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Готові списки джерел за темами / Soluble CD89

Добірка наукової літератури з теми "Soluble CD89"

Автор: Grafiati

Опубліковано: 22 червня 2024

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Статті в журналах з теми "Soluble CD89":

1

Launay, Pierre, Béatrice Grossetête, Michelle Arcos-Fajardo, Emmanuelle Gaudin, Sonia P. Torres, Lucie Beaudoin, Natacha Patey-Mariaud de Serre, Agnès Lehuen та Renato C. Monteiro. "Fcα Receptor (Cd89) Mediates the Development of Immunoglobulin a (Iga) Nephropathy (Berger's Disease)". Journal of Experimental Medicine 191, № 11 (6 червня 1999): 1999–2010. http://dx.doi.org/10.1084/jem.191.11.1999.

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The pathogenesis of immunoglobulin A (IgA) nephropathy (IgAN), the most prevalent form of glomerulonephritis worldwide, involves circulating macromolecular IgA1 complexes. However, the molecular mechanism(s) of the disease remain poorly understood. We report here the presence of circulating soluble FcαR (CD89)-IgA complexes in patients with IgAN. Soluble CD89 was identified as a glycoprotein with a 24-kD backbone that corresponds to the expected size of CD89 extracellular domains. To demonstrate their pathogenic role, we generated transgenic (Tg) mice expressing human CD89 on macrophage/monocytes, as no CD89 homologue is found in mice. These mice spontaneously developed massive mesangial IgA deposition, glomerular and interstitial macrophage infiltration, mesangial matrix expansion, hematuria, and mild proteinuria. The molecular mechanism was shown to involve soluble CD89 released after interaction with IgA. This release was independent of CD89 association with the FcRγ chain. The disease was induced in recombination activating gene (RAG)2−/− mice by injection of serum from Tg mice, and in severe combined immunodeficiency (SCID)-Tg mice by injection of patients' IgA. Depletion of soluble CD89 from serum abolished this effect. These results reveal the key role of soluble CD89 in the pathogenesis of IgAN and provide an in vivo model that will be useful for developing new treatments.

2

van Zandbergen, Ger, Ralf Westerhuis, Ngaisah Klar Mohamad, Jan G. J. van de Winkel, Mohamed R. Daha та Cees van Kooten. "Crosslinking of the Human Fc Receptor for IgA (FcαRI/CD89) Triggers FcR γ-Chain-Dependent Shedding of Soluble CD89". Journal of Immunology 163, № 11 (1 грудня 1999): 5806–12. http://dx.doi.org/10.4049/jimmunol.163.11.5806.

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Abstract CD89/FcαRI is a 55- to 75-kDa type I receptor glycoprotein, expressed on myeloid cells, with important immune effector functions. At present, no information is available on the existence of soluble forms of this receptor. We developed an ELISA for the detection of soluble CD89 (sCD89) forms and investigated the regulation of sCD89 production. PMA/ionomycin stimulation of monocytic cell lines (U937, THP-1, and MM6), but not of neutrophils, resulted in release of sCD89. Crosslinking of CD89 either via its ligand IgA or with anti-CD89 mAbs similarly resulted in sCD89 release. Using CD89-transfected cells, we showed ligand-induced shedding to be dependent on coexpression of the FcR γ-chain subunit. Shedding of sCD89 was dependent on signaling via the γ-chain and prevented by addition of inhibitors of protein kinase C (staurosporine) or protein tyrosine kinases (genistein). Western blotting revealed sCD89 to have an apparent molecular mass of 30 kDa and to bind IgA in a dose-dependent fashion. In conclusion, the present data document a ligand-binding soluble form of CD89 that is released upon activation of CD89-expressing cells. Shedding of CD89 may play a role in fine-tuning CD89 immune effector functions.

3

Esteve Cols, Clara, Freddzia-Amanda Graterol Torres, Bibiana Quirant Sánchez, Helena Marco Rusiñol, Maruja Isabel Navarro Díaz, Jordi Ara del Rey, and Eva Mª Martínez Cáceres. "Immunological Pattern in IgA Nephropathy." International Journal of Molecular Sciences 21, no. 4 (February 18, 2020): 1389. http://dx.doi.org/10.3390/ijms21041389.

