Abstract
Cytokines activate signaling via assembly of cell surface receptors, but it is unclear whether modulation of cytokine-receptor binding parameters can modify biological outcomes. We have engineered IL-6 variants with different affinities to gp130 to investigate how cytokine receptor binding dwell-times influence functional selectivity. Engineered IL-6 variants showed a range of signaling amplitudes and induced biased signaling, with changes in receptor binding dwell-times affecting more profoundly STAT1 than STAT3 phosphorylation. We show that this differential signaling arises from defective translocation of ligand-gp130 complexes to the endosomal compartment and competitive STAT1/STAT3 binding to phospho-tyrosines in gp130, and results in unique patterns of STAT3 binding to chromatin. This leads to a graded gene expression response and differences in ex vivo differentiation of Th17, Th1 and Treg cells. These results provide a molecular understanding of signaling biased by cytokine receptors, and demonstrate that manipulation of signaling thresholds is a useful strategy to decouple cytokine functional pleiotropy.
Keywords:
bias signaling; cytokine engineering; cytokine signaling; endosomal traffic; functional pleiotropy; human; immunology; inflammation.
© 2019, Martinez-Fabregas et al.
Publication types
-
Research Support, N.I.H., Extramural
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Binding Sites
-
Cell Differentiation
-
Cloning, Molecular
-
Cytokine Receptor gp130 / chemistry*
-
Cytokine Receptor gp130 / genetics
-
Cytokine Receptor gp130 / metabolism
-
Endosomes / chemistry
-
Endosomes / metabolism
-
Gene Expression
-
HeLa Cells
-
Humans
-
Interleukin-6 / chemistry*
-
Interleukin-6 / genetics
-
Interleukin-6 / metabolism
-
Kinetics
-
Models, Molecular
-
Phosphorylation
-
Primary Cell Culture
-
Protein Binding
-
Protein Conformation, alpha-Helical
-
Protein Conformation, beta-Strand
-
Protein Engineering / methods
-
Protein Interaction Domains and Motifs
-
Recombinant Proteins / chemistry
-
Recombinant Proteins / genetics
-
Recombinant Proteins / metabolism
-
STAT1 Transcription Factor / genetics
-
STAT1 Transcription Factor / metabolism*
-
STAT3 Transcription Factor / genetics
-
STAT3 Transcription Factor / metabolism
-
Signal Transduction
-
T-Lymphocytes, Regulatory / cytology
-
T-Lymphocytes, Regulatory / immunology
-
T-Lymphocytes, Regulatory / metabolism*
-
Th1 Cells / cytology
-
Th1 Cells / immunology
-
Th1 Cells / metabolism*
-
Th17 Cells / cytology
-
Th17 Cells / immunology
-
Th17 Cells / metabolism*
Substances
-
IL6 protein, human
-
Interleukin-6
-
Recombinant Proteins
-
STAT1 Transcription Factor
-
STAT1 protein, human
-
STAT3 Transcription Factor
-
STAT3 protein, human
-
Cytokine Receptor gp130