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Updated: May 2, 2026
08:28
Validated Immunochemical Assay for Comprehensive Determination of the Human Epidermal Growth Factor Receptor 2 Released from and Bound to Cells
Published on: May 9, 2025
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The epidermal growth factor receptor is a regulator of epidermal complement component expression and complement
Anas H A Abu-Humaidan1, Nageshwar Ananthoju, Tirthankar Mohanty
1Division of Infection Medicine, Department of Clinical Sciences, Lund University, 221 84 Lund, Sweden;
Journal of Immunology (Baltimore, Md. : 1950)
|March 5, 2014
Summary
Epidermal Growth Factor Receptor (EGFR) regulates complement system activation in human skin. Inhibiting EGFR enhances complement component expression and activation, particularly in response to inflammatory stimuli.
Area of Science:
- Immunology
- Dermatology
- Cell Biology
Background:
- The complement system plays a dual role in wound healing, beneficial in acute and detrimental in chronic wounds.
- Epidermal complement component expression is modulated during skin injury.
- Epidermal Growth Factor Receptor (EGFR) signaling is involved in wound healing responses.
Purpose of the Study:
- To investigate the role of EGFR in regulating complement component expression and activation in human epidermis and keratinocytes.
- To determine if EGFR signaling influences the epidermal response to inflammatory stimuli in the context of complement activation.
Main Methods:
- In vivo and ex vivo skin wound models.
- Primary human and murine keratinocyte cultures.
- Stimulation with mononuclear cell supernatants, TGF-α, and proinflammatory cytokines.
- EGFR inhibition using specific inhibitors.
- Assessment of complement component expression via qPCR and Western blotting.
- Complement activation assays using serum and C1q-depleted serum.
Main Results:
- EGFR inhibition significantly enhanced complement component induction in human keratinocytes and epidermis stimulated with proinflammatory cytokines.
- EGFR inhibition alone or with inflammatory stimuli promoted complement system activation in human keratinocytes.
- Complement activation in EGFR-inhibited keratinocytes was dependent on serum C1q, but also occurred with C1q-depleted serum under combined stimulation.
- EGFR inhibition did not affect complement component expression or activation in murine keratinocytes.
Conclusions:
- EGFR plays a crucial role in regulating complement component expression and complement activation in human epidermis and keratinocytes.
- EGFR signaling represents a novel pathway for the epidermal regulation of complement activation.
- These findings highlight a potential therapeutic target for modulating complement-mediated inflammation in skin conditions.
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