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The current gold-standard diagnostic technique for IgA nephropathy (IgAN), the leading form of primary glomerulonephritis, is renal biopsy. CD89 (the main IgA receptor) is expressed on the surface of monocytes and plays a role in disease pathogenesis. Immunocomplexes formed by sCD89 (soluble form) and Gd-IgA1 are related to disease prognosis. We hypothesize that reduced CD89 surface expression on monocytes may be a marker of disease severity. We aimed to analyze leukocyte subpopulations in peripheral blood and CD89 surface expression on monocytes in a prospective study of 22 patients and 12 healthy subjects (HS). Leukocyte subpopulations and CD89 expression were analyzed by flow cytometry. IgAN patients had a higher percentage of activated and effector memory CD4+ and CD8+ T lymphocytes, a lower percentage of transitional B lymphocytes and plasmablasts, and a higher percentage of CD56dimCD16+ NK cells and myeloid dendritic cells compared with HS. Correlations between reduced CD89 expression levels on nonclassical monocytes, histological findings of a poor prognosis on renal biopsy and baseline renal function were observed. IgAN patients show a characteristic immunological pattern in peripheral blood. A reduced expression level of CD89 on nonclassical monocytes identifies patients with a worse renal prognosis.

4

Wu, Haiting, Xiaoyan Wang, Zhe Yang, Qing Zhao, Yubing Wen, Xuemei Li, Wei Zhang, and Ruitong Gao. "Serum Soluble CD89-IgA Complexes Are Elevated in IgA Nephropathy without Immunosuppressant History." Disease Markers 2020 (January 16, 2020): 1–6. http://dx.doi.org/10.1155/2020/8393075.

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Purpose. CD89 (FcαRI), the receptor of IgA, can shed from cells to form complexes with IgA in serum and is supposed to participate in the pathogenesis of IgA nephropathy (IgAN). There are contradictory results on their utility in clinical practice. This study is aimed at investigating whether sCD89-IgA complexes can help in the diagnosis or evaluation of the disease. Methods. A sandwich ELISA was established using anti-CD89 as a capture antibody and HRP-conjugated anti-IgA as a detection antibody. This method was used to measure serum levels of sCD89-IgA complexes in IgAN patients without immunosuppressant history and healthy subjects. Correlations between serum levels of sCD89-IgA complexes and disease severity were analyzed. Results. Serum sCD89-IgA complexes increased with age (P<0.001). IgAN patients had higher sCD89-IgA complex levels compared with age- and gender-matched normal healthy individuals (P<0.001). Serum sCD89-IgAN significantly predicted IgAN diagnosis (AUC = 0.762 (0.640-0.883), P<0.001). But sCD89-IgA complexes did not correlate with baseline clinical manifestations, oxford classification, or renal function deteriorate speed. Conclusions. Serum sCD89-IgA complexes can guide diagnosis of IgAN in patients without immunosuppressant history, but provide limited help in clinicopathologic prediction.

5

Cambier, Alexandra, Patrick J. Gleeson, Lilia Abbad, Fanny Canesi, Jennifer da Silva, Julie Bex-Coudrat, Georges Deschênes, et al. "Soluble CD89 is a critical factor for mesangial proliferation in childhood IgA nephropathy." Kidney International 101, no. 2 (February 2022): 274–87. http://dx.doi.org/10.1016/j.kint.2021.09.023.

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6

Berthelot, Laureline, Thomas Robert, Vincent Vuiblet, Thierry Tabary, Antoine Braconnier, Moustapha Dramé, Olivier Toupance, Philippe Rieu, Renato C. Monteiro, and Fatouma Touré. "Recurrent IgA nephropathy is predicted by altered glycosylated IgA, autoantibodies and soluble CD89 complexes." Kidney International 88, no. 4 (October 2015): 815–22. http://dx.doi.org/10.1038/ki.2015.158.

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7

Vuong, Mai T., Mirjana Hahn-Zoric, Sigrid Lundberg, Iva Gunnarsson, Cees van Kooten, Lars Wramner, Maria Seddighzadeh, et al. "Association of soluble CD89 levels with disease progression but not susceptibility in IgA nephropathy." Kidney International 78, no. 12 (December 2010): 1281–87. http://dx.doi.org/10.1038/ki.2010.314.

