Bibliografie tematiche / Immunomodulation

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Letteratura scientifica selezionata sul tema "Immunomodulation"

Autore: Grafiati
Pubblicato: 4 giugno 2021
Ultima modifica: 31 luglio 2024

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Articoli di riviste sul tema "Immunomodulation"

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Lamoreaux, B., M. Francis-Sedlak, K. Svensson e R. Holt. "OP0173 IMMUNOMODULATION CO-THERAPY WITH PEGLOTICASE: DATABASE TRENDS 2014-2019". Annals of the Rheumatic Diseases 79, Suppl 1 (giugno 2020): 108.2–108. http://dx.doi.org/10.1136/annrheumdis-2020-eular.3893.

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Background:Pegloticase is a PEGylated biologic therapy for patients with uncontrolled gout who have not improved on or could not tolerate conventional urate-lowering therapies.1All biologics have the ability to engender anti-drug antibodies (ADAs) and it is known that some patients given pegloticase develop ADAs that cause them to stop treatment prior to recieving a complete course of therapy.2-3In other rheumatic autoimmune diseases, DMARDs such as methotrexate or azathioprine are used as standard of care to prevent the development of ADAs to biologics. These DMARDs often allow patients to remain on biologic therapies longer and recieve the full therapeutic benefits while minimizing adverse events.4While pegloticase has been used traditionally as monotherapy, recent case series have demonstrated the therapeutic benefit of immunomodulator co-administration, allowing more patients to receive a full course of pegloticase therapy.5-6Little has been published on how widespread this practice is and whether it has changed over time.Objectives:To examine medical claims database from 2014-2019 for trends in immunomodulating therapies being co-prescribed with pegloticase.Methods:An IQVIA claims database (November 2014 to October 2019) representing 1.3 billion claims, covering 30 million patients diagnosed with gout or CKD, was utilized to search for patients who had received pegloticase. Patients who had recieved pegloticase were classified as having been on an immunomodulating co-therapy if they were prescribed methotrexate or azathioprine within 60 days before or after initiation of their first pegloticase infusion.Results:We found relatively steady low rates of immunomodulation co-therapy with pegloticase from 2014 through 2018 ranging from 1% in 2016 to 4% in 2018 (Figure 1). In 2019 however, the proportion of pegloticase patients that were co-treated with methotrexate or azathioprine therapy increased to 15%. Most patients were started on immunomodulating therapy 20 days before to 10 days after initiation of pegloticase. Methotrexate was the more frequently used immunomodulaton co-therapy as compared to azathioprine.Conclusion:We found evidence of a relatively dramatic increasing initiation of immunomodulation therapy with pegloticase beginning soon after a November 2018 presentation of a case series which demonstrated improved response rates of pegloticase when co-administered with methotrexate. These data indicate that clinicians began to more frequently employ a strategy of DMARD co-treatment with pegloticase in 2019 to improve response rates to this important gout medicine.References:[1]Sundy JS, et al.JAMA2011;306:711-20.[2]Abeles AM.Arthritis Research & Therapy2014, 16:112[3]Strand V, et al.BioDrugs2017; 31:299–316.[4]Krieckaert CL, et al.Arthritis Res Ther2010;12:217.[5]Botson J and Peterson J.Ann Rheum Dis.2019; 78: A1289.[6]Bessen SY, et al.Semin Arthritis Rheum.2019;49:56-61.Disclosure of Interests:Brian LaMoreaux Shareholder of: Horizon Therapeutics, Employee of: Horizon Therapeutics, Megan Francis-Sedlak Shareholder of: Horizon Therapeutics, Employee of: Horizon Therapeutics, Karl Svensson Shareholder of: Horizon Therapeutics, Employee of: Horizon Therapeutics, Robert Holt Shareholder of: Horizon Therapeutics, Employee of: Horizon Therapeutics
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Boitard, C. "Immunomodulation.." médecine/sciences 16, n. 12 (2000): 1340. http://dx.doi.org/10.4267/10608/1587.

