CD93 為一個表現在骨髓細胞上的穿膜蛋白，會透過巨噬細胞吞噬凋亡細胞的作用而參與發炎過程。CD93 具有五個不同功能的區域，分別為類凝集素功能區、五個表皮生長因子重複的功能區、黏液素功能區、穿膜功能區，以及一個細胞內尾端。根據先前的文獻指出，人類單核球細胞在脂多醣刺激過後，在其細胞培養液裡發現含有類凝集素功能區的CD93蛋白片段 (CD93-D1)，這代表在發炎時人類單核球細胞膜上的CD93會被切離。然而，此CD93的凝集素功能區在發炎過程所扮演的角色仍然不清楚。在我們的實驗當中，C57BL/6 老鼠在脂多醣刺激後，其血清中CD93的表現量會增加。進一步我們想要了解CD93表現量增加所代表的生理意義及參與的機制為何。首先，利用哺乳類表現系統表現出CD93類凝集素重組蛋白 (rCD93-D1)。接著利用尾靜脈注射方式，將rCD93-D1 注入C57BL/6 老鼠體內，再以腹腔注射將脂多醣注入C57BL/6 老鼠體內。結果發現血液中的細胞激素以及肺部浸潤的多型核中性白血球細胞數都有下降的趨勢。同時在酵素結合免疫吸附分析結果中，也發現rCD93-D1和脂多醣間具有結合的能力。進一步先將rCD93-D1 和脂多醣混合作用，再分別刺激人類單核球細胞以及硫醇乙酸誘導過後的老鼠腹腔細胞。結果顯示，在rCD93-D1的作用下，培養液中細胞激素的濃度會下降。我們的研究也證實rCD93-D1可以促進巨噬細胞吞噬凋亡細胞。從以上結果，我們可以推論，在發炎的過程中，rCD93-D1透過和結合脂多醣以及促進巨噬細胞吞噬凋亡細胞，而發揮抑制發炎的功能。

CD93 is a transmembrane glycoprotein which is expressed on myeloid cells and is involved in inflammatory response via assisting macrophages to engulf apoptotic cells. CD93 is consisted of five different functional domains including a C-type lectin-like domain (domain 1; D1), a multiple epidermal growth factor-like repeats (domain 2; D2), a mucin-like domain (domain 3; D3), a transmembrane domain (domain 4; D4), and a cytoplasmic domain (domain 5; D5). Previous studies showed that different length of D1-containing CD93 fragments (sCD93-D1) were identified in the conditioned medium of human monocytes which were challenged with lipopolysaccharide (LPS) in vitro, suggesting that these sCD93-D1 may be shed from monocytes during inflammation. However, the functions of the lectin-like domain of CD93 in LPS-induced inflammation are mostly unknown. In this study, we found that soluble fragments of CD93 were detected in the serum of LPS-challenged mice. Therefore, we prepared recombinant CD93-D1 protein (rCD93-D1) by a mammalian expression system to dissect the effect of rCD93-D1 in inflammation. We found that intravenous administration of rCD93-D1 into LPS-challenged mice could significantly suppress the release of cytokines in serum and the infiltration of polymorphonuclear cells in lung tissue. We also showed that pre-incubation of rCD93-D1 with LPS could decrease LPS-induced elevations of cytokines in THP-1 cells and thioglycollate-elicited peritoneal cells. Furthermore, rCD93-D1 could dose-dependently bind to LPS in an ELISA assay, suggesting that rCD93-D1 may function as an anti-inflammatory factor through neutralization of LPS. We also found that rCD93-D1 enhanced phagocytosis percentages of apoptotic cells. In conclusion, we demonstrated that the rCD93-D1 may play an anti-inflammatory role in neutralizing LPS-induced inflammation and in phagocytosis of apoptotic cells by thioglycollate-elicited peritoneal macrophages.

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