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      Low-dose interleukin-2 treatment selectively modulates CD4(+) T cell subsets in patients with systemic lupus erythematosus.

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          Abstract

          Systemic lupus erythematosus (SLE) is a potentially life-threatening autoimmune disease characterized by altered balance of activity between effector and regulatory CD4(+) T cells. The homeostasis of CD4(+) T cell subsets is regulated by interleukin (IL)-2, and reduced production of IL-2 by T cells is observed in individuals with SLE. Here we report that treatment with low-dose recombinant human IL-2 selectively modulated the abundance of regulatory T (Treg) cells, follicular helper T (TFH) cells and IL-17-producing helper T (TH17) cells, but not TH1 or TH2 cells, accompanied by marked reductions of disease activity in patients with SLE.

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          Updating the American college of rheumatology revised criteria for the classification of systemic lupus erythematosus

          Marc Hochberg (1997)
          Article 0 comments Cited 1315 times – based on 0 reviews     Review now
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            Systemic lupus erythematosus.

            George C. Tsokos (2011)
            Article 0 comments Cited 563 times – based on 0 reviews     Review now
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              Interleukin-2 and regulatory T cells in graft-versus-host disease.

              John Koreth, Ken-ichi Matsuoka, Haesook T. Kim … (2011)
              Dysfunction of regulatory T (Treg) cells has been detected in diverse inflammatory disorders, including chronic graft-versus-host disease (GVHD). Interleukin-2 is critical for Treg cell growth, survival, and activity. We hypothesized that low-dose interleukin-2 could preferentially enhance Treg cells in vivo and suppress clinical manifestations of chronic GVHD. In this observational cohort study, patients with chronic GVHD that was refractory to glucocorticoid therapy received daily low-dose subcutaneous interleukin-2 (0.3×10(6), 1×10(6), or 3×10(6) IU per square meter of body-surface area) for 8 weeks. The end points were safety and clinical and immunologic response. After a 4-week hiatus, patients with a response could receive interleukin-2 for an extended period. A total of 29 patients were enrolled. None had progression of chronic GVHD or relapse of a hematologic cancer. The maximum tolerated dose of interleukin-2 was 1×10(6) IU per square meter. The highest dose level induced unacceptable constitutional symptoms. Of the 23 patients who could be evaluated for response, 12 had major responses involving multiple sites. The numbers of CD4+ Treg cells were preferentially increased in all patients, with a peak median value, at 4 weeks, that was more than eight times the baseline value (P<0.001), without affecting CD4+ conventional T (Tcon) cells. The Treg:Tcon ratio increased to a median of more than five times the baseline value (P<0.001). The Treg cell count and Treg:Tcon ratio remained elevated at 8 weeks (P<0.001 for both comparisons with baseline values), then declined when the patients were not receiving interleukin-2. The increased numbers of Treg cells expressed the transcription factor forkhead box P3 (FOXP3) and could inhibit autologous Tcon cells. Immunologic and clinical responses were sustained in patients who received interleukin-2 for an extended period, permitting the glucocorticoid dose to be tapered by a mean of 60% (range, 25 to 100). Daily low-dose interleukin-2 was safely administered in patients with active chronic GVHD that was refractory to glucocorticoid therapy. Administration was associated with preferential, sustained Treg cell expansion in vivo and amelioration of the manifestations of chronic GVHD in a substantial proportion of patients. (Funded by a Dana-Farber Dunkin' Donuts Rising Star award and others; ClinicalTrials.gov number, NCT00529035.).
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                Author and article information

                Journal
                Journal ID (iso-abbrev): Nat. Med.
                Title: Nature medicine
                Publisher: Springer Nature
                ISSN (Electronic): 1546-170X
                ISSN (Print): 1078-8956
                Publication date (Electronic): Sep 2016
                Volume: 22
                Issue: 9
                Affiliations
                [1 ] Department of Rheumatology and Immunology, Peking University People's Hospital, Beijing, China.
                [2 ] Laboratory of Immunology for Environment and Health, Shandong Analysis and Test Center, Shandong Academy of Sciences, Jinan, China.
                [3 ] Laboratory for Molecular Immunomodulation, Department of Biochemistry and Molecular Biology, Infection and Immunity Program, Monash Biomedicine Discovery Institute, Monash University, Clayton, Victoria, Australia.
                [4 ] China-Australia Centre for Personalised Immunology, Shanghai Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
                [5 ] Centre for Inflammatory Diseases, School of Clinical Sciences at Monash Health, Monash University, Clayton, Victoria, Australia.
                Article
                Publisher Item ID: nm.4148
                DOI: 10.1038/nm.4148
                PubMed ID: 27500725
                SO-VID: ad51442c-3389-4037-99cd-1e2ef326d052
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