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Holland, S. "Immunomodulation". Current Opinion in Pharmacology 2, n. 4 (1 agosto 2002): 425–27. http://dx.doi.org/10.1016/s1471-4892(02)00188-1.

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&NA;. "Immunomodulation". Shock 10, Supplement (1998): 1. http://dx.doi.org/10.1097/00024382-199812001-00006.

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Jiao, Qing, Liwen Li, Qingxin Mu e Qiu Zhang. "Immunomodulation of Nanoparticles in Nanomedicine Applications". BioMed Research International 2014 (2014): 1–19. http://dx.doi.org/10.1155/2014/426028.

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Nanoparticles (NPs) have promising applications in medicine. Immune system is an important protective system to defend organisms from non-self matters. NPs interact with the immune system and modulate its function, leading to immunosuppression or immunostimulation. These modulating effects may bring benefits or danger. Compositions, sizes, and surface chemistry, and so forth, affect these immunomodulations. Here we give an overview of the relationship between the physicochemical properties of NPs, which are candidates to be applied in medicine, and their immunomodulation properties.
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Demase, Kathryn, Cassandra K. Monitto, Robert D. Little e Miles P. Sparrow. "The Role of Low-Dose Oral Methotrexate in Increasing Anti-TNF Drug Levels and Reducing Immunogenicity in IBD". Journal of Clinical Medicine 12, n. 13 (29 giugno 2023): 4382. http://dx.doi.org/10.3390/jcm12134382.

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Concomitant immunomodulation is utilised in combination with anti-TNF therapy for IBD primarily to increase drug levels and prevent anti-drug antibody formation. Whilst thiopurines have traditionally been the immunomodulator of choice in IBD populations, there are concerns regarding the long-term safety of the prolonged use of these agents: particularly an association with lymphoproliferative disorders. Given this, we have explored the existing literature on the use of low-dose oral methotrexate as an alternative immunomodulator for this indication. Although there is a lack of data directly comparing the efficacies of methotrexate and thiopurines as concomitant immunomodulators, the available literature supports the use of methotrexate in improving the pharmacokinetics of anti-TNF agents. Furthermore, low-dose oral methotrexate regimens appear to have comparable efficacies to higher-dose parenteral administration and are better tolerated. We suggest that clinicians should consider the use of low-dose oral methotrexate as an alternative to thiopurines when the primary purpose of concomitant immunomodulation is to improve anti-TNF pharmacokinetics.
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Patole, S., P. Vijayakumar e S. Jog. "Perinatal immunomodulation". Journal of Maternal-Fetal & Neonatal Medicine 11, n. 5 (gennaio 2002): 290–301. http://dx.doi.org/10.1080/jmf.11.5.290.301.

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LOWELL, JEFFREY A., HOWARD L. PARNES e GEORGE L. BLACKBURN. "Dietary immunomodulation". Critical Care Medicine 18, Supplement (febbraio 1990): S149. http://dx.doi.org/10.1097/00003246-199002003-00010.

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House, Robert V., e Kenneth L. Hastings. "Multidimensional Immunomodulation". Journal of Immunotoxicology 1, n. 2 (gennaio 2004): 123–29. http://dx.doi.org/10.1080/15476910490503646.

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Pastore, Chiara. "Liver immunomodulation". Nature Nanotechnology 14, n. 3 (marzo 2019): 194. http://dx.doi.org/10.1038/s41565-019-0410-5.

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Tesi sul tema "Immunomodulation"

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Hoopen, Petra ten. "Immunomodulation of jasmonate functions". [S.l. : s.n.], 2002. http://deposit.ddb.de/cgi-bin/dokserv?idn=969394403.

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DeClue, Amy E. "Ketamine immunomodulation during endotoxemia". Diss., Columbia, Mo. : University of Missouri-Columbia, 2007. http://hdl.handle.net/10355/6276.

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Thesis (M.S.)--University of Missouri-Columbia, 2007.
The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. "August 2007" Includes bibliographical references.
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Kaplan, Jennifer Melissa. "Immunomodulation During Systemic Inflammation". University of Cincinnati / OhioLINK, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1186158205.

