Finerty J F, Krehl E P, McKelvin R L
Infect Immun. 1978 May;20(2):464-7. doi: 10.1128/iai.20.2.464-467.1978.
When mice were immunized intravenously, subcutaneously, or by the footpad route with formaldehyde-killed Trypanosoma rhodesiense, delayed-type hypersensitivity was elicited by the use of frozen-thawed trypanosomal antigen. The delayed footpad swelling technique was used to measure delayed hypersensitivity. Hypersensitivity induction was dose dependent (greater than or equal to 10(6) formaldehyde-treated T. rhodesiense) and was affected by the route of immunization. The footpad route induced higher levels of hypersensitivity than other routes of immunization. Mice immunized with a single dose of formaldehyde-treated antigen and challenged with live T. rhodesiense did not survive. Yet, mice immunized subcutaneously with formaldehyde-treated antigen and then injected with frozen-thawed antigen and challenged 28 days after immunization survived. The results suggest that T-cell activation, manifested by delayed hypersensitivity responses, was a necessary component in the protective response, perhaps functioning in a helper cell capacity.
当用甲醛灭活的罗德西亚锥虫通过静脉内、皮下或足垫途径对小鼠进行免疫时,使用冻融的锥虫抗原可引发迟发型超敏反应。采用足垫肿胀延迟技术来测量迟发型超敏反应。超敏反应的诱导呈剂量依赖性(≥10⁶甲醛处理的罗德西亚锥虫),并且受免疫途径的影响。足垫途径诱导的超敏反应水平高于其他免疫途径。用单剂量甲醛处理的抗原免疫并用活的罗德西亚锥虫攻击的小鼠未能存活。然而,用甲醛处理的抗原皮下免疫小鼠,然后注射冻融抗原并在免疫后28天进行攻击,小鼠存活了下来。结果表明,以迟发型超敏反应表现的T细胞活化是保护性反应的必要组成部分,可能以辅助细胞的能力发挥作用。