Kyoto University · Medicine
Professor Saeko Nakajima's research lab focuses on the immunological mechanisms underlying chronic inflammatory skin diseases, particularly atopic dermatitis and psoriasis. The lab investigates key immune regulators such as TSLP, PGI2-IP signaling, and microbiota-driven T cell responses to understand how innate and adaptive immunity shape barrier immunity and tissue inflammation. Using translational models and multi-omics approaches—including transcriptomics, proteomics, and lipidomics—the lab aims to uncover molecular pathways linking environmental triggers, immune cell activation, and disease pathogenesis. Their work highlights the role of stromal and dendritic cells in orchestrating type 2 and Th17-mediated inflammation at epithelial barriers.
Figures are computed from collected data and may differ slightly.
TSLP is an epithelial cell-derived cytokine synthesized in response to various stimuli, including protease allergens and microorganisms like viruses and bacteria. Biological functions of TSLP require heterodimer formation between the TSLP receptor (TSLPR) and IL-7 receptor-α, which polarize dendritic cells to induce type 2 inflammation and directly expand and/or activate Th2 cells, group 2 innate lymphoid cells, basophils, and other immune cells. TSLP is thus considered a master regulator of typ
Under steady-state conditions, the immune system is poised to sense and respond to the microbiota. As such, immunity to the microbiota, including T cell responses, is expected to precede any inflammatory trigger. How this pool of preformed microbiota-specific T cells contributes to tissue pathologies remains unclear. Here, using an experimental model of psoriasis, we show that recall responses to commensal skin fungi can significantly aggravate tissue inflammation. Enhanced pathology caused by f
PGI(2), which exerts its actions via its specific Gs-coupled I prostanoid receptor (IP), is known to be present in the lymph nodes, but its roles in acquired cutaneous immune responses remain unclear. To investigate the role of PGI(2)-IP signaling in cutaneous immune responses, we applied IP-deficient (Ptgir(-/-)) mice to contact hypersensitivity as a model of acquired immune response and found that Ptgir(-/-) mice exhibited a significantly decreased contact hypersensitivity response. Lymph node
Atopic dermatitis (AD), a complex and heterogeneous chronic inflammatory skin disorder, manifests in a spectrum of clinical subtypes. The application of genomics has elucidated the role of genetic variations in predisposing individuals to AD. Transcriptomics, analyzing gene expression alterations, sheds light on the molecular underpinnings of AD. Proteomics explores the involvement of proteins in AD pathophysiology, while epigenomics examines the impact of environmental factors on gene expressio
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