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Sanders, Robert A. "GABAA immunomodulation & infection". Thesis, Imperial College London, 2012. http://hdl.handle.net/10044/1/9981.

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Abstract (sommario):
GABAergic drugs, such as benzodiazepines, are widely used in clinical practice yet their immune side effects are poorly understood. Preliminary studies have suggested that immune cells express GABAA receptors indicating that they may be controlled by GABA signaling. Herein parallel preclinical, translational and epidemiological approaches are described to help understand the importance of GABAA immunomodulation. The hypothesis is that GABA signaling acts to reduce responsiveness to a pathogen and thus that GABAergic drugs will increase susceptibility to infection. To inform on the clinical importance of this work, data from a subgroup analysis of the Maximizing Efficacy of Targeted Sedation and Reducing Neurological Dysfunction (MENDS) trial (where the relative effects of lorazepam, and dexmedetomidine were compared) are described in septic and non‐septic patients. Consistent with the hypothesis, avoidance of lorazepam sedation decreased mortality by 70% in septic patients but did not affect outcome in non‐septic patients. As preclinical data suggests that benzodiazepines increase mortality at subsedative doses we next conducted a population‐based cohort and nested case‐control design analysis of The Health Improvement Network (THIN), a comprehensive UK general practice database. Benzodiazepines exposure increased the incidence of community acquired pneumonia (CAP) and both 30‐day and long‐term mortality from CAP. Based on these significant accumulating data of the harm of exposure to benzodiazepines during an infection, animal studies were conducted to understand (i) the biological plausibility of our findings and (ii) the mechanism of the effect. In a series of mouse studies the prototypical benzodiazepine, diazepam, increased mortality from Streptococcus pneumoniae through potentiation of GABAA signaling. The increased mortality was associated with increased pathogen load and a delayed cytokine response to the infection. However cellular recruitment was not affected, indicating that local mechanisms were perturbed. Immune cell profiling revealed that alveolar macrophage and monocytes abundantly expressed subunits of the GABAA receptor, compatible with benzodiazepine sensitivity. Ex vivo studies showed that GABAA receptor activation decreased cytokine responses, phagocytosis and bacterial killing by alveolar macrophage likely via inducing an intracellular acidosis. Finally based on the immune cell profile of GABAA receptors we predicted that benzodiazepines that do not target the α1 GABAA subunit would lack the immune suppression observed by nonselective drugs. In accordance with this hypothesis we show that these selective benzodiazepines do not provoke intracellular acidosis, affect cytokine release or bacterial killing of macrophage ex vivo. In vivo the selective benzodiazepine did not increase mortality from infection or increase pathogen load.
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Demols, Anne. "Immunomodulation de la pancreatite experimentale". Doctoral thesis, Universite Libre de Bruxelles, 2003. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/211321.

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Islander, Ulrika. "Immunomodulation by estrogen and estren /". Göteborg : Department of Rheumatology and Inflammation Research, The Sahlgrenska Academy at Göteborg University, 2007. http://hdl.handle.net/2077/3123.

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Mattsson, Lars. "Immunomodulation of collagen-induced arthritis /". Stockholm, 2000. http://diss.kib.ki.se/2000/91-628-4369-9/.

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Barber, K. A. "Immunomodulation in the NOD mouse". Thesis, University of Cambridge, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.596341.

