Stephen Grimes

Induction of latent immunological memory in genetically nonresponsive mice.

Abstract C57BL/10 mice exhibit major histocompatibility complex linked nonresponsiveness to hen egg white lysozyme (HEL). When these animals are primed with HEL in Freunds complete adjuvant (FCA), their secondary splenic plaque forming cell responses to aqueous HEL challenge are minimal to nonexistent. This notwithstanding, we show here that concomitant priming with both HEL and keyhole limpet hemocyanin (KLH) leads to an enhanced response to the HEL component following secondary challenge with an HEL-KLH conjugate. This enhancing effect can be transferred by nylon wool nonadherent spleen cells from HEL/FCA primed animals. Adoptive transfer studies with fractionated spleen cell populations suggest also that B cells are primed in these animals. Thus, animals which are incapable of mounting a secondary response to this antigen nevertheless appear to be primed at both the T-cell and B-cell levels following exposure to the antigen in FCA. The implications of this finding are discussed.

Cellular Basis of Genetic Nonresponsiveness to Egg White Lysozyme

Abstract Utilizing radiation chimeras, we have investigated the cellular level at which the low immunological responsiveness to egg white lysozyme C57B1/10 mice is expressed. Both NR > F1 (responder) and F1 > NR combinations were assessed. The results demonstrate that C57B1/10 bone marrow can give rise to hen egg white lysozyme responsive cells, but this response requires that the antigen be presented by cells derived from high responder animals.