on Natural ST2 Gene Products in the Human Leukemic Cell Line UT-7 Using Monoclonal Antihuman ST2 Antibodies." Hybridoma 14, no. 5 (October 1995): 419–27. http://dx.doi.org/10.1089/hyb.1995.14.419.
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Chen, Mengjiao, Peijun Ding, Lili Yang, Xufeng He, Chunjie Gao, Guoxun Yang, and Huimin Zhang. "Evaluation of Anti-Inflammatory Activities of Qingre-Qushi Recipe (QRQS) against Atopic Dermatitis: Potential Mechanism of Inhibition of IL-33/ST2 Signal Transduction." Evidence-Based Complementary and Alternative Medicine 2017 (2017): 1–11. http://dx.doi.org/10.1155/2017/2489842.
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To evaluate the anti-inflammatory activities of QRQS against AD and the inhibitory molecular mechanisms of IL-33/ST2 signal transduction, BALB/c mice were divided into six groups (normal control, OVA control, low-dose of QRQS, middle-dose of QRQS, high-dose of QRQS, and cetirizine) and epicutaneously exposed to ovalbumin or PBS for 3 weeks and treated with QRQS for 2 weeks. Skin biopsies and blood samples were obtained for histological study, antibody analysis, and RNA isolation. HaCaT cells, stimulated by TNF-α and IFN-γ, were treated with QRQS to evaluate mRNA and protein expression by RT-PCR and ELISA. QRQS decreased both epidermal and dermal thickness, alleviated dermatitis, and reduced IL-33 and ST2 positive cell numbers. The concentration of specific IgE, IgG, IgG1, and IgG2a antibodies in serum and the expression of IL-33, ST2, IL-1RAcP, IL-4, and IL-13 mRNA in the skin were suppressed. No significant difference exists in TNF-α or IFN-γ. QRQS decreased IL-33 mRNA and protein secretion in HaCaT cells exposed to TNF-α and IFN-γ in a time- and concentration-dependent manner. QRQS regulates related molecule expression of ovalbumin-induced dermatitis involved in the IL-33/ST2 signaling axis in the treatment of acute AD.
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Martin, Rebecca, Joseph Cornelius Lownik, Jared Farrar, Grayson Way, Matthew Zellner, Bin Ni, Francesco Celi, and Daniel H. Conrad. "Loss of ADAM17 from macrophages induces ST2+ T regulatory cells that limit obesity-induced metabolic inflammation in mice through changes in both membrane and soluble TNF." Journal of Immunology 208, no. 1_Supplement (May 1, 2022): 46.14. http://dx.doi.org/10.4049/jimmunol.208.supp.46.14.
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Abstract Obesity is known to contribute to changes in immune cells, cytokines and metabolism. Secreted TNF (sTNF) levels are directly correlated in obesity with weight gain and morbidity, as well as metabolic dysregulation. ADAM17 cleaves transmembrane TNF (mTNF) into its soluble form. This is well defined, but the mechanism behind the regulation of TNF, the source of TNF, as well as the downstream action of TNF is less clear. Our data showed that mice with ADAM17 deleted from the myeloid lineage (ADAM17LysM) had a significant metabolic advantage as illustrated by an increase in glucose tolerance and decrease in body weight. Immunophenotyping of the fatpad of these mice using high dimensional flow cytometry after high fat diet (HFD) feeding showed an increase in activated ST2+ T regulatory cells (Tregs). Based on these findings, we hypothesized that modulation of TNF on macrophages through loss of ADAM17, helps maintain a healthy metabolic state through recruitment and activation of ST2+ Treg cells that limit metabolic dysregulation. Next, we showed that the accumulation and activation of these Tregs occurred through two separate mechanistic actions of TNF. First, the loss of sTNF production from macrophages decreased soluble ST2 (sST2) production by adipocytes. This loss of sST2 augments ST2+ Treg recruitment and expansion in the fatpad due to increased bioavailable IL-33. These experiments were controlled using a myeloid-specific knockout of TNF. Second, utilizing TNFR blocking antibodies, we demonstrated that ST2+ Treg activation was dependent on macrophage mTNF acting through TNFR2. Supported by grants from NIH (R56 AI139658 and R01 AI018697)
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Fu, Denggang, Hua Jiang, Alan Long, Hong fen Guo, Maegan L. Capitano, Baskar Ramdas, Reuben Kapur, Nai-Kong V. Cheung, and Sophie Paczesny. "Immunotherapy Targeting ST2/IL-33 Signaling in Myeloid Leukemia Stem Cells." Blood 138, Supplement 1 (November 5, 2021): 23. http://dx.doi.org/10.1182/blood-2021-149672.
