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金黃色葡萄球菌 B 型腸毒素(staphylococcal enterotoxin B; SEB)是超
級抗原的一種,可被antigen-presenting cells (APC)上的 MHC class
II molecule 表現出來,而刺激帶特定 TCR Vb chains 的 T 細胞大量增
殖.我們的實驗發現,以靜脈注射方式將 SEB 打入 BALB/c 小鼠,其後於體
外用 SEB, Con A 以及 anti-CD3 刺激這些小鼠的脾臟細胞,其細胞增殖
反應明顯低下,但對 SEA 之刺激則仍有相當程度的增殖反應.注射 SEB 後
取出小鼠脾臟細胞在體外以 SEB, Con A 再度刺激,其增殖反應低下的情
形可因 anti-CD28 加入劑量逐而有漸次回升的現象.B 細胞淋巴瘤 A20
細胞以及活化態脾臟 B 細胞等 APC 的加入也可防止這種由 SEB 誘導的
免疫低反應.利用 Propidium Iodide 及免疫螢光染色來分析脾臟細胞亞
群及其細胞週期變化,發現活化後導致的細胞死亡可能是造成免疫低反應
的原因之一.在 coculture 的實驗中,曾注射過 SEB 之小鼠的脾臟細胞會
抑制 naive 脾臟細胞受 SEB 及 Con A 刺激後的增殖反應,而且這樣的免
疫抑制作用是透過 CD4+ 及 CD8+ 的 T 細胞來執行.在 SEB 誘發之免疫
抑制作用中發現,細胞培養上清液中 IL-2 含量減低許多,然而高劑量的
IL-2 (200 U/ML)只能部分補回由 SEB 造成之免疫抑制,而 anti-CD28 則
可以完全逆轉這種免疫抑制作用.
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Staphylococcal enterotoxin B is a polyclonal activator which
stimulates in particular those T cells bearing certain Vb TCR
and requires the presence of accessory cells that express class
II MHC molecules. We showed that in vivo SEB-primed splenocytes
exhibited a reduced level of cell proliferation in response to
further stimulation with SEB, Con A and anti-CD3, but not to
SEA. By propidium iodide staining and FACScan analysis, our
results showed that activation-induced cell death might be
involved in the SEB-induced hyporesponsiveness. The reduction
in cell proliferation of these in vivo SEB-primed cells in
response to further SEB or Con A stimulation could be reversed
by anti-CD28 mAb in a dose-dependent manner. The addition of
activated B cells and A20 as the APCs to these SEB-primed cells
could also overcome the suppressive effect. Furthermore, in
vitro cocultures demonstrated that naive cell prolifertion to
SEB and Con A was suppressed by SEB-primed spleen cells, and
this immunosuppressive activity was mediated by CD4+ and CD8+ T
cells. The suppression of cell proliferation could only be
partially reversed by addition of up to 200 U/ml of exogenous
rIL-2 to the cultures. However, anti-CD28 mAb could reverse the
suppressive effect of SEB-primed cells in the cocultures.
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