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8

Hahn-Zoric, Mirjana, Mai Vuong, Sigrid Lundberg, Lars Wramner, Jarl Ahlmen, Lars Å. Hanson, Iva Gunnarsson, Stefan Jacobson, and Leonid Padyukov. "Su.82. Evidence for Genetic Regulation of Fc Alpha Receptor (CD89) Expression: Study of Soluble CD89 in Plasma of IgA Nephropathy Patients and Healthy Controls." Clinical Immunology 127 (January 2008): S151. http://dx.doi.org/10.1016/j.clim.2008.03.433.

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9

Hahn-Zoric, Mirjana, Neda Tahmasebifar, Cees van Kooten, Jarl Ahlmen, Svante Swerkersson, Sverker Hansson, Ulla Berg, Lars Åke Hanson, Leonid Padyukov, and Stefan H. Jacobson. "Immunoassays for Detection of Soluble Fc Alpha Receptor (CD89) in Plasma of IgA Nephropathy Patients." Clinical Immunology 123 (2007): S54—S55. http://dx.doi.org/10.1016/j.clim.2007.03.335.

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10

Berthelot, Laureline, Christina Papista, Thiago T. Maciel, Martine Biarnes-Pelicot, Emilie Tissandie, Pamela H. M. Wang, Houda Tamouza, et al. "Transglutaminase is essential for IgA nephropathy development acting through IgA receptors." Journal of Experimental Medicine 209, no. 4 (March 26, 2012): 793–806. http://dx.doi.org/10.1084/jem.20112005.

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IgA nephropathy (IgAN) is a common cause of renal failure worldwide. Treatment is limited because of a complex pathogenesis, including unknown factors favoring IgA1 deposition in the glomerular mesangium. IgA receptor abnormalities are implicated, including circulating IgA–soluble CD89 (sCD89) complexes and overexpression of the mesangial IgA1 receptor, TfR1 (transferrin receptor 1). Herein, we show that although mice expressing both human IgA1 and CD89 displayed circulating and mesangial deposits of IgA1–sCD89 complexes resulting in kidney inflammation, hematuria, and proteinuria, mice expressing IgA1 only displayed endocapillary IgA1 deposition but neither mesangial injury nor kidney dysfunction. sCD89 injection into IgA1-expressing mouse recipients induced mesangial IgA1 deposits. sCD89 was also detected in patient and mouse mesangium. IgA1 deposition involved a direct binding of sCD89 to mesangial TfR1 resulting in TfR1 up-regulation. sCD89–TfR1 interaction induced mesangial surface expression of TGase2 (transglutaminase 2), which in turn up-regulated TfR1 expression. In the absence of TGase2, IgA1–sCD89 deposits were dramatically impaired. These data reveal a cooperation between IgA1, sCD89, TfR1, and TGase2 on mesangial cells needed for disease development. They demonstrate that TGase2 is responsible for a pathogenic amplification loop facilitating IgA1–sCD89 deposition and mesangial cell activation, thus identifying TGase2 as a target for therapeutic intervention in this disease.

Більше джерел

Дисертації з теми "Soluble CD89":

1

Staab, Christine [Verfasser], and Lars [Akademischer Betreuer] Nitschke. "Production of Recombinant Human Soluble CD83 in an Eukaryotic System and Generation of Tissue-Specific CD83 Knock-out Mice / Christine Staab. Betreuer: Lars Nitschke." Erlangen : Universitätsbibliothek der Universität Erlangen-Nürnberg, 2011. http://d-nb.info/1015475329/34.

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2

Sanchez, Vidales Maria Del Mar. "Release of Soluble Interleukin-7 α Receptor (CD127) from CD8+ T-Cells and Human Thymocytes". Thesis, Université d'Ottawa / University of Ottawa, 2016. http://hdl.handle.net/10393/34631.

