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Key Documents

SRP8053

Sigma-Aldrich

IL-35 (mouse): FC (human)

recombinant, expressed in CHO cells

Synonym(s):

Interleukin-35, T-cell immunoglobulin and mucin domain-containing protein 4

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About This Item

UNSPSC Code:
12352200
NACRES:
NA.32

biological source

human
mouse

recombinant

expressed in CHO cells

Assay

≥98% (SDS-PAGE)

form

lyophilized

mol wt

monomer 23 kDa by calculation (IL-12a (p35))
monomer 46 kDa by calculation (Ebi3)

packaging

pkg of 5 μg

technique(s)

activity assay: suitable

impurities

<0.06 EU/μg endotoxin, tested

color

white

UniProt accession no.

shipped in

wet ice

storage temp.

−20°C

Gene Information

General description

Research area: IMMUNO AND CKS. Interleukin-35 (IL-35) is a novel IL-12 family cytokine produced by regulatory T cells (Treg) but not by resting or activated effector T cells (Teff). IL-35 is a heterodimeric protein composed of EBI3 (Epstein-Barr-Virus-induced gene 3) and IL-12a (p35). EBI3 is a downstream target of Foxp3, a transcription factor required for Treg-cell development and function, and thus Treg-cell restriction of IL35 occurs.

Application

IL-35 has been used to study its immunosuppressive effect on acute graft-versus-host disease in a mouse model.Ithas also been used to study its effects on the differentiation of granulocytemacrophage-colony-stimulating factor-producing T helper cells (ThGM). IL-35has been used to study its effects on bleomycin-induced pulmonary fibrosis.

Biochem/physiol Actions

Regulatory T cells are essential for maintaining self tolerance and preventing autoimmunity, and IL-35 is identified as a molecule that mediates the immune suppression function of Treg-cell. As an inhibitory cytokine, IL-35 induces proliferation of Treg-cell populations but suppresses Th17 cell development. Studies in mice show the absence of either IL-35 chain from Treg-cell reduces the cells′ ability to suppress inflammation using an experimental model for inflammatory bowel disease. IL-35 is suggested as a potential target of immunotherapy.IL-35 is produced inresponse to agonists of toll-like receptors 3 and 4 (TLR 3 & 4) and interferon γ (IFN-γ). It is secreted mainly by activated B cells, CD4+ Foxp3+ regulatoryT cells (Tregs), and at a lower concentration by monocytes, smooth muscle cells, and endothelial cells.

Physical form

Lyophilized from 0.2 μm-filtered solution in PBS.

Reconstitution

Reconstitute at 100 μg/mL in sterile PBS.

Other Notes

The mouse IL-35 complex composed of the Ebi3 subunit (aa 23-228) and the IL-12a (p35) subunit (aa 23-215) is fused through a polypeptide linker to the Fc region of human IgG1.

Storage Class Code

10 - Combustible liquids

WGK

WGK 2

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable


Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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Jinjung Choi et al.
Clinical reviews in allergy & immunology, 49(3), 327-332 (2015-01-27)
Interleukin 35 (IL-35) is the most recently identified member of the IL-12 family of cytokines and offers the potential to be a target for new therapies for autoimmune, inflammatory, and infectious diseases. Similar to other members of the IL-12 family
The inhibitory cytokine IL-35 contributes to regulatory T-cell function.
Collison LW
Nature, 450, 566-569 (2007)
IL-35 is a novel cytokine with therapeutic effects against collagen-induced arthritis through the expansion of regulatory T cells and suppression of Th17 cells.
Niedbala W
European Journal of Immunology, 37, 3021-3029 (2007)
Fengqin Lin et al.
Molecular immunology, 164, 28-38 (2023-11-09)
The immune system contributes to the pathophysiology of endometriosis. The role of ThGM cells, which produce granulocyte macrophage-colony-stimulating factor (GM-CSF), in the pathogenesis of endometriosis remains unknown. To analyze the features of ThGM cells in endometriosis, a mouse endometriosis model
IL-35 inhibits acute graft-versus-host disease in a mouse model
Zhang X H, et al.
International Immunopharmacology, 29(2), 383-392 (2015)

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