Miller J F, Gamble J, Mottram P, Smith F I
Scand J Immunol. 1979;9(1):29-38. doi: 10.1111/j.1365-3083.1979.tb02703.x.
Antigen-pulsed macrophages (Mph) could sensitize syngeneic mice for delayed-type hypersensitivity (DTH) and also elicit sensitivity from mice sensitized to antigen in adjuvant provided these were syngeneic or semi-allogeneic to the strain providing the Mph. Sensitivity could not be elicited with antigen-pulsed allogeneic Mph. Antigen-pulsed Mph from low-responder (LR) strains could not sensitize LR mice nor F1 hybrids between responder (R) and LR strains. Normal F1 mice could be sensitized to respond to antigen presented on Mph or either parental type (i.e. P1 or P2): if, however, they were sensitized to antigen on P1 Mph, DTH transfer was restricted to naive P1 mice, not to P2 (restriction imposed by priming). F1 T cells derived from stem cells differentiating in a P1 thymus graft could be sensitized but could transfer sensitivity only to naive P1 mice, not to P2 (restriction imposed in thymus). When an antigen under Ir gene control was used, LR derived T cells differentiating in an (R X LR)F1 thymus could be sensitized but only if antigen was presented on (R X LR)F1 Mph not on LR Mph. Totally allogeneic chimaeras could be sensitized but only if given antigen in association with the appropriate Mph. These findings suggest that restriction of T cell activities can be imposed as a result of priming in some cases and as a result of differentiation within the thymus in others. LR strains appear to have a lesion at the level of antigen presentation by Mph; whether they also have a defect at the level of generation of T cell repertoire cannot be determined from the present investigations.
抗原脉冲巨噬细胞(Mph)可使同基因小鼠对迟发型超敏反应(DTH)致敏,并且还能使在佐剂中对抗原致敏的小鼠产生敏感性,前提是这些小鼠与提供Mph的品系是同基因或半同种异体的。抗原脉冲的同种异体Mph不能引发敏感性。来自低反应性(LR)品系的抗原脉冲Mph既不能使LR小鼠致敏,也不能使反应性(R)和LR品系之间的F1杂种致敏。正常的F1小鼠可被致敏以对Mph或任一亲本类型(即P1或P2)上呈递的抗原作出反应:然而,如果它们在P1 Mph上对抗原致敏,DTH转移仅限于未致敏的P1小鼠,而不是P2小鼠(由致敏施加的限制)。源自于在P1胸腺移植中分化的干细胞的F1 T细胞可被致敏,但只能将敏感性转移至未致敏的P1小鼠,而不是P2小鼠(在胸腺中施加的限制)。当使用受Ir基因控制的抗原时,在(R×LR)F1胸腺中分化的源自LR的T细胞可被致敏,但前提是抗原呈现在(R×LR)F1 Mph上,而不是LR Mph上。完全同种异体嵌合体可被致敏,但前提是给予与适当的Mph相关联的抗原。这些发现表明,T细胞活性的限制在某些情况下可能是由于致敏导致的,而在其他情况下则是由于在胸腺内的分化导致的。LR品系似乎在Mph呈递抗原的水平上存在缺陷;从目前的研究中无法确定它们在T细胞库产生水平上是否也存在缺陷。