Characterization of the interaction of staphylococcal enterotoxin B with CD1d expressed in human renal proximal tubule epithelial cells

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• 作者：Rasha Hammamieh ; Nabarun Chakraborty ; Yixin Lin ; Jeffrey W Shupp…
• 刊名：BMC Microbiology
• 出版年：2015
• 出版时间：December 2015
• 年：2015
• 卷：15
• 期：1
• 全文大小：952 KB
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• 作者单位：Rasha Hammamieh (1) <br> Nabarun Chakraborty (1) <br> Yixin Lin (2) <br> Jeffrey W Shupp (3) <br> Stacy-Ann Miller (1) <br> Sam Morris (2) <br> Marti Jett (1) <br><br>1. Integrative Systems Biology, US Army Center for Environmental Health Research Fort Detrick, 568 Doughten Drive, Fort Detrick, MD, 21702-5010, USA <br> 2. Axela, Inc., 50 Ronason Drive, Suite 105, Toronto, ON, M9W 1B3, Canada <br> 3. The Burn Center, Department of Surgery, Washington Hospital Center, Washington, DC, 20010, USA <br>
• 刊物主题：Microbiology; Biological Microscopy; Fungus Genetics; Parasitology; Virology; Life Sciences, general;
• 出版者：BioMed Central
• ISSN：1471-2180

文摘

Background Participation of renal cells in the pathogenesis of staphylococcal enterotoxin B (SEB) is critical for late cleansing and sequestration of the antigens facilitated by CD1d mediated antigen sensing and recognition. This is a noted deviation from the typical antigen recognition process that recruits the major histocompatibility complex class II (MHC II) molecules. The immunological importance of CD1d is underscored by its influences on the performances of natural killer T-cells and thereby mediates the innate and adaptive immune systems. Results Using diffraction-based dotReady?immunoassays, the present study showed that SEB directly and specifically conjugated to CD1d. The specificity of the conjugation between SEB and CD1d expressed on human renal proximal tubule epithelial cells (RPTEC) was further established by selective inhibition of CD1d prior to its exposure to SEB. We found that SEB induced the expression of CD1d on the cell surface prompting a rapid conjugation between them. The mRNA transcripts encoding CD1d remained elevated potentially after completing the antigen cleansing process. Conclusion Molecular targets associated with the delayed pathogenic response have essential therapeutic values. Particularly in the event of bioterrorism, the caregivers are typically able to intervene much later than the toxic exposures. Given circumstances mandate a paradigm shift from the conventional therapeutic strategy that counts on targeting the host markers responding to the early assault of pathogens. We demonstrated the role of CD1d in the late stage of pathogen recognition and cleansing, and thereby underscored its clinical potential in treating bioweaponizable antigens, such as Staphylococcal enterotoxin B (SEB).