Target intelligence / Profile preview

Interleukin-4 and Interleukin-10 (IL-4 and IL-10)

Target
IL-4 and IL-10
Molecular classification
Cytokine, Interleukin
01

Overview

Interleukin-4 (IL-4) and Interleukin-10 (IL-10) are critical regulatory cytokines that modulate immune responses and maintain tissue homeostasis (UniProt P05112, P22301). IL-4, primarily produced by Th2 cells and mast cells, drives B-cell class switching to IgE and Th2 cell differentiation, making it a key player in allergic diseases such as asthma and atopic dermatitis (Wikipedia, NIH). Conversely, IL-10 is a potent anti-inflammatory mediator that inhibits the production of pro-inflammatory cytokines like TNF-alpha and IL-1beta, thereby preventing excessive tissue damage during infection or inflammation (StatPearls, NIH). Therapeutically, these cytokines are targeted in two main ways: through antagonism to treat Th2-driven allergic conditions or through agonism/supplementation to suppress autoimmune and inflammatory diseases. For instance, dupilumab is a monoclonal antibody that blocks the IL-4 receptor alpha subunit, effectively inhibiting both IL-4 and IL-13 signaling for the treatment of atopic dermatitis (PubMed). In contrast, recombinant IL-10 (e.g., pegilodecakin) and novel IL-4/IL-10 fusion proteins are being investigated for their potential to treat rheumatoid arthritis and osteoarthritis by leveraging their synergistic anti-inflammatory effects (NIH, PubMed). Safety concerns associated with these therapies include an increased risk of infections due to immunosuppression and potential paradoxical inflammatory responses (NIH).

Other names
IL4IL10B-cell stimulatory factor 1Cytokine synthesis inhibitory factorCSIFBCGF-1B-cell growth factor 1Lymphocyte stimulatory factor 1
02

Mechanism of action

Therapeutic strategies involve either the antagonism of IL-4/IL-10 signaling to treat allergic or Th2-mediated diseases (e.g., monoclonal antibodies) or the administration of recombinant cytokines/fusion proteins to suppress excessive inflammation in autoimmune and inflammatory conditions.

03

Biological functions

Immune responseInflammation regulationCell differentiationB-cell activationT-cell differentiationTissue regenerationImmunosuppression
04

Disease associations

AsthmaAtopic dermatitisRheumatoid arthritisInflammatory bowel diseaseOsteoarthritisCancerPsoriasisMultiple sclerosis
05

Safety considerations

Increased risk of infectionImmunosuppressionInjection site reactionsPotential for paradoxical pro-inflammatory effectsEosinophilia
06

Interacting drugs

5 more in the full profile.

07

Biomarkers

Serum IL-4 levelsSerum IL-10 levelsTotal serum IgESTAT6 phosphorylationSTAT3 phosphorylationEosinophil count

Beyond the preview

Go deeper on Interleukin-4 and Interleukin-10 (IL-4 and IL-10).

Explore the evidence, development activity, and competitive landscape with Gosset’s full data platform.

Drug pipeline

Full profile access

Explore the programs pursuing this target and their development progress.

  • Drug candidates
  • Developers
  • Development stage

Clinical trials

Full profile access

Follow the clinical studies evaluating therapies directed at this target.

  • Trial design
  • Status
  • Readouts

Competitive landscape

Full profile access

Compare approaches across drug candidates, modalities, and indications.

  • Programs
  • Modalities
  • Indications

Literature & evidence

Full profile access

Investigate the research and source evidence behind target biology and development.

  • Publications
  • Sources
  • Analysis

Patents

Full profile access

Explore patent activity around therapies and technologies addressing this target.

  • Patents
  • Assignees
  • Technologies

Research & analysis

Full profile access

Connect target biology, drug development, and emerging evidence in your research.

  • Biology
  • Development news
  • Analysis

Bring the full picture into focus.

See how Gosset can support your research on Interleukin-4 and Interleukin-10 (IL-4 and IL-10).

Explore the full profile

Gosset Free

Get started with Gosset.

Enter your work email and we’ll be in touch with next steps.

Work email preferred.

Book a call