soluble form of the interleukin-2 receptor (sIL-2R)

Introduction

IL-2 exerts its effects by binding to IL-2 receptors expressed by lymphocytes
activated CD4+ T cells and CD8+ T cells are the primary sources of IL-2
upon T-cell activation, in addition to increased cellular expression of IL-2R, they also shed the soluble form of the interleukin-2 receptor (sIL-2R), resulting in elevated serum concentrations of sIL-2R in patients with various conditions associated with an ongoing immune response
binding of IL-2 to the soluble IL-2 receptor (sIL-2R) can have varying effects on the immune response, depending on the specific target cell involved in either immunity or self-tolerance
the precise role of sIL-2R is yet to be elucidated but it may:
- primarily play a role in the regulation of IL-2-dependent cell function
- complex with IL-2 and prolong the half-life of IL-2
- present IL-2 to CD4+ T lymphocytes, leading to their differentiation into regulatory T cells (Tregs) instead of T-helper (Th)1 or Th17 lymphocytes, which can subsequently suppress immune activity
- contribute to (auto)immune processes by promoting enhanced Th17 generation, which involves sequestering the IL-2 that normally inhibits early Th17 differentiation

renal insufficiency
sepsis
Grave's disease
systemic lupus erythematosus (SLE)
rheumatoid arthritis
sarcoidosis
- sensitivity is 79% (and higher if there is also uveitis)
- levels may correlate with Rx success
- compared to soluble angiotensin-converting enzyme (sACE), serum sIL-2R tests demonstrate superior ability in determining pulmonary severity and unlike ACE levels is not affected by drug or immunosuppressant use ¹⁾
- high levels of serum sIL-2R can predict the need for therapy in sarcoidosis patients
Lőfgren syndrome
haematologic malignancies
other granulomatous diseases
post-transplantation
various other autoimmune disorders

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