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. 1999 Dec 7;96(25):14541–14546. doi: 10.1073/pnas.96.25.14541

Figure 1.

Figure 1

Bcl-2 prevents apoptosis in sepsis. Thymocytes or splenocytes from septic or sham-operated Bcl-2 transgenic or B6C3F1 mice were examined for apoptosis by flow cytometry and the apoptosis indicator annexin V. Different classes of T or B cells were determined by labeling cell markers, i.e., CD4, CD8, CD3, or CD19 with fluorophore-conjugated Abs from PharMingen. Sepsis increased apoptosis in T and B cells from thymi and spleens of B6C3F1 mice; *, P < 0.05 septic vs. sham. Although there was no protection from apoptosis in thymocytes from septic Bcl-2 transgenic mice, both T and B cells in spleens from septic Bcl-2 mice were protected against sepsis-induced apoptosis; *, P < 0.05 septic vs. sham, n = 5 sham and n = 7–8 septic for both Bcl-2 and B6C3F1 mice. The protection by Bcl-2 was consistent with the greater expression of Bcl-2 in spleen vs. thymus, as seen in immunohistochemical stains (see Fig. 2).