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A CD8+ T cell clone was generated by priming non-diabetic NOD mice with C2, a Kd-binding, 10-mer peptide (WYIPQSLRGV) derived from the large isoform of GAD. This clone (αC2.4) lyses NOD fibroblast targets transfected with a construct encoding human GAD67. This molecule is entirely homologous with mouse and rate GAD67 at the C2 region and as such this observation indicates that C2 is a naturally processed epitope. The object of this project was to investigate the role of the C2 epitope and altered peptide ligand (APL) derivatives in IDDM pathogenesis in the NOD mouse, with the ultimate aim of modifying disease by induction of antigen specific tolerance. Adoptive transfers into neonatal NOD and NOD-scid recipients have shown αC2.4 not to cause disease. Neither do these cells home to the pancreas. Surface marker characterization demonstrated that αC2.4 did not express β7 integrin, a horning receptor thought to play a key role in infiltration of the pancreas by autoreactive cells. However, administration of the C2 peptide was shown to reduce the incidence of spontaneous but not cyclophospamide induced disease, although this effect was dependent on the route of administration. Knowledge of the specificity of the CD8+T cell clone allowed investigation of the nature of T cell recognition of peptide/MHC as a basis for the search for an APL. Three residues of positions 5, 7 and 8 of the C2 peptide were shown to be critical for recognition of peptide/MHC by αC2.4. On the basis of these findings variant peptides were synthesized and screened by antagonistic properties. None was identified with the ability to alter recognition of C2/MHC by αC2.4. Cytokine intervention has been shown to be an important approach for immune modulation in IDDM in the NOD mouse. The aim of this aspect of the project was to use recombinant retroviral vector technology to modify islet specific T cell clones for targeted expression of immunosuppressive cytokines. Transduction of T cells was achieved although the efficiency of this process was limited. This approach may prove useful in altering the local cytokine milieu towards a non-pathogenic Th2 environment.
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Dua, Harminder Singh. "Immunomodulation of experimental autoimmune uveitis". Thesis, University of Aberdeen, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.317710.

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Chronic posterior uveitis is a relatively common clinical disorder and an importance cause of visual impairment in young adults. Experimental autoimmune uveitis (EAU) and its associated experimental autoimmune pinealitis (EAP) induced by retinal autoantigens are predominantly CD4+ T cell mediated (auto) immune disease of the retina and uveal tract of the eye and the pineal gland respectively. EAU bears a close clinical and pathological resemblance to chronic posterior uveitis in humans and seves as a good animal model for the study of posterior uveitis. The EAU model was used to study means of modulating the host's immune response to suppress or inhibit the onset of uveitis. The onset of retinal S-antigen induced EAU could be successfully inhibited by pre-treating Lewis rats with a retinal S-antigen (carboxy terminus) specific monoclonal antibody called S2.4.C5. This however did not suppress the associated EAP indicating that the monoclonal antibody acted via the efferent arc of the immune mediated response. This prompted a study of the 'Blood-retinal and Blood-pineal barrier sites' during the active stages of EAU and EAP. Transmission electron microscopy of the vascular endothelium revealed changes resembling 'High endothelial venules' of lymph nodes in the retinal and pineal vasculature. In an attempt to identify one or more immunodominant epitopes of S-antigen that may be relevant to tolerance induction, an in-vitro and in-vivo study using enzyme digested preparations of S-antigen was carried out. This revealed that digestion of S-antigen by a protease derived from staphylococcus aureus V8 strain, not only inhibited the binding of the monoclonal S2.4.C5 in-vitro but was also associated with an in-vivo attenuation of the pathogenic response to S-antigen indicating that a dominant immunogenic epitope of S-antigen was located at the C-terminus of the molecule.
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Merly, Liza. "Immunomodulation by Shark Cartilage Extracts". FIU Digital Commons, 2011. http://digitalcommons.fiu.edu/etd/420.

