IL-10 induces the tyrosine phosphorylation of tyk2 and Jak1 and the differential assembly of STAT1 α and STAT3 complexes in human T cells and monocytes
Abstract
IL-10 affects monocytes and T cells by driving the progression of immune responsiveness such that Th2 lymphocyte-mediated effects predominate. In this report, we show that in monocytes and T cells IL-10 stimulates tyrosine phosphorylation of the signal transducers and activators of transcription, STAT1 alpha and STAT3, in a differential manner such that the relative formation of homo- and heterodimers varies between the two cell types. Moreover, monocytes express a novel IL-10-stimulated STAT protein with an M(r) of 70 kDa that is recognized by the anti-STAT3 Ab but is not observed in T cells. IL-10 treatment of both T cells and monocytes results in the ligand-induced tyrosine phosphorylation of tyk2 and Jak1, but not Jak2 or Jak3. Selective modulation of immune responsiveness by IL-10 in cells such as monocytes and T cells may result in part from the differential activation of STAT protein pairs.
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IL-10 suppresses LPS-stimulated secretion of TNFα, a marker of its anti-inflammatory actions.
“IL-10 suppresses the LPS-stimulated secretion of TNF␣, a marker of its anti-inflammatory actions (24).”
From Cytokine Response Is Determined by Duration of Receptor and Signal Transducers and Activators of Transcription 3 (STAT3) Activation (2013) · cites this paper as [24]
STAT1 has been reported to be activated by IL-10.
“Because STAT1 has been reported to be activated by IL-10 (24, 25), the specificity of the patterns of JAK-STAT signaling was evaluated by measuring the levels of STAT1 activation.”
From Cytokine Response Is Determined by Duration of Receptor and Signal Transducers and Activators of Transcription 3 (STAT3) Activation (2013) · cites this paper as [24]
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- Authors
- Finbloom, D. S., & Winestock, K. D.
- Affiliations
- Center for Biologics Evaluation and Research (US)
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 1995-08-01
- Volume
- 155
- Issue
- 3
- Pages
- 1079-1090
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- OpenAlex
- W1499527462
- Cited by
- 421
- References
- 0
- Citations by year
- 2026: 6 · 2025: 4 · 2024: 8 · 2023: 9 · 2022: 11 · 2021: 10 · 2020: 8 · 2019: 14 · 2018: 8 · 2017: 12 · 2016: 17 · 2015: 5 · 2014: 22 · 2013: 17 · 2012: 18
- FWCI
- 7.96
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- The Journal of Immunology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
- Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Keywords
- IL-10, STAT3, tyrosine phosphorylation, TYK2, JAK1, monocytes, T cells, Th2 immune response, cytokine signaling
- MeSH terms
- Cells, Cultured, DNA-Binding Proteins, Humans, Monocytes, Phosphorylation, Protein Processing, Post-Translational, Protein-Tyrosine Kinases, Proteins, T-Lymphocytes, Tyrosine, Signal Transduction, Trans-Activators, Interleukin-10, Th2 Cells, Phosphotyrosine, STAT1 Transcription Factor, STAT3 Transcription Factor, Janus Kinase 1, TYK2 Kinase
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