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ABSTRACT Background Interleukin-7 (IL-7) is a cytokine crucial for T-cell development and homeostasis. IL-7 is thought to be a limited resource, and its interaction with the IL-7 receptor (IL-7R) has effects on increasing cell survival, proliferation and cytolytic function. Considering the roles of IL-7, it is no surprise that the expression of the IL-7 receptor alpha chain (CD127) is tightly regulated. Despite increased levels of soluble CD127 (sCD127) being detected in a number of disease states and being associated with disease activity, the biological function of sCD127 and its clinical relevance remains to be established. In this study, I explore the post-translational mechanisms leading to the release of the soluble form of CD127 receptor through IL-7 and αCD3/αCD28 stimulation. Here I specifically established two different mechanisms by which CD127 is processed; shedding of the receptor ectodomain and clipping. Results In CD8+ T-cells, IL-7 plus TcR stimulation resulted in an increased release of sCD127. Here I found that matrix metalloproteases (MMPs), in particular MMP-9, have a role in the proteolytic clipping of CD127 resulting in the release of sCD127. In addition, I found that IL-7 plus TcR stimulation resulted in an increase in MMP activity and this activity was particularly dampened when MMP-2 and -9 inhibitors were used. I also found that neither MMP-3 nor cysteine and serine proteases seem to be directly involved in the generation of sCD127. Using a biotinylation assay I found that CD127 is being shed from the surface of CD8+ T-cells as well as thymocytes through a MMP-independent mechanism. Conclusion These results demonstrate that MMPs (in particular MMP-9) have a role in the generation of sCD127. Further studies are required to determine the specific sheddase responsible for the ectodomain shedding of CD127, as well as the details behind the regulation of MMP-9 activity both in CD8+ T-cells and thymocytes. A thorough understanding of these mechanisms will aid in the development of alternative and more specific strategies to control IL-7 mediated processes in both normal and disease states.

3

Aloufi, Nawaf. "The role of sCD127 in IL-7-Mediated T Cell Homeostasis in Vivo." Thesis, Université d'Ottawa / University of Ottawa, 2020. http://hdl.handle.net/10393/41089.

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Interleukin-7 is an essential cytokine that plays a major role in the development and homeostatic maintenance of T-cells. The presence of soluble forms of various cytokine receptors have been proposed to be involved in the endogenous regulation of cytokine activity. Due to the natural ability of soluble CD127 (sCD127) to bind to IL-7, there is an interest in its potential application as an immunotherapeutic agent in diseases, where IL-7 has been found to be relevant, including HIV infection. In this study, I hypothesize that by administering sCD127 to healthy mice, IL-7 activity should be enhanced, thus enhancing T cell proliferation in vivo. The work presented here focuses on three main objectives: 1) evaluating the effect of IL-7 with or without sCD127 on T cell proliferation in healthy mice; 2) validating a mouse model of T cell depletion using anti-CD4 and CD8 antibodies; and 3) determining the effect of sCD127 treatment with or without IL-7 on T cell reconstitution and proliferation in the T cell depletion model. To assess the effect of administering exogenous sCD127, IL-7 or the combination on T cell proliferation, peripheral blood mononuclear cells and spleen were isolated, and stained to characterize T cell number, proliferation, and surface CD127 expression by flow cytometry. For the T cell depletion model, wild type C57BL/6 mice were injected intra-peritoneally with 150 μg single dose of anti-CD4 and anti-CD8 depleting antibodies. Consequently, mice were bled weekly to demonstrate the kinetics of T cell reconstitution following depletion (from d7 to d63). Our results demonstrated that in healthy mice daily treatment with murine IL-7 significantly stimulated T cell proliferation and consequently increased cell number. This observation was further boosted by pre-complexing IL-7 with sCD127. For T cell depletion experiments, the kinetics of T-cell reconstitution was different between the CD4+ and CD8+ T cells. CD4+ T cell reconstitution was almost complete 6 weeks following T cell depletion, while CD8+ T cells were only partially reconstituted at this time point. Treatment with IL-7 or combined therapy had a transient and significant effect on T cell proliferation and reconstitution, and this influence was abrogated after treatment discontinuation. Interestingly, CD8+ T cells exert greater responses to our treatments in that a more pronounced proliferation and significant increase in cell number was observed relative to the effect seen on CD4+ T cells in both healthy and depleted mice. In conclusion, antibody-mediated T cell depletion is a potentially valuable tool to investigate lymphopenia-induced proliferation and potential therapies thereof. This study suggests that combining sCD127 and IL-7 therapies enhances IL-7-mediated T cell proliferation, and provides important information for the potential therapeutic use of sCD127 and its impact on IL-7 function.