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Abstract Therapies for acute myeloid leukemia (AML) has barely changed over 30 years, while treatment for other blood cancers have made remarkable leaps forward. Recent advances in genomics have allowed molecular targeted therapies (i.e. FLT3-ITD, IDH, c-KIT inhibitors) extending survival, but most patients still succumb (Burd et al. Nat Med 2020). Therefore, developing more efficient, less toxic, and immune-based therapies for AML is an urgent unmet need. Previous studies showed that stromal cell-derived IL-33 stimulates myeloproliferative neoplasms (Mager et al. J Clin Invest 2015). Stimulation-2 (ST2), IL-33 receptor, contributes to leukemia stem cells (LSCs) survival in Cbfb-MYH11 mice (Wang et al . Sci Rep 2019). We showed that ST2 blockade enhanced graft versus leukemia activity against MLL-AF9 egfp AML after hematopoietic cell transplantation (Zhang et al . Sci Transl Med 2015). We and others, also, found that ST2 is expressed on normal murine and human hematopoietic stem cells (HSCs), respectively (Capitano et al. Blood Cells Mol Dis 2020; Alt et al. Biol Blood Marrow Transplant 2019). These data suggest a leukemia-promoting role of ST2/IL-33 signaling. To determine clinical relevance of ST2 in AML, we generated Kaplan-Meier curves using TCGA (n=173) and TARGET AML (n=187) databases. Decreased survival was observed in patients with high IL1RL1 (ST2 gene) which was validated in an independent database (AMLCG 1999 trial, n=417) (Fig. 1A). Since ST2 is expressed on HSCs, we interrogated if ST2 is expressed on LSCs defined as CD34 +CD38 - in the Princess Margaret Leukemia biobank (n=192), and found ST2 is higher on LSCs vs CD34 -CD38 +/- cells (Fig. 1B). We then sought to analyze ST2 on bone marrow samples comparing complete responders vs refractory patients to note that ST2 expression was increased in refractory patients' LSCs (Fig. 1C). To scrutinize the role of ST2 in initiating leukemogenesis, we performed limiting dilution transplantation using 500, 200, and 50 Lin -Sca-1 +c-KIT +-sorted LSCs from WT vs ST2 -/- MLL-AF9 egfp transduced cells. Frequency of LSCs in ST2 -/- cells was decreased by ~15-fold as opposed to WT cells [1:2141 (1:546-1:8405) vs 1:145 (1:75-1:283), p=3.37e-05] (Fig. 2A). We also tested leukemia maintenance, secondary transplantations from the primary recipients resulted in leukemia growth delay in ST2 -/- vs WT cells which was confirmed in tertiary transplantations (Fig. 2B-E). Self-renewal ability of LSCs is correlated to reactive oxygen species (ROS) (Testa et al. Exp Hematol 2016), and we found that ROS levels in ST2 -/- leukemic cells are markedly diminished in contrast to WT leukemic cells (Fig. 2F). ST2 deficiency in leukemic cells arrests G2/S/M cell cycle progression in LSCs (Fig. 2G-J). These data indicated that ST2 is indispensable for initiating and maintaining LSCs in MLL-AF9 AML. We next developed murine and human Fc-silenced-bispecific antibodies engaging mouse or human ST2 and CD3 (BsAb) built on the IgG[L]-scFv platform with proven ability to drive T cells into human tumors for effective tumor ablation (Santich et al. Sci Transl Med 2020; Park et al. J Immunother Cancer 2021) (Fig. 3A, 3E). Both BsAbs showed >90% purity by HPLC, stability under heat stress and low endotoxin. Animals did not exhibit any in vivo toxicity at BsAb doses of 0.4, 2, 5, 10 μg ip q 3 days x 6 doses (not shown). In the immunocompetent MLL-AF9 mice, murine anti-ST2 BsAb (BC281) treatment (10 μg i.p, 4 days post-AML challenge and given every three days for a total of 6 injections) resulted in extended survival compared to isotype control mice (Fig. 3B). Leukemic cells and LSCs were accordingly decreased in treated vs control group (Fig. 3C-D). We modeled humanized leukemic mice with MOLM-14 egfp cells and weekly injection of human CD8 + T cells in NOD.Cg-Prkdc scid Il2rg tm1Wjl/SzJ (NSG) mice (Fig. 3F). Animals treated with human anti-ST2 BsAb (BC282), using a similar regimen as for the immunocompetent model, led to better survival when compared to animals treated with mutated non-functional anti-ST2 BsAb (BC283) (Fig. 3G). Frequency of MOLM-14 egfp cells was lower in the BC282 vs BC283 group (Fig. 3H). These results suggested that anti-ST2 BsAbs can inhibit AML growth to improve survival. We concluded that ST2 is a potential therapeutic target, and ST2-specific T cell engaging BsAbs represent promising immunotherapeutics for AML. Figure 1 Figure 1. Disclosures Cheung: Medical University of South Carolina: Patents & Royalties: inventor on the ST2 bispecific antibody patent application; Y-mabs Therapeutics and Abpro-Labs Inc: Patents & Royalties: inventor on multiple patents filed by MSK, including those licensed to Ymabs Therapeutics, Biotec Pharmacon, and Abpro-labs; Eureka Therapeutics: Membership on an entity's Board of Directors or advisory committees. Paczesny: Medical University of South Carolina: Patents & Royalties: inventor on the ST2 bispecific antibody patent application.
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Huang, Qiong, Chen Duo Li, Yi Ran Yang, Xiao Feng Qin, Jing Jing Wang, Xin Zhang, Xiao Nan Du, et al. "Role of the IL-33/ST2 axis in cigarette smoke-induced airways remodelling in chronic obstructive pulmonary disease." Thorax 76, no. 8 (February 15, 2021): 750–62. http://dx.doi.org/10.1136/thoraxjnl-2020-214712.
