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Ives, Megan L., BAdvSc; Ma, Cindy S., PhD; Palendira, Umaimainthan, PhD; Chan, Anna, MSc; Bustamante, Jacinta, MD, PhD; Boisson-Dupuis, Stephanie, PhD; Arkwright, Peter D., FRCPCH, DPhil; Engelhard, Dan, MD; Averbuch, Diana, MD; Magdorf, Klaus, MD; Roesler, Joachim, MD, PhD; Peake, Jane, MBBS; Wong, Melanie, MBBS, PhD, FRCPA; Adelstein, Stephen, MBBS, PhD, FRACP, FRCPA; Choo, Sharon, MBBS, FRACP, FRCPA; Smart, Joanne M., MBBS, FRACP; French, Martyn A., MB ChB, MD, FRACP, FRCPath, FRCP; Fulcher, David A., MBBS, PhD, FRACP, FRCPA; Cook, Matthew C., MBBS, PhD, FRACP, FRCPA; Picard, Capucine, MD, PhD; Durandy, Anne, MD, PhD; Tsumura, Miyuki, MSc; Kobayashi, Masao, MD, PhD; Uzel, Gulbu, MD; Casanova, Jean-Laurent, MD, PhD; Tangye, Stuart G., PhD; Deenick, Elissa K., PhD
Journal of allergy and clinical immunology, 08/2013, Letnik: 132, Številka: 2Journal Article
Background The capacity of CD8+ T cells to control infections and mediate antitumor immunity requires the development and survival of effector and memory cells. IL-21 has emerged as a potent inducer of CD8+ T-cell effector function and memory development in mouse models of infectious disease. However, the role of IL-21 and associated signaling pathways in protective CD8+ T-cell immunity in human subjects is unknown. Objective We sought to determine which signaling pathways mediate the effects of IL-21 on human CD8+ T cells and whether defects in these pathways contribute to disease pathogenesis in patients with primary immunodeficiencies caused by mutations in components of the IL-21 signaling cascade. Methods Human primary immunodeficiencies resulting from monogenic mutations provide a unique opportunity to assess the requirement for particular molecules in regulating human lymphocyte function. Lymphocytes from patients with loss-of-function mutations in signal transducer and activator of transcription 1 (STAT1) , STAT3 , or IL-21 receptor (IL21R) were used to assess the respective roles of these genes in human CD8+ T-cell differentiation in vivo and in vitro. Results Mutations in STAT3 and IL21R , but not STAT1 , led to a decrease in multiple memory CD8+ T-cell subsets in vivo , indicating that STAT3 signaling, possibly downstream of IL-21R, regulates the memory cell pool. Furthermore, STAT3 was important for inducing the lytic machinery in IL-21–stimulated naive CD8+ T cells. However, this defect was overcome by T-cell receptor engagement. Conclusion The IL-21R/STAT3 pathway is required for many aspects of human CD8+ T-cell behavior but in some cases can be compensated by other signals. This helps explain the relatively mild susceptibility to viral disease observed in STAT3- and IL-21R–deficient subjects.
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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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in: SICRIS
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