4

Morice, Yoann. "Le virus de l'hépatite C : études de la variabilité inter- et intra-génomique : production sous forme soluble de protéines membranaires impliquées dans l'interaction virus-cellule hôte." Paris 7, 2002. http://www.theses.fr/2002PA077217.

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5

SADAT, SOWTI COMBADIERE BEHAZINE. "Controle des reponses cytotoxiques par les lymphocytes cd8+cd57+ au cours de l'infection par le vih et apres transplanttion de moelle osseuse / caracterisation d'un facteur soluble inhibiteur (icf)." Paris 7, 1993. http://www.theses.fr/1993PA077357.

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L'infection par le vih induit une reponse cytotoxique specifique d'antigene intense mais incapable de proteger les patients infectes par le vih. Nous avons contribue a l'etude de ce probleme en decrivant une nouvelle propriete des lymphocytes t cd8+ coexprimant le marqueur cd57. En effet, les cellules cd8+cd57+ augmentees chez les patients infectes par le vih et apres transplantation de moelle osseuse, sont spontanement capables d'inhiber la phase effectrice des activites cytotoxiques mediees par les ctl specifiques d'antigenes, les cellules nk et lak. De plus, les cellules cd8+cd57+ exercent leur activite inhibitrice par l'intermediaire d'une glycoproteine soluble inhibitrice (icf inhibitor of cytotoxic functions), different des cytokines telles que le tgfb, le tnfa et b, l'ifng ou les pge2. Les caracteristiques physicochimiques de l'icf ont permis de mettre au point une methode de purification en vue du sequencage de l'extremite nh2-terminale de l'icf. En effet, l'activite inhibitrice de l'icf est sensible a la pronase e, mais resistante a la trypsine et a la chaleur. Son affinite pour la concanavalin a, suggere l'existence d'une ou des proteines glycosylees de poids moleculaire de 20 et 30 kdaltons. De plus, l'interferon gamma et l'interleukine-4 sont capables d'induire une levee d'activite inhibitrice de l'icf de maniere a restaurer l'activite cytotoxique des cellules lak, nk et ctl. Ces derniers resultats suggerent un role probable de l'icf dans le reseau de cytokines. Ces cellules ainsi que les molecules inhibitrices relarguees semblent jouer un role important dans le controle des reponses immunitaires apres l'infection par le vih et transplantation de moelle osseuse.

6

Kastenmüller, Kathrin [Verfasser], Dirk [Akademischer Betreuer] Busch, Wolfgang [Akademischer Betreuer] Wurst, and Siegfried [Akademischer Betreuer] Scherer. "Generation of CD8+ T cell mediated protective immunity upon vaccination with soluble antigen : involvement of immunmodulatory factors like adjuvant or regulatory lymphocytes / Kathrin Kastenmüller. Gutachter: Wolfgang Wurst ; Siegfried Scherer. Betreuer: Dirk Busch." München : Universitätsbibliothek der TU München, 2006. http://d-nb.info/1058141163/34.

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7

Dioszeghy, Vincent. "Etude des activités antivirales solubles non cytolytiques des lymphocytes CD8+ au cours de l'infection par SIV : Effet d'un traitement par polychimiothérapie post-exposition, effet d'un traitement immuno-modulateur par l'interleukine 2 et mécanismes de reconstitution lymphocytaire T CD4+." Paris 11, 2006. http://www.theses.fr/2006PA11T012.

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8

Müssig, Oliver. "Bedeutung des löslichen CD14-Rezeptors in Plasma und Urin als immunologischer Parameter nach Nierentransplantation und sein Verhältnis zu den löslichen Rezeptoren IL2R, CD4 und CD8." Doctoral thesis, 2011. http://hdl.handle.net/11858/00-1735-0000-0006-B1DF-C.

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9

Berg, Martina [Verfasser]. "Induction of cytotoxic CD8+ T cells by a soluble HLA-derived tumor-associated peptide and regulation of CD8+ T cell activation by CTLA-4 / vorgelegt von Martina Berg." 2005. http://d-nb.info/977277305/34.