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The immune system is composed of innate and adaptive mechanisms. Innate immune responses are significantly modulated by immunomodulatory factors that act through the induction of specific patterns of cytokine production in responding cells. Human leukocytes have been shown to respond to substance(s) present in acid extracts of commercial shark cartilage (SC). Shark cartilage is a food supplement taken by consumers as a prophylaxis and for the treatment of conditions ranging from arthritis to cancer. No reliable scientific evidence in the literature supports the alleged usefulness of shark cartilage supplements, but their use remains popular. Cartilage extracts exhibit immunomodulatory properties by inducing various inflammatory, Th1-type cytokines and potent chemokines in human peripheral blood leukocytes (HPBL) in vitro. The objectives of the study were to (1) to determine the nature of the active component(s), (2) to define the scope of cellular response to SC extract, and (3) to elucidate the molecular mechanisms underlying bioactivity. Results showed that there are at least two cytokine-inducing components which are acid stable. One anionic component has been identified as a small (14-21 kDa) glycoprotein with at least 40% carbohydrate content. Shark cartilage stimulated HPBL to produce cytokines resembling an inflammatory, Th1 polarized response. Leukocyte-specific responses consist of both initial cytokine responses to SC directly (i.e., TNF-a) and secondary responses such as the IFN-γ response by lymphocytes following initial SC stimulation. Response of RAW cells, a murine macrophage cell line, indicated that TNF-α could be induced in macrophages of another mammalian species in the absence of other cell types. The results suggest that the human monocyte/macrophage is most likely to be the initial responding cell to SC stimulation. Stimulation of cells appears to engage at least one ligand-receptor interaction with TLR 4, although the role of TLR 2 cannot be ruled out. Initial activation is likely followed by the activation of the JNK and p38 MAPK signal transduction pathways resulting in activation, release, and translocation of transcription factor nuclear factor κB (Nf-kB). This dissertation research study represents the first in-depth study into characterizing the bioactive component(s) of commercial shark cartilage responsible for its immunomodulating properties and defining cellular responses at the molecular level.
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Libri sul tema "Immunomodulation"

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Bernard, Bizzini, Bonmassar Enzo e International Symposium on Immunomodulation (1986 : Copanello, Italy), a cura di. Advances in immunomodulation. Roma: Pythagora Press, 1988.

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1937-, Cruse Julius M., e Lewis R. E. 1947-, a cura di. Immunomodulation of neoplasia. Basel: Karger, 1988.

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Grogan, Jane Louise. Immunomodulation in human schistomiasis. Leiden: University of Leiden, 1998.

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Sangwan, Neelam S., Mohamed A. Farag e Luzia Valentina Modolo, a cura di. Plants and Phytomolecules for Immunomodulation. Singapore: Springer Nature Singapore, 2022. http://dx.doi.org/10.1007/978-981-16-8117-2.

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Malemud, Charles J., e Eben Alsberg, a cura di. Mesenchymal Stem Cells and Immunomodulation. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-46733-7.

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Friedman, Herman, John J. Madden e Thomas W. Klein, a cura di. Drugs of Abuse, Immunomodulation, and Aids. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-5347-2.

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1946-, D'Alessandro Natale, North Atlantic Treaty Organization. Scientific Affairs Division. e NATO Advanced Study Institute on Specific Approaches in Cancer Therapy: Differentiation, Immunomodulation, and Angiogenesis (1992 : Erice, Italy), a cura di. Cancer therapy: Differentiation, immunomodulation, and angiogenesis. Berlin: Springer-Verlag, 1993.

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1931-, Friedman Herman, Madden John J, Klein Thomas W e Symposium on Drugs of Abuse, Immunomodulation, and AIDS (5th : 1997 : Nashville, Tenn.), a cura di. Drugs of abuse, immunomodulation, and AIDS. New York: Plenum, 1998.

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Eisenstein, Toby K., Ward E. Bullock e Nabil Hanna, a cura di. Host Defenses and Immunomodulation to Intracellular Pathogens. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4757-5421-6.

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Eastern, Pennsylvania Branch of the ASM Symposium on Host Defenses and Immunomodulation to Intracellular Pathogens (1986 Philadelphia Pa ). Host defenses and immunomodulation to intracellular pathogens. New York, N.Y: Plenum Press, 1988.

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Capitoli di libri sul tema "Immunomodulation"

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Dias Da Silva, Wilmar. "Immunomodulation". In Fundamentals of Immunology, 415–37. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-70393-5_14.

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Wisniewski, Thomas, e Fernando Goñi. "Immunomodulation". In Prions and Diseases, 269–87. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-5338-3_17.

