Immunology letters · 2026
Analysis of Tim-4 expression in ulcerative colitis and its association with inflammation-related immune infiltration.
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Liu Yunyun, Wang Yuxin, Wang Xin, Zhu Luyu, Zhao Chengguang, Zhu Jijun, Wang Xiaoyan
Аннотация
PURPOSE: To investigate the role of T-cell immunoglobulin and mucin domain 4 (Tim-4) in ulcerative colitis (UC) and its association with inflammation-related immune cell infiltration.
METHOD: We analyzed Tim-4 expression in patients with UC using the GSE87466 dataset and validated these findings through qPCR, ELISA, and immunohistochemistry of intestinal mucosal tissues collected from patients with UC and healthy control subjects. To evaluate the inflammatory response, hematoxylin and eosin (HE) staining was performed to assess the extent of inflammatory cell infiltration into the intestinal mucosa. Additionally, CIBERSORT analysis was performed to explore the correlation between Tim-4 expression and immune cell infiltration in patients with UC. Flow cytometry was used to quantify the proportion of immunosuppressive cells, such as regulatory T cells (Tregs) and CD14+HLA-DR-/low myeloid-derived suppressor cells (MDSCs), in both UC and control groups.
RESULTS: Tim-4 expression was significantly elevated in patients with UC. It positively correlated with increased inflammatory cell infiltration and cytokine levels, particularly IL-17. Tim-4 was also associated with pro-inflammatory immune cells and a reduction in immunosuppressive cells, such as Tregs and MDSCs.
CONCLUSION: Our findings indicate that Tim-4 expression is elevated in UC and is associated with alterations in both proinflammatory and immunosuppressive immune cell populations. These correlations suggest that Tim-4 may participate in the inflammatory processes of UC, potentially influencing immune cell infiltration and immune regulation. However, further mechanistic studies are required to determine the causal relationship and clarify the precise role of Tim-4 in UC pathogenesis.
METHOD: We analyzed Tim-4 expression in patients with UC using the GSE87466 dataset and validated these findings through qPCR, ELISA, and immunohistochemistry of intestinal mucosal tissues collected from patients with UC and healthy control subjects. To evaluate the inflammatory response, hematoxylin and eosin (HE) staining was performed to assess the extent of inflammatory cell infiltration into the intestinal mucosa. Additionally, CIBERSORT analysis was performed to explore the correlation between Tim-4 expression and immune cell infiltration in patients with UC. Flow cytometry was used to quantify the proportion of immunosuppressive cells, such as regulatory T cells (Tregs) and CD14+HLA-DR-/low myeloid-derived suppressor cells (MDSCs), in both UC and control groups.
RESULTS: Tim-4 expression was significantly elevated in patients with UC. It positively correlated with increased inflammatory cell infiltration and cytokine levels, particularly IL-17. Tim-4 was also associated with pro-inflammatory immune cells and a reduction in immunosuppressive cells, such as Tregs and MDSCs.
CONCLUSION: Our findings indicate that Tim-4 expression is elevated in UC and is associated with alterations in both proinflammatory and immunosuppressive immune cell populations. These correlations suggest that Tim-4 may participate in the inflammatory processes of UC, potentially influencing immune cell infiltration and immune regulation. However, further mechanistic studies are required to determine the causal relationship and clarify the precise role of Tim-4 in UC pathogenesis.