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10

DI, FILIPPO ALESSANDRA. "Immune profile of cancer patients to improve selection and efficacy of immunotherapeutic strategies." Doctoral thesis, 2022. https://hdl.handle.net/11573/1665638.

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Over the years, the clinical outcome of cancer patients has remarkably improved with the introduction of immune checkpoint inhibitors (ICIs) and tyrosine kinase inhibitors (TKIs), that by targeting immune system restore an efficient anti-tumor immune response. Despite the potential of immunotherapy as cancer leading treatment, initial response rates with ICIs are however limited and depend on the host pre-existing anti-cancer immunity and the degree of immunosuppression present in the patient. Most of patients fail to respond and to increase the number of responder patients is necessary a more in-depth understanding of the underlying immunity and the identification of biomarkers. In this research project we investigate and characterize the immune system of cancer patients (mRCC, NSCLC, HNSCC, UM) before and during treatment with TKIs or ICIs, in order to investigate the relation between circulating immune profile, tumor microenvironment (TME), the gut microbiome and clinical outcome. The aim was the identification of possible biomarkers/immune profile able to select patients and improve clinical outcome. We assessed immunological analysis to evaluate exhausted/activated circulating T cells by cytofluorimetric assay, 14 immune checkpoint-related proteins and 20 inflammation cytokines/chemokines using Luminex assay. The immunological profile was correlated with survival (PFS and OS), clinical parameters and response to treatment. Gut microbiota composition was evaluated through metagenomic analysis and immunohistochemistry was used to characterize tumor microenvironment. Our results demonstrated that TKIs and ICIs modulate immune system. We observed a decrease of soluble immune checkpoint molecules in serum of mRCC (sPDL2, sHVEM, sPD1, sGITR) and NSCLC patients (sPD1, sPDL2) during treatment (p<0.05). In particular, the decrease of sPD1 and sPDL2 resulted associated with response to treatments (p=0.03 and p=0.01, respectively). Moreover, the immune profile of responder (R) patients was characterized by low levels of soluble protein (sCTLA4, sPD-L1 in mRCC vs sCD137, sTIM3, sPDL1, sPDL2 in NSCLC) (p<0.05) and by a high proportion of eubiosis-associated gut metabolites. These data resulted also associated with better clinical status, PS=0 (performance status). Profiling circulating immune cells in patients undergoing ICI treatment (anti-PD1) we identified CD3+CD137+ and CD3+CD8+CD137+ T cells that correlate with improved response to therapy. The percentage of both CD3+CD137+ and CD3+CD8+CD137+ T population was higher in R patients (p=0.03 and p=0.02) and correlated to a better survival in terms of PFS and OS (p<0.05). Moreover, R patients had higher levels of CD3+CD137+PD1+ and of CD8+CD137+PD1+ lymphocytes (p=0.02 and p=0.01), but only CD3+CD137+PD1+ resulted associated with a low number of metastasis (p=0.01) and longer survival (OS)(p=0.015). Instead, the high concentration of the immunosuppressive sCD137 in the serum was associated with a lower PFS (p=0.038) and OS (p=0.012). In tumor microenvironment, patients with a complete pathological response showed a high percentage of CD137+ and CD8+ T cells. Results were validated in an independent cohort of metastatic cancer patients. These results identified immunological parameters that, independently from tumor setting and administered therapy, predict clinical outcome of cancer patients, monitor immune response and help clinicians in the decision-making.

Частини книг з теми "Soluble CD89":

1

Lusso, Paolo. "Suppression of Primate Immunodeficiency Lentiretroviruses by CD8+ T-Cell-Derived Soluble Factors." In AIDS Pathogenesis, 133–53. Dordrecht: Springer Netherlands, 2000. http://dx.doi.org/10.1007/978-94-017-0685-8_8.

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2

Weiss, C., S. Hohaus, E. Ogniben, M. Dörner, and R. Haas. "Effect of Recombinant Human Granulocyte—Macrophage Colony-Stimulating Factor on Serum Levels of Soluble CD25, CD8, and CD4 in Patients with Hodgkin’s Disease in Sensitive Relapse." In Cytokines in Hemopoiesis, Oncology, and AIDS II, 587–93. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-48715-6_74.