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Chauhan, Ramswaroop Singh, Yashpal Singh Malik, M. Saminathan e Bhupendra Nath Tripathi. "Immunomodulation". In Essentials of Veterinary Immunology and Immunopathology, 143–68. Singapore: Springer Nature Singapore, 2024. http://dx.doi.org/10.1007/978-981-99-2718-0_6.

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Wisniewski, Thomas, e Fernando Goñi. "Immunomodulation". In Prions and Diseases, 757–85. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-20565-1_37.

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Yang, Bob, e Steve Foley. "Immunomodulation Vaccines". In Female Urinary Tract Infections in Clinical Practice, 79–83. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-27909-7_13.

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Nelson, Steve, Carol M. Mason, Ping Zhang, Warren R. Summer e Gregory J. Bagby. "Immunomodulation in Sepsis". In Critical Care Infectious Diseases Textbook, 225–43. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1679-8_11.

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Kumar, Rajiv, Susanna S. Ng e Christian R. Engwerda. "Immunomodulation in Malaria". In Encyclopedia of Malaria, 1–13. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4614-8757-9_136-1.

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Bomford, R., M. Stapleton e S. Winsor. "Immunomodulation by Adjuvants". In Vaccines, 25–32. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-3848-6_4.

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Perdue, M. H. "Immunomodulation of epithelium". In Inflammatory Bowel Disease, 139–48. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-009-0371-5_14.

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Agarwal, Neeraj. "Immunomodulation and Photocarcinogenesis". In Photocarcinogenesis & Photoprotection, 45–51. Singapore: Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-10-5493-8_5.

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Atti di convegni sul tema "Immunomodulation"

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Leichtle, A., CS Draf, Allen F. Ryan e Karl-Ludwig Bruchhage. "Immunomodulation in Cholesteatoma". In Abstract- und Posterband – 91. Jahresversammlung der Deutschen Gesellschaft für HNO-Heilkunde, Kopf- und Hals-Chirurgie e.V., Bonn – Welche Qualität macht den Unterschied. © Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1711281.

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Leichtle, A., D. Leffers, CS Draf, Allen F. Ryan e K.-L. Bruchhage. "Immunomodulation in Cholesteatoma". In 100 JAHRE DGHNO-KHC: WO KOMMEN WIR HER? WO STEHEN WIR? WO GEHEN WIR HIN? Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1728511.

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Disis, Mary L. "Abstract IA27: Immunomodulation of breast cancer". In Abstracts: AACR Special Conference on Advances in Breast Cancer Research: Genetics, Biology, and Clinical Applications - October 3-6, 2013; San Diego, CA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1557-3125.advbc-ia27.

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Pukhova, Yana, Alexander S. Provorov e Vladimir V. Salmin. "Immunomodulation action of ultraviolet N2-laser radiation". In Laser Applications in Life Sciences: 5th International Conference, a cura di Pavel A. Apanasevich, Nikolai I. Koroteev, Sergei G. Kruglik e Victor N. Zadkov. SPIE, 1995. http://dx.doi.org/10.1117/12.197485.

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BASTIDE, MADELEINE, e FREDERIC BOUDARD. "HIGH DILUTIONS AS A TOOL OF IMMUNOMODULATION". In Proceedings of the International School of Biophysics. WORLD SCIENTIFIC, 1998. http://dx.doi.org/10.1142/9789812816887_0016.

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Cao, Xiaohong, Chaolong Han, Lei Shi e Xiaoye Wang. "Immunomodulation of Polyunsaturated Fatty Acids Purified from Nitzschia Laevis". In 2009 2nd International Conference on Biomedical Engineering and Informatics. IEEE, 2009. http://dx.doi.org/10.1109/bmei.2009.5305609.

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Bissell, B. D., J. L. Sturgill, M. Starr e E. D. Lewis. "Opioid Immunomodulation and Impact Within a Murine Sepsis Model". In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a2706.

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Yano, Max, Priscilla Do, Xiaokui Mo, Natarajan Muthusamy e John C. Byrd. "Abstract 3959: Ibrutinib immunomodulation via CTLA4 downregulation in CLL". In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-3959.