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BackgroundEfficient therapy and potential prophylaxis are confounded by current ignorance of the pathogenesis of airway remodelling and blockade in COPD.ObjectiveTo explore the role of the IL-33/ST2 axis in cigarette smoke (CS) exposure-induced airways remodelling.MethodsC57BL/6, BALB/c and IL-1RL1-/- mice exposed to CS were used to establish an animal surrogate of COPD (air-exposed=5~8, CS-exposed=6~12). Hallmarks of remodelling were measured in mice. Cigarette smoke extract (CSE)-induced proliferation and protein production in vitro by fibroblasts in the presence of anti-interleukin-33 (anti-IL-33) or hST2 antibodies were measured. Expression of IL-33 and ST2 and other remodelling hallmarks were measured, respectively, in bronchoalveolar lavage fluid (BALF) (controls=20, COPD=20), serum (controls=59, COPD=90) and lung tissue sections (controls=11, COPD=7) from patients with COPD and controls.ResultsWild-type mice exposed to CS elevated expression of hallmarks of tissue remodelling in the lungs and also in the heart, spleen and kidneys, which were significantly abrogated in the IL-1RL1-/- mice. Fibroblasts exposed to CSE, compared with control, exhibited early cellular translocation of IL-33, accompanied by proliferation and elevated protein synthesis, all inhabitable by blockade of IL-33/ST2 signalling. Expression of IL-33 and ST2 and hallmarks of tissue remodelling were significantly and proportionally elevated in BALF, serum and tissue samples from patients with COPD.ConclusionsExposure to CS induces remodelling changes in multiple organs. The data support the hypothesis that CS-induced lung collagen deposition is at least partly a result of CS-induced IL-33 translocation and release from local fibroblasts.
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Mohd Jaya, Fatin Nurizzati, Zhongyi Liu, and Godfrey Chi-Fung Chan. "Early Treatment of Interleukin-33 can Attenuate Lupus Development in Young NZB/W F1 Mice." Cells 9, no. 11 (November 10, 2020): 2448. http://dx.doi.org/10.3390/cells9112448.
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Interleukin-33 (IL-33), a member of the IL-1 cytokine family, has been recently associated with the development of autoimmune diseases, including systemic lupus erythematosus (SLE). IL-33 is an alarmin and a pleiotropic cytokine that affects various types of immune cells via binding to its receptor, ST2. In this study, we determine the impact of intraperitoneal IL-33 treatments in young lupus, NZB/W F1 mice. Mice were treated from the age of 6 to 11 weeks. We then assessed the proteinuria level, renal damage, survival rate, and anti-dsDNA antibodies. The induction of regulatory B (Breg) cells, changes in the level of autoantibodies, and gene expression were also examined. In comparison to the control group, young NZB/W F1 mice administered with IL-33 had a better survival rate as well as reduced proteinuria level and lupus nephritis. IL-33 treatments significantly increased the level of IgM anti-dsDNA antibodies, IL-10 expressing Breg cells, and alternatively-induced M2 macrophage gene signatures. These results imply that IL-33 exhibits a regulatory role during lupus onset via the expansion of protective IgM anti-dsDNA as well as regulatory cells such as Breg cells and M2 macrophages.
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Michigami, Toshimi, Nobuaki Shimizu, Paul J. Williams, Maria Niewolna, Sarah L. Dallas, Gregory R. Mundy, and Toshiyuki Yoneda. "Cell–cell contact between marrow stromal cells and myeloma cells via VCAM-1 and α4β1-integrin enhances production of osteoclast-stimulating activity." Blood 96, no. 5 (September 1, 2000): 1953–60. http://dx.doi.org/10.1182/blood.v96.5.1953.
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Abstract Myeloma is a unique hematologic malignancy that exclusively homes in the bone marrow and induces massive osteoclastic bone destruction presumably by producing cytokines that promote the differentiation of the hematopoietic progenitors to osteoclasts (osteoclastogenesis). It is recognized that neighboring bone marrow stromal cells influence the expression of the malignant phenotype in myeloma cells. This study examined the role of the interactions between myeloma cells and neighboring stromal cells in the production of osteoclastogenic factors to elucidate the mechanism underlying extensive osteoclastic bone destruction. A murine myeloma cell line 5TGM1, which causes severe osteolysis, expresses α4β1-integrin and tightly adheres to the mouse marrow stromal cell line ST2, which expresses the vascular cell adhesion molecule-1 (VCAM-1), a ligand for α4β1-integrin. Co-cultures of 5TGM1 with primary bone marrow cells generated tartrate-resistant acid phosphatase-positive multinucleated bone-resorbing osteoclasts. Co-cultures of 5TGM1 with ST2 showed increased production of bone-resorbing activity and neutralizing antibodies against VCAM-1 or α4β1-integrin inhibited this. The 5TGM1 cells contacting recombinant VCAM-1 produced increased osteoclastogenic and bone-resorbing activity. The activity was not blocked by the neutralizing antibody to known osteoclastogenic cytokines including interleukin (IL)-1, IL-6, tumor necrosis factor, or parathyroid hormone-related peptide. These data suggest that myeloma cells are responsible for producing osteoclastogenic activity and that establishment of direct contact with marrow stromal cells via α4β1-integrin/VCAM-1 increases the production of this activity by myeloma cells. They also suggest that the presence of stromal cells may provide a microenvironment that allows exclusive colonization of myeloma cells in the bone marrow.
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Michigami, Toshimi, Nobuaki Shimizu, Paul J. Williams, Maria Niewolna, Sarah L. Dallas, Gregory R. Mundy, and Toshiyuki Yoneda. "Cell–cell contact between marrow stromal cells and myeloma cells via VCAM-1 and α4β1-integrin enhances production of osteoclast-stimulating activity." Blood 96, no. 5 (September 1, 2000): 1953–60. http://dx.doi.org/10.1182/blood.v96.5.1953.h8001953_1953_1960.
