Selective Stimulation of T Cell Subsets with Antibody-Cytokine Immune Complexes
By O. Boyman, M. Kovář, M. Rubinstein, C. Surh, J. Sprent. Science, 2006
928 citations recorded by the source corpus.
Subfields: Immunology, Oncology
View Paper: https://www.semanticscholar.org/paper/49b49c3d611a7450d168df73a65c0f8b94568887
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Immunology
In Oncology
Citations in the corpus
- Interleukin-2 at the Crossroads of Effector Responses, Tolerance, and Immunotherapy (2013, neutral): “…cell dysfunction due to defective IL-2 production results in the breakdown of self-tolerance, but administering low doses of IL-2 and IL-2 mAbs (Boyman et al., 2006), which form stable immune complexes, increased Treg cell survival and decreased the incidence of diabetes (Tang et al., 2008),…”
- A Special Population of Regulatory T Cells Potentiates Muscle Repair (2013, positive): “For the gain-of-function experiments, we made use of the published observation that complexes of recombinant IL-2 and a particular anti-IL-2 mAb (clone JES6-1A12) can preferentially expand Treg populations after injection into mice (Boyman et al., 2006).”
- The role of interleukin-2 during homeostasis and activation of the immune system (2012, background): “Cells expressing high levels of the dimeric IL-2R are sensitive to exogenously administered IL-2, but these cells are presumably unresponsive to the low physiological levels of IL-2 found in vivo”
- The transcription factors Blimp-1 and IRF4 jointly control the differentiation and function of effector regulatory T cells (2011, neutral): “, we investigated whether increasing the IL-2 concentration by injecting complexes of IL-2 and antibody to IL-2 (anti-IL-2”
- Central role of defective interleukin-2 production in the triggering of islet autoimmune destruction. (2008, background): “memory T cells in C57BL/6 mice ( Boyman et al., 2006 ), led to a marked increase in CD25 expression in Treg cells (Figure 5A) and a systemic increase in the percentage of Treg cells (Figure 5B).”
- Shaping and reshaping CD8+ T-cell memory (2008, background): “The functionality of CD25-deficient memory CD8 + T cells could be restored by injection of a complex of IL-2 and an IL-2-specific antibody that allows signalling through the low affinity IL-2 receptor ( CD122”
- Fat Treg cells: a liaison between the immune and metabolic systems (2009, methodology): “Therefore, as an alternative means to achieve gain-of-function, we turned to in situ expansion of T reg cells via injection of a complex consisting of recombinant IL-2 and a particular–IL-2–specific monoclonal antibody (mAb), previously shown to selectively elicit T reg cell”