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Yano, Max, Priscilla Do, Xiaokui Mo, Natarajan Muthusamy e John C. Byrd. "Abstract 3959: Ibrutinib immunomodulation via CTLA4 downregulation in CLL". In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-3959.

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Lukyanov, Sergey, Konstantine Shapovalov, Pavel Tereshkov, Yuri Smolyakov, Ayagma Vanchikova e Boris Kuznik. "Thymalin as an immunomodulation option in severe COVID-19". In ERS International Congress 2021 abstracts. European Respiratory Society, 2021. http://dx.doi.org/10.1183/13993003.congress-2021.pa3667.

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Rapporti di organizzazioni sul tema "Immunomodulation"

1

Guha, Chandan. Immunomodulation of Hyperthermia for Recurrent Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, marzo 2005. http://dx.doi.org/10.21236/ada437721.

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2

Guha, Chandan. Immunomodulation of Hyperthermia for Recurrent Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, marzo 2006. http://dx.doi.org/10.21236/ada456006.

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3

Cendales, Linda C. Immunomodulation to Optimize Vascularized Composite Allograft Integration in Limb Loss Therapy. Fort Belvoir, VA: Defense Technical Information Center, ottobre 2013. http://dx.doi.org/10.21236/ada596553.

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4

Lee, W. P. Mesenchymal Stem Cell Therapy for Nerve Regeneration and Immunomodulation after Composite Tissue Allotransplantation. Fort Belvoir, VA: Defense Technical Information Center, agosto 2012. http://dx.doi.org/10.21236/ada574699.

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5

Lee, W. P. Mesenchymal Stem Cell Therapy for Nerve Regeneration and Immunomodulation After Composite Tissue Allotransplantation. Fort Belvoir, VA: Defense Technical Information Center, febbraio 2011. http://dx.doi.org/10.21236/ada559244.

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Loria, Roger M. Preliminary Studies on the Effects of Androstenetriol Induced Immunomodulation in the Treatment of Traumatic Shock. Fort Belvoir, VA: Defense Technical Information Center, maggio 2005. http://dx.doi.org/10.21236/ada456654.

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7

Kamaruzzaman, Mohd Amir, Muhammad Hibatullah Romli, Razif Abas, Sharmili Vidyadaran, Mohamad Taufik Hidayat Baharuldin, Muhammad Luqman Nasaruddin, Vishnnumukkala Thirupathirao et al. Impact of Endocannabinoid Mediated Glial Cells on Cognitive Function in Alzheimer’s Disease: A Systematic Review and Meta-Analysis of Animal Studies. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, agosto 2022. http://dx.doi.org/10.37766/inplasy2022.8.0094.

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Abstract (sommario):
Review question / Objective: This review aims to review systematically, and meta-analyse published pre-clinical research about the mechanism of endocannabinoid system modulation on glial cells and their effects on cognitive function in designated Alzheimer’s Disease (AD) in the animal model. Condition being studied: Its been acknowledged that the cure of Alzheimer's disease is still vague. Current medicine is working on symptoms only but never stop the disease progression due to neuronal loss. In recent years, researches have found that cannabinoid which is derived from cannabis sativa plant and its compounds exert neuroprotective effects in vitro and in vivo. In fact, cognitive improvement has been shown in some clinical studies. Therefore, the knowledge of cannabinoids and its interaction with living physiological environment like glial cells is crucial as immunomodulation to strategize the potential target of this substance. The original articles from related study relating endocannabinoid mediated glial cell were extracted to summarize and meta-analyze its impact and possible mechanism against cognitive decline in AD.
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Velkova, Lyudmila, Asya Daskalova, Alexandar Dolashki, Pavlina Dolashka e Tchavdar Vassilev. Immunomodulating Potential of IgG Antibodies with Induced Polyspecificity. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, ottobre 2021. http://dx.doi.org/10.7546/crabs.2021.10.08.

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