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Myeloma is a unique hematologic malignancy that exclusively homes in the bone marrow and induces massive osteoclastic bone destruction presumably by producing cytokines that promote the differentiation of the hematopoietic progenitors to osteoclasts (osteoclastogenesis). It is recognized that neighboring bone marrow stromal cells influence the expression of the malignant phenotype in myeloma cells. This study examined the role of the interactions between myeloma cells and neighboring stromal cells in the production of osteoclastogenic factors to elucidate the mechanism underlying extensive osteoclastic bone destruction. A murine myeloma cell line 5TGM1, which causes severe osteolysis, expresses α4β1-integrin and tightly adheres to the mouse marrow stromal cell line ST2, which expresses the vascular cell adhesion molecule-1 (VCAM-1), a ligand for α4β1-integrin. Co-cultures of 5TGM1 with primary bone marrow cells generated tartrate-resistant acid phosphatase-positive multinucleated bone-resorbing osteoclasts. Co-cultures of 5TGM1 with ST2 showed increased production of bone-resorbing activity and neutralizing antibodies against VCAM-1 or α4β1-integrin inhibited this. The 5TGM1 cells contacting recombinant VCAM-1 produced increased osteoclastogenic and bone-resorbing activity. The activity was not blocked by the neutralizing antibody to known osteoclastogenic cytokines including interleukin (IL)-1, IL-6, tumor necrosis factor, or parathyroid hormone-related peptide. These data suggest that myeloma cells are responsible for producing osteoclastogenic activity and that establishment of direct contact with marrow stromal cells via α4β1-integrin/VCAM-1 increases the production of this activity by myeloma cells. They also suggest that the presence of stromal cells may provide a microenvironment that allows exclusive colonization of myeloma cells in the bone marrow.
Dissertations / Theses on the topic "ST2 antibodies"
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Jonsson, Monica. "Sexually transmitted diseases and sexual behaviour among young Swedish women : a population-based study." Doctoral thesis, Umeå universitet, Allmänmedicin, 1998. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-96898.
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Most epidemiologic studies of sexually transmitted diseases (STD) are based on patients seeking help or advice at various health care settings. Because many STD:s are subclinical, epidemiologic surveys can be strengthened by a population-based approach. The aims of the present study were to investigate the prevalence and incidence of STDs in a population of young women, and to assess associations between STDs and social background, education, previous genital infections, sexual behaviour, contraceptive use and reproductive experience. All women belonging to the 19-, 21-, 23- and 25-year age cohorts and living in the catchment area of a community health center, were invited by mail to participate in the study. In the presence of the investigator, participants answered a structured questionaire regarding their social background, education, previous genital infections, sexual behaviour, contraceptive use and reproductive experience. A gynecologic examination was performed. Cervical scrapes for human papillomavirus (HPV) DNA, as well as samples for wet smear, cervical pap smear, and Chlamydia trachomatis (CT) culture were taken. The presence of genital warts was noted, and a colposcopy was performed 2-5 minutes after application of 5% acetic acid on the cervix and vulva. Acetowhite changes were then assessed. A serologic test for CT and herpes simplex virus type 2 (HSV-2) antibodies were performed. Of the 816 women available, 611 (75%) participated in the study. One out of four women reported symptoms from the lower genital tract. The most common were itching, followed by discharge and soreness. There was a significant correlation between the womens" complaint of vaginal discharge, and previous CT infection, lack of lactobacilli and the presence of leucocytosis in wet smear. Twenty-two percent of the women were HPV DNA positive and acetowhitening at the cervix was observed in 16% of the women. The sensitivity of detection of HPV infection by acetowhitening of the cervix was 22% (95%CI 18%, 26%), and the specificity was 90% (95% Cl 87%, 93%). C.trachomatis culture positivity was found in 2.7% of the women and the seroprevalence of CT was 24.7 %. Atypical cytology was found in 3.4% of the women and 6.6% was HSV-2 seropositiv. Of the women studied 23.6% reported having had at least one STD previously and the laboratory analysis showed 45.4% to have had at least one STD. Multivariate logistic regression analysis showed that the number of sexual partners, age at first coitus, history of therapeutic abortion, and previous pelvic inflammatory disease (PID) was independently correlated with CT seropositivity. Lifetime number of sexual partners was the only independent risk factor for HPV. Multivariate analysis showed that increasing age, early sexual debut, and a history of spontaneous abortion were independently related to the presence of HSV-2 antibodies. The lifetime number of sexual partners and coitus on first date were independently associated with a previous STD. Conclusion, We found that one out of four women had some kind of lower genital tract complaint, almost every other women had at sometime in their life an STD, and STDs were often asymptomatic. Acetowhitening of the cervix and vulva has low sensitivity, to low to warrant its use as a predictor of subclinical HPV infection. The pattern of risk factors differed between STDs.Härtill 6 uppsatser
digitalisering@umu
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Nierras, Ma Concepcion R. "Characterization of monoclonal antibodies against Escherichia coli ribosomal protein S12." 1990. http://catalog.hathitrust.org/api/volumes/oclc/23601203.html.
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Thesis (Ph. D.)--University of Wisconsin--Madison, 1990.Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 218-233).
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Brunner, David. "Why people fail to use condoms for STD and HIV prevention." 2009. http://digital.library.duq.edu/u?/etd,98265.
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Garcia, Carolina Yvette. "Immunogenicity characterization of enterotoxigenic Escherichia coli (ETEC) toxoid fusion and adhesin MEFA antigens in intradermally or intramuscularly immunized mice." Thesis, 2018. http://hdl.handle.net/2097/38870.
