[7][8][9] Several frequent point mutations, single nucleotide polymorphism (SNP), have been identified in or in close proximity to IL2RA gene in the population.

These SNPs have been linked mainly to susceptibility to immune dysregulation disorders, with majority found in research on multiple sclerosis (MS) and type 1 diabetes mellitus.

[10][11][12][13][14] IL2RA gene orthologues with identical protein functionality are relatively abundant and constant among animal species, especially in mammals subgroups.

[5][18] IL2RA protein can be expressed in many types of neoplastic cells, such as in most B-cell neoplasms, T-cell lymphomas, some acute nonlymphocytic leukemias, neuroblastomas, mastocytosis, Waldenstrom macroglobuliaemia and tumor infiltrating lymphocytes.

However, while extracellular part is able to function as a binding site for interleukin-2, short cytoplasmic domain lacks an ability to induce intracellular signalling and therefore needs to oligomerise with other IL-2 receptor subunits.

[5][18][27] Roifman's group was the first to identify immunological consequences of CD25 loss and the patient has suffered from chronic infections and severe autoimmunity resembling Immune dysregulation, Polyendocrinopathy, Enteropathy X-linked (IPEX) syndrome, caused by mutations in FOXP3 gene.

Similarly in Chagas disease, caused by the protozoan Trypanosoma cruzi, patients have increased levels of sIL-2Rα and autoantibodies.

Concerning CVD (cardiovascular diseases) soluble IL-2Rα has positive correlation with hypertension, type 2 diabetes mellitus, cardiac sarcoidosis, stroke and heart failure.

[32] Antibodies directly against CD25 have been altered to contain  ‘activating’ Fc regions for the purpose of antibody-dependent cell-mediated cytotoxicity, in this case Treg depletion.

[33][34] From the other side, treatment strategies for autoimmune and inflammatory diseases need selectivity for Tregs and suppression of immune system.

Low-dose IL-2 therapy is used for graft-versus-host disease, type 1 diabetes mellitus, hepatitis C virus-induced vasculitis and systemic lupus.