GMP IL-12 Protein, Human (HEK293, His)

Interleukin-12 subunit alpha (IL-12A; IL-12p35), an immune-suppressive cytokine, encodes a subunit of the cytokine IL-12 that acts on T and natural killer cells, and has a broad array of biological activities. IL-12A is a disulfide-linked heterodimer composed of the 35-kD subunit encoded by this gene, and a 40-kD subunit that is a member of the cytokine receptor family. IL-12 is primarily produced by professional antigen-presenting cells (APCs) such as B-cells and dendritic cells (DCs) as well as macrophages and granulocytes, induces the production of IFN-gamma, favors the differentiation of Th1 cells and is an important link between innate resistance and adaptive immunity^[1][2].
The amino acid sequence of human IL-12A protein has low homology between mouse IL-12A protein. While, human IL-12A shares 94% aa sequence identity with Rhesus Macaque IL-12A protein.
IL-12 family cytokines are pleiotropic immunological playmakers that coordinate innate and adaptive immune responses mainly via regulation of T-cell populations. The four core members of the Interleukin-12 (IL-12) family of cytokines, IL-12, IL-23, IL-27 and IL-35 are heterodimers which share α-cytokine subunits (IL-12p35 (IL-12A), IL-23p19, and IL-27p28) and β-cytokine subunits (IL-12p40, Ebi3). The subunits are each encoded by separate chromosomes and their expression is regulated independently. Among them, the IL-12A subunit has immunoregulatory functions hitherto attributed to IL-35. Pairing of the α-subunits, IL-12A or IL-23p19 with IL-12p40, gives rise to the two pro-inflammatory members IL-12 and IL-23, respectively, whereas the two immunosuppressive members of the family, IL-27 and IL-35, derive from pairing of IL-27p28 or IL-12A with Ebi3^[1][2].
IL-12A suppresses lymphocyte proliferation, induces expansion of IL-10-expressing and IL-35-expressing B cells and ameliorates autoimmune uveitis in mice by antagonizing pathogenic Th17 responses. IL-12A-mediated expansion of Treg and Breg cells and its amelioration of experimental autoimmune encephalomyelitis (EAE) correlated with inhibition of cytokine-induced activation of STAT1/STAT3 pathways. IL-12A may be utilized for in vivo expansion of Tregs and Bregs cells and autologous Tregs and Bregs cell immunotherapy^[1][2].

IL-12 Protein, Human (10 ng/mL; for 5 days) results in the induction of IFN-γ secretion by Dermatophagoides pteronyssinus group 1 antigen (Der p 1)-specific CD4+ T cells in dendritic cell (DC)-T cell cocultures, whereas their production of IL-5 is not inhibited^[3].