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Master of ScienceDepartment of Diagnostic Medicine/Pathobiology
Weiping Zhang
Enterotoxigenic Escherichia coli (ETEC) strains are the most common bacterial cause of diarrhea. ETEC bacterial adherence to the small intestinal epithelial cells and delivery of enterotoxins cause diarrhea in children living in developing countries and international travelers. Currently, there are no vaccines licensed for ETEC associated children’s diarrhea and travelers’ diarrhea. Recently, toxoid fusion 3xSTa[subscript N12S]-mnLT[subscript R192G/L211A] (toxoid fusion), adhesin MEFA (multiepitope fusion antigen) CFA/I/II/IV (CFA MEFA), and toxoid-adhesin MEFA CFA/I/II/IV-3xSTa[subscript N12S]-mnLT[subscript R192G/L211A] (CFA-toxoid MEFA) are demonstrated to induce neutralizing antitoxin and/or anti-adhesin antibodies in intraperitoneal (IP) or subcutaneous (SC) immunized mice, suggesting these antigens are potential candidates for ETEC subunit vaccines. However, these antigens have not been examined for immunogenicity using intradermal (ID) or intramuscular (IM) routes, the routes perhaps are more suitable for human vaccine administration. In this study, toxoid fusion 3xST[subscript aN12S]-mnLT[subscript R192G/L211A], CFA/I/II/IV MEFA, alone or combined, or toxoid-adhesin MEFA CFA-3xSTa[subscript N12S]-mnLT[subscript R192G/L211A] were ID or IM immunized to mice (8 mice per group) induced antigen-specific antibodies were titrated, and antibody neutralization activities were assessed in vitro. Data showed that mice ID or IM immunized with the toxoid fusion 3xSTa[subscript N12S]-mnLT[subscript R192G/L211A] antigen developed anti-LT and anti-STa antibodies and mice immunized with the CFA/I/II/IV MEFA developed antibody responses to all seven adhesins (CFA/I, CS1-CS6). In addition, mice co-administered ID or IM with toxoid fusion 3xSTa[subscript N12S]-mnLT[subscript R192G/L211A] and CFA/I/II/IV MEFA, or with toxoid-adhesin MEFA CFA-3xSTa[subscript N12S]-mnLT[subscript R192G/L211A] developed antibodies to both toxins and all seven adhesins. Antibody neutralization studies of the serum samples of the immunized mice showed that the induced antibodies neutralized enterotoxicity of LT and STa and/or inhibited adherence of ETEC or E. coli bacteria producing any of these seven adhesins. These data confirmed immunogenicity of these ETEC subunit vaccine target antigens and provide useful information for vaccine development against ETEC diarrhea.
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Sousa, Diana Isabel Pacheco de. "Improving the anti-tumor immune responses against cancer cells." Master's thesis, 2016. http://hdl.handle.net/10362/19550.
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Cancer is one of the leading causes of death worldwide. Dendritic cells (DCs) can capture cancer antigens and present them to T lymphocytes, after a maturation process, inducing specific immune responses. Sialyl-Tn (STn) is a tumor-associated carbohydrate antigen that is expressed by several carcinomas. STn downregulates the immune responses towards STn-expressing tumor cells by inducing a tolerogenic phenotype on DCs. For this reason, a successful therapeutic approach against this antigen has to take in consideration the activation of the immune response.
The main goal of this thesis was to assess if the use of anti-STn antibodies to block the STn antigen could improve anti-tumor immune responses by reestablishing the mature phenotype on DCs. To do this, STn-expressing cancer cell lines were cultured and DCs were obtained from differentiation of monocytes. Initially, the work comprised the development and characterization of anti-STn antibodies produced by the group through hybridoma technology, using mainly ELISA and flow cytometry. Three hybridoma clones producing IgM anti-STn antibodies were obtained and will be further characterized. A second part of the work included a functional in vitro characterization of humanized anti-STn antibodies. This comprised the establishment of co-cultures between cancer cells and DCs and assessment of the immune response of DCs against STn-expressing cancer cells, with and without STn blockade by those antibodies. The expression of MHC-II and co-stimulatory molecules was assessed by flow cytometry, and the expression of cytokines was assessed by ELISA and RT-PCR. However, the reestablishment of the mature phenotype was not observed.
The work developed contributed to understanding that further improvements and assays are necessary; and also that the production of antibodies comprises many variants that can be modified throughout the development and characterization procedures, thus being a long process and needing many optimizations before success can be achieved.
Book chapters on the topic "ST2 antibodies"
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Goebel, F. D., V. Erfle, H. Piechowiak, P. Hien, H. Schloz, and R. Hehlmann. "The Relations of HTLV-III antibodies to Neopterin and Beta-2- Microglobulin in the Serum of Patients with AIDS or Persons at Risk." In February 23–March 2, 1985, St. Christoph, Arlberg, Austria, edited by Helmut Wachter, H. Ch Curtius, and W. Pfleiderer, 319–34. Berlin, Boston: De Gruyter, 1985. http://dx.doi.org/10.1515/9783110860566-029.
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Kashyout, Abd El-Hady B., and Feby Youssef. "Science, Technology, and Innovation Response to the COVID-19 Pandemic." In Advances in Human Services and Public Health, 108–32. IGI Global, 2022. http://dx.doi.org/10.4018/978-1-7998-8973-1.ch006.
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The COVID-19 pandemic has caused deep changes all over the world. Great efforts to stop the spread of the contagious are still under actions in economy, social works, STI through many activities. The study highlights the Egyptian efforts in the STI sector for facing the pandemic effects. Conceptual and methodology framework of the study is built up and discussed. Egyptian government emergency response package greatly minimized its effects. Also, HEI's policies suggested an innovation framework to strengthen the Egyptian market. STI institutions in both MOHESR and MOHP worked on the effects of drugs clinical trials, vaccine manufacturing, and therapeutic approaches. Internationally recognized publications in Egyptian top universities and research centers focused on many topics including the effect of drugs and antibiotics on the infected patients with the virus for efficient therapy, the genetic development of the virus in Egypt, monitoring of the extent possibilities for the formation of collective immunity in Egyptians, the movement of antibodies in their bodies, and many other activities.
