Garzelli C, Colizzi V, Campa M, Bozzi L, Falcone G
Infect Immun. 1979 Oct;26(1):4-11. doi: 10.1128/iai.26.1.4-11.1979.
The cellular basis of depression of contact sensitivity to oxazolone in mice injected with Pseudomonas aeruginosa was studied. Cells from draining lymph nodes of mice sensitized with oxazolone 18 h previously were able to induce contact sensitivity to normal mice when administered in their footpads. In contrast, cells from draining lymph nodes of P. aeruginosa-injected and oxazolone-sensitized donors failed to induce contact sensitivity when injected in the footpad of normal mice and were capable of actively blocking the immunizing process brought about by lymph node cells from sensitized mice when injected together in the footpad of normal recipients. The P. aeruginosa-induced suppressor cells required antigenic stimulation, had precursors sensitive to cyclophosphamide, and did not affect the effector mechanisms of contact sensitivity. Thus, the results suggest that P. aeurginosa depresses contact sensitivity to oxazolone by enhancing the activity of suppressor cells which normally arise during the sensitization process and which affect the afferent limb of the immune response, probably by inhibiting the normal recruitment of T lymphocytes in the draining lymph nodes.
研究了注射铜绿假单胞菌的小鼠对恶唑酮接触敏感性降低的细胞基础。18小时前用恶唑酮致敏的小鼠引流淋巴结中的细胞,当注射到正常小鼠的脚垫中时,能够诱导正常小鼠产生接触敏感性。相反,来自注射铜绿假单胞菌并致敏恶唑酮的供体的引流淋巴结细胞,当注射到正常小鼠的脚垫中时,不能诱导接触敏感性,并且当与致敏小鼠的淋巴结细胞一起注射到正常受体的脚垫中时,能够积极阻断致敏小鼠的淋巴结细胞所引发的免疫过程。铜绿假单胞菌诱导的抑制细胞需要抗原刺激,具有对环磷酰胺敏感的前体,并且不影响接触敏感性的效应机制。因此,结果表明铜绿假单胞菌通过增强抑制细胞的活性来降低对恶唑酮的接触敏感性,这些抑制细胞通常在致敏过程中产生,并且可能通过抑制引流淋巴结中T淋巴细胞的正常募集来影响免疫反应的传入环节。