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. Annu. Rev. Immunol., 2000, 18, 53–81. Delong, T., Baker, R. L., He, J., et al.: Diabetogenic T-cell clones recognize an altered peptide of chromogranin A. Diabetes, 2012, 61 (12), 3239

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Clari MA, Aguilar G, Benet I, et al. Evaluation of cytomegalovirus (CMV)-specific T-cell immunity for the assessment of the risk of active CMV infection in non-immunosuppressed surgical and trauma intensive care

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Orvosi Hetilap
Authors: Lenke Jenei Kluch, Irén Erdei, Éva Remenyik, Éva Surányi, Ferenc Bodnár, Gabriella Emri, and Andrea Szegedi

2020; 75: 781–797. 11 Naisbitt DJ, Farrell J, Wong G, et al. Characterization of drug-specific T cells in lamotrigine hypersensitivity. J Allergy Clin Immunol

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,  6 ]. In this case, the number of naive T-cells in the periphery is reduced [ 7 ] with the proliferation of resident T-cells, which later stops the proliferation. This is followed by a decline in immune function, consequently the weakness of immune

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. Early experience with CliniMACS Prodigy CCS (IFN-gamma) System in selection of virus-specific T-cells from third-party donors for pediatric patients with severe viral infections after

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The lentiviral protein Nef recruits cellular signalling proteins to lipid rafts at the cell membrane and acts thereby as a master regulator affecting the transcription of a series of cellular genes. By activating resting T cells, Nef creates an optimal environment for lentivirus replication. In human immunodeficiency virus (HIV) infected macrophages and microglial cells Nef activates the production of T-cell attracting chemokines and contributes to the development HIV infection associated brain damage. Nef also functions as an adaptor or connector protein downregulating CD4 and CCR5, the key receptor and one of the coreceptors for HIV. It also downregulates cell surface expression of a subset of class I MHC molecules which contributes to viral immune evasion. Extracellular, soluble Nef may facilitate the spread of T-cell-tropic HIV variants and mediate a switch in dominant replicating HIV strains (from macrophage- tropic to T-cell-tropic viruses) in AIDS (acquired immunodeficiency syndrome) patients. Virion-bound Nef enhances infectivity. Nef is a potential target of antiretroviral therapy and nef-deleted (attenuated) retroviruses have been considered as candidate vaccines against HIV. We suggest that nef-deleted or highly mutated defective HIV (dHIV) genomes interfere with replication of “wild type” HIV in certain long-term non-progressor individuals. This implies that introduction of artificially constructed dHIV genomes (by infusion of leukocytes carrying dHIV proviruses) into HIV infected individuals could slow disease progression and could be considered as a therapeutic possibility.

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the autoimmune regulator AIRE are associated with common organ-specific autoimmune disease. Immunity 2015; 42: 1185–1196. 10 Maródi L. Inborn errors of T cell immunity

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in T cells from women with systemic lupus erythematosus. J. Rheumatol., 2001, 28 (12), 2644–2649. 17 Cutolo, M., Sulli, A., Straub, R. H.: Estrogen metabolism and

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Immune cells synthesize, store and secrete hormones, the level of which changes in ALL. In previous experiments the level of histamine, serotonin and triiodothyronine (T3)was studied, while at present that of ACTH, insulin and epinephrine, using flow cytometric analysis for the determination of cell subsets and detection of hor-mone content. The measurements were done in children at the time of diagnosis. ACTH was significantly elevated in each T cell subsets (total T, Th, Tc, activated T), while B and NK cells were not touched. The alterations in the insulin content (decrease in Tc and activated T cells) were uncertain, and NK cells contained significantly less insulin. The disease did not influence the cells’ epinephrine content. There is not clear explanation for the importance of changes in the cells’ hormone content, however, it is discussed in the text.

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Szabolcs-Szatmár-Bereg megyei leukaemia/lymphoma regiszterben.] Magy. Belorv. Arch., 1998, 51 (5), 367–370. [Hungarian] Nikl, J., Barakonyi, I., Sipos, J.: Primary central nervous system T-cell lymphoma. [Központi

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