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Hefter, Harald, and Sara Samadzadeh. "Clinical Relevance of Neutralizing Antibodies in Botulinum Neurotoxin Type A." In Botulinum Toxin - Recent Topics and Applications [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.102896.
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The precise definition of prevalence of neutralizing antibodies (NABs) affords cross-sectional testing of a cohort. But in most studies, only selected patients are tested. This leads to gross underestimation of NAB-prevalence, and the opinion that induction of NABs is a rare phenomenon in botulinum neurotoxin (BoNT)/A-therapy. However, recent cross-sectional studies report annual incidences between 1 and 2% in patients being treated with a complex protein (CP)-containing preparation. This implies that NAB-prevalence above 10% has to be expected in patients being treated for more than 10 years. High dose per session and long duration of treatment are relevant risk factors for induction of NABs. In patients exclusively treated with the CP-free incobotulinumtoxin A (incoBoNT/A) preparation Xeomin® no NAB-induction has been reported so far. In patients with NABs switching to incoBoNT/A may lead to a decline of NAB-titers. In patients with NABs under treatment with a CP-containing BoNT/A-preparation it may take years of treatment until a second treatment failure (STF) becomes clinical manifest. In a cohort of 59 patients with partial STF patients’ reports on the reduction of BoNT-activity predicted the presence of NABs better than treatment related data produced by the treating physicians.
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Danks, Janine A., and Samantha J. Richardson. "Endocrinology and evolution: lessons from comparative endocrinology." In Oxford Textbook of Endocrinology and Diabetes, 14–23. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199235292.003.1013.
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Comparative endocrinology is the study of the endocrine glands and their hormones in different species of animals. It is undergoing a renaissance because of the new tools and techniques provided by genome sequencing and molecular biology. Until relatively recently, characterization and detection of hormones in lower vertebrates relied on biological assays and protein chemistry approaches, whereas now gene sequences can be readily revealed from whole genome sequencing. Gene expression and synthesis can be used to develop antibodies and other reagents for sensitive assays and revealing physiological experiments can be carried out. Endocrinology traditionally used a range of animal species, including many lower vertebrates. Comparative endocrinology became a separate specialty only in the last 50 years when endocrinologists concentrated on rodents as their model animals. In 1933, Riddle demonstrated that an avian pituitary factor that promoted growth of the pigeon crop-sac was identical to a mammalian pituitary factor that earlier had been found to initiate and maintain milk secretion in mammals. Riddle called this avian factor prolactin and the response of the crop-sac provided a sensitive assay for the detection of human prolactin in pituitary extracts. Pigeon prolactin was the first pituitary hormone to be crystallized and purified in 1937 and led to the purification of mammalian prolactin. Prolactin has a number of roles in lower vertebrates, including a vital role as a hypercalcaemic factor in fish. The first part of this chapter focuses on the calcium-regulating factors including parathyroid hormone (PTH), parathyroid hormone-related protein (PTHrP), and stanniocalcin (STC), and the second part will discuss comparative endocrinology of thyroid hormones and transthyretin (a thyroid hormone distributor in blood the cerebrospinal fluid).
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Leòn-Vizcaino, L., M. Molera, A. Gasca, F. Garrido, M. D. Rodriguez, M. L. Rodriguez, and M. L. Hierro. "Serological Survey of Prevalence of Antibodies to Brucellosis In Wild Ruminants in Jaén (Spain)." In 9. Juni bis 13. Juni 1985 in St. Vincent/Torino, 455–62. De Gruyter, 1985. http://dx.doi.org/10.1515/9783112520802-068.
Full textConference papers on the topic "ST2 antibodies"
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Shattil, S. J., J. A. Hoxie, M. Cunningham, C. S. Abrahms, J. O’Brien, and Z. Budzynski. "DETECTION OF ACTIVATED PLATELETS IN WHOLE BLOOD BY FLOW CYTOMETRY." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643830.
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Platelets may become activated in a number of clinical disorders and participate in thrombus formation. We have developed a direct test for activated platelets in whole blood that utilizes dual-color flow cytometry and requires no washing steps. Platelets were distinguished from erythrocytes and white blood cells in the flow cytometer by labeling the platelets with biotin-AP1, an antibody specific for membrane glycoprotein lb, and analyzing the cells for phycoerythrin-streptavidin fluorescence. Membrane surface changes resulting from platelet activation were detected with three different FITC-labeled monoclonal antibodies: 1) PAC1, an antibody specific for the fibrinogen receptor on activated platelets; 2) 9F9, which binds to the D-domain of fibrinogen and detects platelet-bound fibrinogen; and 3) S12, which binds to an alpha-granule membrane protein that associates with the platelet surface during secretion. Unstimulated platelets demonstrated no PAC1, 9F9, or S12-specific fluorescence, indicating that they did not bind these antibodies. Upon stimulation with agonists, however, the platelets demonstrated a dose-dependent increase in FITC-fluorescence. The binding of 9F9 to activated platelets required fibrinogen. Low concentrations of ADP and epinephrine, which induce fibrinogen receptors but little secretion, stimulated near-maximal PAC1 or 9F9 binding but little S12 binding. On the other hand, a concentration of phorbol myristate acetate that evokes full platelet aggregation and secretion induced maximal binding of all three antibodies. When blood samples containing activated and non-activated platelets were mixed, as few as 0.8% activated platelets could be detected by this technique. There was a direct correlation between ADP-induced FITC-PAC1 binding and binding determined in a conventional 125I-PAC1 binding assay (r = 0.99; p < 0.001). These studies demonstrate that activated platelets can be reliably detected in whole blood using activation-dependent monoclonal antibodies and flow cytometry. This method may be useful to assess the degree of platelet activation and the efficacy platelet inhibitor therapy in thrombotic disorders.
