CD300e is an immune receptor expressed on myeloid cells, where it contributes to the regulation of innate immune responses. CD300e has recently attracted attention because of its upregulation in several inflammatory conditions, including bacterial infections, obesity, and colorectal cancer. These observations have raised interest in the molecular mechanisms regulating CD300e transcription. This study aims to investigate the transcriptional regulation of CD300e following lipopolysaccharide (LPS) stimulation in primary human monocytes. In silico promoter analysis revealed putative STAT-binding sites within the CD300e promoter, suggesting the involvement of the JAK/STAT signalling pathway. Among the STAT family members, western blot analysis identified STAT3 as the most likely candidate involved in CD300e regulation. Among the cytokines released upon LPS stimulation, IL-6 and IL-10 are major activators of the JAK/STAT3 pathway. Their potential contribution to CD300e regulation is therefore currently under investigation. Our findings indicate that cytokine-mediated JAK/STAT signalling regulates CD300e expression, although the specific upstream mediator responsible for this effect has yet to be identified. Elucidating the mechanisms controlling CD300e expression may provide new insights into the role of this receptor during inflammation and help clarify whether it contributes to the maintenance or resolution of inflammatory responses in different pathological contexts.

Investigation on CD300e transcriptional regulation

CAMPAGNOLO, SERENA
2025/2026

Abstract

CD300e is an immune receptor expressed on myeloid cells, where it contributes to the regulation of innate immune responses. CD300e has recently attracted attention because of its upregulation in several inflammatory conditions, including bacterial infections, obesity, and colorectal cancer. These observations have raised interest in the molecular mechanisms regulating CD300e transcription. This study aims to investigate the transcriptional regulation of CD300e following lipopolysaccharide (LPS) stimulation in primary human monocytes. In silico promoter analysis revealed putative STAT-binding sites within the CD300e promoter, suggesting the involvement of the JAK/STAT signalling pathway. Among the STAT family members, western blot analysis identified STAT3 as the most likely candidate involved in CD300e regulation. Among the cytokines released upon LPS stimulation, IL-6 and IL-10 are major activators of the JAK/STAT3 pathway. Their potential contribution to CD300e regulation is therefore currently under investigation. Our findings indicate that cytokine-mediated JAK/STAT signalling regulates CD300e expression, although the specific upstream mediator responsible for this effect has yet to be identified. Elucidating the mechanisms controlling CD300e expression may provide new insights into the role of this receptor during inflammation and help clarify whether it contributes to the maintenance or resolution of inflammatory responses in different pathological contexts.
2025
Investigation on CD300e transcriptional regulation
Immunoreceptor
Transcription
Inflammatory disease
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/20.500.12608/114531