Central role of defective interleukin-2 production in the triggering of islet autoimmune destruction.

By Q. Tang, J. Y. Adams, C. Penaranda, Kristin Melli, E. Piaggio, Evridiki Sgouroudis, C. Piccirillo, B. Salomon, J. Bluestone. Immunity, 2008

783 citations recorded by the source corpus.

Subfields: Immunology

View Paper: https://www.semanticscholar.org/paper/43f851554ce4c32b5f70a1cf8d6e632880a0d3e5

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In Immunology

1. Jian-Xin Lin
2. W. Liao
3. T. Malek
4. W. Leonard
5. I. Castro
6. J. Buckner
7. Y. Belkaid
8. J. Bluestone

Citations in the corpus

• IL-2 Family Cytokines: New Insights into the Complex Roles of IL-2 as a Broad Regulator of T helper Cell Differentiation (2011, background): “Consistent with this, Il2, Il2ra, or Il2rb deficient mice exhibit severe autoimmunity [53–56], and defective IL-2 production contributes to diminished tolerance and the development of autoimmune diabetes in the NOD mouse [57].”
• Decrease of Foxp3+ Treg cell number and acquisition of effector cell phenotype during lethal infection (2009, background): “A link between defective IL-2 production and Treg cell dysfunction has been previously proposed as one of the mechanisms associated with breakdown of tolerance in nonobese diabetic mice (Tang et al., 2008).”
• Type 1 diabetes immunotherapy using polyclonal regulatory T cells (2015, background): “Recently, we and others have shown that Tregs are defective in a wide variety of autoimmune diseases, including T1D (17).”
• Intestinal tolerance requires gut homing and expansion of FoxP3+ regulatory T cells in the lamina propria. (2011, neutral): “Because previous studies revealed a high rate of constitutive FoxP3+ Treg cell proliferation (Tang et al., 2008a, 2008b), we compared the proliferation of endogenous FoxP3+ Treg cells in the LP to secondary lymphoid organs.”
• The role of interleukin-2 during homeostasis and activation of the immune system (2012, background): “and to impair the development of several autoimmune diseases, including type 1 diabetes in non-obese diabetic mice (NOD mice”
• Type 1 diabetes: etiology, immunology, and therapeutic strategies. (2011, background): “Experts in the field acknowledge the numerous technical problems that are likely to be encountered: a bona fide set of markers for “pure” human Tregs [currently set at CD4 CD127CD25 (343, 420)], a low frequency in the circulation ( 5–7% of CD4 T cells)(28), the number of cells to be transferred, the”
• Mechanisms of impaired regulation by CD4+CD25+FOXP3+ regulatory T cells in human autoimmune diseases (2010, positive): “In addition, in NOD mice (a spontaneous model of type 1 diabetes), T Reg cell numbers and FOXP3 expression decrease with the age of the animals despite ongoing autoimmunit”
• Interleukin-2 at the Crossroads of Effector Responses, Tolerance, and Immunotherapy (2013, positive): “…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), without activating effector CD8+ T cells.”
• Interleukin-2 Receptor Signaling: At the Interface between Tolerance and Immunity (2010, positive): “Thus, IL-2 therapy using anti-IL-2-IL-2 complexes directed at the highaffinity IL-2R, which increases Treg cell numbers, protects NODmice fromdiabetes and experimental autoimmune encephalomyelitis (EAE), a mouse model of multiple sclerosis (Tang et al., 2008; Webster et al., 2009).”
• 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”
• Foxp3 instability leads to the generation of pathogenic memory T cells in vivo (2009, positive): “T reg cells are a specialized CD4 + T cell lineage that is central to the preservation of self-tolerance and whose dysfunction has been linked to autoimmune diseases, including type 1 diabete”