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Cervantes, Ana Jazmín Otero, Cynthia Rodríguez-Nava, Karen Cortés Sarabia, Luz Del Carmen Alarcón Romero, Isela Parra Rojas, and Amalia Vences Velazquez. "P1.02 Production of polyclonals antibodies againstgardnerella vaginalis." In STI and HIV World Congress Abstracts, July 9–12 2017, Rio de Janeiro, Brazil. BMJ Publishing Group Ltd, 2017. http://dx.doi.org/10.1136/sextrans-2017-053264.110.
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Marcovina, S., R. Coppola, M. P. Protti, C. Gelfi, and P. M. Mannucci. "EDTA-DEPENDENT MONOCLONAL ANTIBODIES TO HUMAN PROTEIN S." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644294.
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Splenocytes from a Balb/c mouse immunized with purified human protein S (PS) were fused with murine hybridoma cell line SP2/0-Agl4 and cultured in Iscove's medium without addition of fetal bovine serum. Hybrid supernatants were screened for the presence of specific antibodies by solid-phase ELISA and cloned by the limiting dilution technique. Pour clones, named S2, S3, S8, and S10, were selected, recloned several times, and injected intraperitoneally into Balb/c mice for the production of antibody-rich ascitic fluid. The monoclonal antibodies (Mabs), all of IgGl subclass with k light chain, were purified from ascitic fluid by Protein-A chromatography. The specificity of Mabs was controlled by the immunoblotting technique: the Mabs appeared to react only with two plasma proteins, one with a MW of about 70.000 dal tons comigrating with purified PS, and the other with a MW >300.000 da that is likely to be the C4b-binding protein-PS complex. No interaction has been observed with PS-depleted plasma. As tested by a fluid phase radio immunoassay, the binding of Mabs to PS was significantly higher in the presence of EDTA while was totally inhibited in the presence of Ca2+. Scatchard plot analysis of the binding between 125I-PS and Mabs showed that the binding affinity of the antibodies ranged from 108 to 109 1/mol. Each EDTA-dependent Mab was then immobilized on Sepharose 4B-CNBr and used to purify PS from barium precipitation of citrated plasma. The fraction eluted with 2 mmol of CaCl2 from the immunoadsorbent appeared to contain only two proteins when stained with Cocmassie Blue. By immuno blotting, all Mabs reacted with both proteins, one comigrating with purified PS and the other with a MW >300.000. Essentially homogeneous PS, free from the high MW component, was obtained when the barium citrate adsorbate was applied to a DEAE-Sephadex column and the protein peack containing the balk of PS was sussequently applied to the immunoadsorbent and eluted with 2 mmol CaCl2.In summary, we have described an unusual set of EDTA-dependent monoclonal antibodies to PS and their use for the purification of homogeneous protein S from human plasma.
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Kim, C., L. Manheart, C. Gillespie, C. Khosropour, M. Lowens, P. Totten, and G. Wood. "P388 Mycoplasma genitalium-reactive antibodies in serum and urethral specimens of persistently infected men." In Abstracts for the STI & HIV World Congress, July 14–17 2021. BMJ Publishing Group Ltd, 2021. http://dx.doi.org/10.1136/sextrans-2021-sti.423.
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Sah, Manoj Kumar, Prabhakar Verg Shah, Rupa Adhikari, Shyam Kumar Mishra, and Keshab Parajuli. "P3.143 Serological prevalence of antibodies to human immunodeficiency virus among nepalese population." In STI and HIV World Congress Abstracts, July 9–12 2017, Rio de Janeiro, Brazil. BMJ Publishing Group Ltd, 2017. http://dx.doi.org/10.1136/sextrans-2017-053264.378.
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Mbugua, Njeri, Elizabeth Ann Bukusi, Asunta Wagura, and Elizabeth Ngugi. "P3.175 Early development of broadly neutralising antibodies in hiv-1-infected infants." In STI and HIV World Congress Abstracts, July 9–12 2017, Rio de Janeiro, Brazil. BMJ Publishing Group Ltd, 2017. http://dx.doi.org/10.1136/sextrans-2017-053264.410.
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Kazama, M., H. Ishii, J. Tsubouchi, M. Nakano, N. Hiramoto, T. Abe, and P. W. Majerus. "PREPARATION OF ANTI-HUMAN THROMBOMODULIN ANTIBODIES AND THEIR APPLICATION FOR STUDY ON PLASMA THROMBOMODULIN." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643962.
