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10.1016/j.ajpath.2014.07.006

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C4215033!4215033!25194661
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suck abstract from ncbi


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pmid25194661      Am+J+Pathol 2014 ; 184 (11): 3130-41
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  • B2 Cells Suppress Experimental Abdominal Aortic Aneurysms #MMPMID25194661
  • Meher AK; Johnston WF; Lu G; Pope NH; Bhamidipati CM; Harmon DB; Su G; Zhao Y; McNamara CA; Upchurch GR; Ailawadi G
  • Am J Pathol 2014[Nov]; 184 (11): 3130-41 PMID25194661show ga
  • Recent reports of rupture in patients with abdominal aortic aneurysm (AAA) receiving B-cell depletion therapy highlight the importance of understanding the role of B cells (B1 and B2 subsets) in the development of AAA. We hypothesized that B2 cells aggravate experimental aneurysm formation. The IHC staining revealed infiltration of B cells in the aorta of wild-type (C57BL/6) mice at day 7 after elastase perfusion and persisted through day 21. Quantification of immune cell types using flow cytometry at day 14 showed significantly greater infiltration of mononuclear cells, including B cells (B2: 93% of total B cells) and T cells in elastase-perfused aortas compared with saline-perfused or normal aortas. muMT (mature B-cell deficient) mice were prone to AAA formation similar to wild-type mice in two different experimental AAA models. Contradicting our hypothesis, adoptive transfer of B2 cells suppressed AAA formation (102.0% � 7.3% versus 75.2% � 5.5%; P�<�0.05) with concomitant increase in the splenic regulatory T cell (0.24% � 0.03% versus 0.92% � 0.23%; P�<�0.05) and decrease in aortic infiltration of mononuclear cells. Our data suggest that B2 cells constitute the largest population of B cells in experimental AAA. Furthermore, B2 cells, in the absence of other B-cell subsets, increase splenic regulatory T-cell population and suppress AAA formation.



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