Especially significant are the IL-2 receptor- (CD25-) and CD3-directed antibodies.

Last, a signal is induced by the interaction between IL-2 and the high-affinity IL-2 receptor.

IL-2 mediates its effects by binding to IL-2 receptors, which are expressed by lymphocytes.

It can also decrease the expression levels of cytokine receptors, such as the IL-2 receptor to down-regulate the activity of immune cells.

Endogenous melatonin in human lymphocytes has been related to interleukin-2 (IL-2) production and to the expression of IL-2 receptor.

Glucocorticoids cause B cells to express smaller amounts of IL-2 and of IL-2 receptors.

Drugs that inhibit IL-2 receptors, such as basiliximab and daclizumab are used in conjunction with other drugs to prevent immune rejection of transplants.

The three IL-2 receptor chains span the cell membrane and extend into the cell, thereby delivering biochemical signals to the cell interior.

It consists of an interleukin 15 receptor, alpha subunit and shares common beta and gamma subunits with the IL-2 receptor.

IL-2 has direct effects on immune cells carrying the IL-2 receptor, which in turn release soluble factors and/or activate other cells by cell-cell interactions.

The cell then releases IL-2, which binds to its own new IL-2 receptors, causing self-stimulation and ultimately a monoclonal population of T cells.

Daclizumab (trade name Zenapax) is a therapeutic humanized monoclonal antibody to the alpha subunit of the IL-2 receptor of T cells.

Substantial reduction, and even stabilization of both vitreous inflammation and retinal vasculitis has been evident via electroretinography, during daclizumab (IL-2 receptor blocker) therapy.

In addition, other specific markers of macrophage activation (e.g. soluble CD163), and lymphocyte activation (e.g. soluble IL-2 receptor) can be helpful.

The IL-2 receptor (IL-2R) was the first interleukin receptor to be described and characterized by Kendall Smith and his team at Dartmouth Medical School.

Antigen binding to the T cell receptor (TCR) stimulates the secretion of IL-2, and the expression of IL-2 receptors IL-2R.

Upon activation, "low-affinity" IL-2 receptors are replaced by "high-affinity" IL-2 receptors consisting of α, β, and γ chains.

Also, because T-Reg cells constitutively express IL-2 receptors, they bind, internalize and degrade IL-2, thereby depriving neighboring effector T cells of IL-2.

The IL-2 receptor belongs to this chain, whose γ-chain (common to several other cytokines) deficiency is directly responsible for the x-linked form of Severe Combined Immunodeficiency (X-SCID).

As IL-2 is an important inducer of lymphocyte proliferation, the absence of highly sensitive IL-2 receptors may also significantly hinder activation and clonal expansion of CD8+ and CD4+ lymphocytes and NK cells.

Activated T cells also produce the alpha sub-unit of the IL-2 receptor (CD25 or IL-2R), enabling a fully functional receptor that can bind with IL-2, which in turn activates the T cell's proliferation pathways.

Smith's group also showed TCGF to be the first cytokine to mediate its effects via a specific IL-2 receptor, and it was also the first interleukin to be cloned and expressed from a complementary DNA (cDNA) library by Tadatsugu Taniguchi's group.