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Thrombomodulin is an endothelial cell membrane protein that is cofactor required for rapid activation of plasma protein C. Recently, thrombomodulin was found also in plasma in normal subject. However, the information of the soluble thrombomodulin in plasma is very poor. We now report the preparation of polyclonal and monoclonal anti-human thrombomodulin and their application for study on plasma thrombomodulin.Thrombomodulin was extracted from human placenta by 0.5% of Triton X-100 and purified by DIP-thrombin column chromatography. Polyclonal anti-thrombomodulin antibody was obtained from rabbit serum. The three types of monoclonal anti-human thrombomodulin antibodies were obrained from hybrid cell of BALB/C spleen cell and SP2 mouse myeloma cell. The type 1 monoclonal antibody inhibited the thrombomodulin activity. The type 2 of the antibody did not inhibit the activity. The type 3 of antibody cross reacted with rabbit lung thrombomodulin. The IgGs of these antibodies were separated by protein A Sepharose. The plasma thrombomodulin was separated using polyclonal anti-thrombomodulin IgG Sepharose. The apparent molecular weight of plasma thrombomodulin was estimated by immunoblot analysis using monoclonal anti-thrombomodulin IgG. When run with mercaptoethanol, plasma thrombomodulin migrated mainly at Mr=85,000 against Mr=105,000 of tissue thrombomodulin. The plasma thrombomodulin had an apparent Km for 1 nM compared with 0.3nM for tissue thrombomodulin. The apparent Km for protein C was same between tissue and plasma thrombomodulin.
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McBride, S., M. Ferguson, M. Kelly, K. Hawley, A. Luthra, H. Driscoll, J. Montezuma-Rusca, et al. "P401 Development and Utilization of Antibodies Specific for Extracellular Loops of the Treponema pallidum outer membrane protein BamA (TP0326)." In Abstracts for the STI & HIV World Congress, July 14–17 2021. BMJ Publishing Group Ltd, 2021. http://dx.doi.org/10.1136/sextrans-2021-sti.431.
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Osbak, Kara, S. Abdellati, A. Tsoumanis, M. Van Esbroeck, T. Crucitti, and C. Kenyon. "P1.46 Comparison of two enzyme immunoassays for the detection of igg and igm anti-treponema pallidum antibodies." In STI and HIV World Congress Abstracts, July 9–12 2017, Rio de Janeiro, Brazil. BMJ Publishing Group Ltd, 2017. http://dx.doi.org/10.1136/sextrans-2017-053264.153.
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Towns, J., D. Leslie, I. Denham, F. Azzato, T. Karapanagiotidis, D. Williamson, S. Graves, et al. "P067 Timing of primary syphilis treatment and impact on the development of treponemal antibodies: A cross-sectional clinic-based study." In Abstracts for the STI & HIV World Congress, July 14–17 2021. BMJ Publishing Group Ltd, 2021. http://dx.doi.org/10.1136/sextrans-2021-sti.205.
Full textReports on the topic "ST2 antibodies"
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Schat, Karel Antoni, Irit Davidson, and Dan Heller. Chicken infectious anemia virus: immunosuppression, transmission and impact on other diseases. United States Department of Agriculture, 2008. http://dx.doi.org/10.32747/2008.7695591.bard.
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1. Original Objectives. The original broad objectives of the grant were to determine A) the impact of CAV on the generation of cytotoxic T lymphocytes (CTL) to reticuloendotheliosis virus (REV) (CU), B). the interactions between chicken anemia virus (CAV) and Marek’s disease virus (MDV) with an emphasis on horizontal spread of CAV through feathers (KVI), and C) the impact of CAV infection on Salmonella typhimurium (STM) (HUJI). During the third year and the one year no cost extension the CU group included some work on the development of an antigen-antibody complex vaccine for CAV, which was partially funded by the US Poultry and Egg Association. 2. Background to the topic. CAV is a major pathogen causing clinical disease if maternal antibody-free chickens are infected vertically or horizontally between 1 and 14 days of age. Infection after 3 weeks of age when maternal antibodies are not longer present can cause severe subclinical immunosuppression affecting CTL and cytokine expression. The subclinical immunosuppression can aggravate many diseases including Marek’s disease (MD) and several bacterial infections. 3. Major conclusions and achievements. The overall project contributed in the following ways to the knowledge about CAV infection in poultry. As expected CAV infections occur frequently in Israel causing problems to the industry. To control subclinical infections vaccination may be needed and our work indicates that the development of an antigen-antibody complex vaccine is feasible. It was previously known that CAV can spread vertically and horizontally, but the exact routes of the latter had not been confirmed. Our results clearly show that CAV can be shed into the environment through feathers. A potential interaction between CAV and MD virus (MDV) in the feathers was noted which may interfere with MDV replication. It was also learned that inoculation of 7-day-old embryos causes growth retardation and lesions. The potential of CAV to cause immunosuppression was further examined using CTL responses to REV. CTL were obtained from chickens between 36 and 44 days of age with REV and CAV given at different time points. In contrast to our earlier studies, in these experiments we were unable to detect a direct impact of CAV on REV-specific CTL, perhaps because the CTL were obtained from older birds. Inoculation of CAV at one day of age decreased the IgG antibody responses to inactivated STM administered at 10 days of age. 4. Scientific and Agricultural Implications The impact of the research was especially important for the poultry industry in Israel. The producers have been educated on the importance of the disease through the many presentations. It is now well known to the stakeholders that CAV can aggravate other diseases, decrease productivity and profitability. As a consequence they monitor the antibody status of the breeders so that the maternal antibody status of the broilers is known. Also vaccination of breeder flock that remain antibody negative may become feasible further reducing the negative impact of CAV infection. Vaccination may become more important because improved biosecurity of the breeder flocks to prevent avian influenza and Salmonella may delay the onset of seroconversion for CAV by natural exposure resulting in CAV susceptible broilers lacking maternal antibodies. Scientifically, the research added important information on the horizontal spread of CAV through feathers, the interactions with Salmonella typhimurium and the demonstration that antigen-antibody complex vaccines may provide protective immunity.