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3

Bayhan, Ülkü, and Remziye Banka. "Nobel Molecule Artemisia-Annua and T-CD8+ Receptor Bestfit Interactions." In Matematik ve Fen Bilimleri Üzerine Araştırmalar-II. Özgür Yayınları, 2023. http://dx.doi.org/10.58830/ozgur.pub165.c799.

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Effector T cells, one of the body's defense cells, have an active role in the regulation of immune responses. These T cells have assumed the role of defense between the soluble substances they produce and the ligand interactions on their surface, and the regulators of the immune system. The CD8+ cells surface receptor control intracellular pathogens. CD8+ cells directly mark cells infected with intracellular organisms. In this study, the interactions between Artemisia annua ligand molecule and CD8+ surface protein molecules were investigated. AutoDock 4 –MGLTolls package program was used for the calculations, taking into account the basic energy data by determining the best binding site of the protein to the ligand interaction.

4

"CD8 Antiviral Soluble Factors and Human Immunodeficiency Virus (HIV) Control." In Soluble Factors Mediating Innate Immune Responses to HIV Infection, edited by Nitin K. Saksena, Jing Qin Wu, Katherine Lau, Li Zhou, Maly Soedjono, and Bin Wang, 1–16. BENTHAM SCIENCE PUBLISHERS, 2012. http://dx.doi.org/10.2174/978160805006211001010001.

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5

Magnin, Morgane, Philippe Guillaume, George Coukos, Alexandre Harari, and Julien Schmidt. "High-throughput identification of human antigen-specific CD8+ and CD4+ T cells using soluble pMHC multimers." In Methods in Enzymology, 21–42. Elsevier, 2020. http://dx.doi.org/10.1016/bs.mie.2019.05.019.

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Тези доповідей конференцій з теми "Soluble CD89":

1

Soodaeva, Svetlana K., Nailya Kubysheva, Larisa Postnikova, Viktor Novikov, Tatyana Eliseeva, and Igor A. Klimanov. "The level of soluble CD8 molecules in serum and sputum in COPD patients with an exacerbation." In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.pa3653.

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2

Asai, Kazuhisa, Nahoko Shiratsuchi-Nakagawa, Gakuya Tamagaki, Tetsuya Watanabe, Yumiko Imahashi, Yukikazu Ichimaru, Yoshihiro Tochino, Hiroshi Kamoi, Hiroshi Kanazawa, and Kazuto Hirata. "Soluble Perforin, A Marker Of CD8+ T Lymphocyte Activation In Epithelial Lining Fluid In COPD Patients." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a4545.

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3

Haile, Samuel, Sonia P. Dalal, Virginia Clements, Koji Tamada, and Suzanne Ostrand-Rosenberg. "Abstract 462: Soluble CD80 restores T-cell activation and overcomes tumor cell programmed death ligand-1-mediated suppression." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-462.

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4

Horn, Lucas, Virginia Clements, and Suzanne Ostrand-Rosenberg. "Abstract B013: A soluble form of CD80 enhances anti-tumor immunity by inhibiting PDL1 immune suppression and does not suppress via CTLA-4." In Abstracts: CRI-CIMT-EATI-AACR Inaugural International Cancer Immunotherapy Conference: Translating Science into Survival; September 16-19, 2015; New York, NY. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/2326-6074.cricimteatiaacr15-b013.

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5

Long, Tiha M., and Suzanne Ostrand-Rosenberg. "Abstract B017: A soluble form of CD80 inhibits PD-L1 immune suppression and stimulates T cells through CD28-specific pathways indicating potential for increased therapeutic activity over checkpoint inhibition alone." In Abstracts: CRI-CIMT-EATI-AACR Inaugural International Cancer Immunotherapy Conference: Translating Science into Survival; September 16-19, 2015; New York, NY. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/2326-6074.cricimteatiaacr15-b017.

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6

Zhang, Jinyu, Pablo Larrocha, Payal Dhar, and Jennifer Wu. "Abstract A77: Antibody targeting tumor-derived soluble NKG2D ligand sMIC provides dual costimulation of CD8 T cells and enables sMIC+ tumors to respond to PD1/PD-L1 blockade therapy." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; November 17-20, 2019; Boston, MA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/2326-6074.tumimm19-a77.

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