Pregnancy and the susceptibility of Lewis rats to experimental allergic encephalomyelitis.

Pregnant Lewis rats challenged with encephalitogen during the second or third week of gestation were afforded a high level of protection against experimental allergic encephalomyelitis, whilst females sensitised during the first week of pregnancy enjoyed only limited protection from clinical signs of disease. When rechallenged with encephalitogen, females which had been sensitised during pregnancy were marginally more susceptible to reinduction of clinical signs of disease than their virgin counterparts. Mothers inoculated during the first week of gestation were the only group to produce abnormal young.

The effect of sensitization of pregnant Lewis rats with encephalitogen on the subsequent susceptibility of their offspring to allergic encephalomyelitis.

In a previous report (Smith & Rumjanek, 1984), it was shown that offspring of female Lewis rats which had been sensitized with encephalitogen during the second, but not the third or first, week of pregnancy, were resistant to the induction of EAE at 10 weeks of age. These observations have been extended to show that transfer of protection, from mothers to offspring, occurs during lactation. It is shown, furthermore, that sensitization leads to decreased incidence of disease in offspring, maternal clinical status simply determining the duration of protection enjoyed by offspring. The possible source of this protection is discussed.

Modulation of the host-versus-graft reaction of the popliteal lymph node by small numbers of dendritic cells injected at a distant site.

This paper demonstrates that dendritic cells (DC) injected intraperitoneally into CBA mice can alter the popliteal lymph node response of the animals to semi-allogeneic spleen cells injected into the footpad. This effect is antigen specific, for both cell populations must share the same foreign antigenic determinants. The alteration is expressed as an augmentation of node swelling following injection of very low numbers of DC, whilst a slight increase in the numbers of DC leads to suppression of the host-versus-graft response. Therefore it would appear that, in addition to their role as antigen-presenting cells, DC are also capable of modulating the response to an allogeneic stimulus in an antigen-specific manner. It is postulated that such antigen-specific modulation arises from formation of complexes between prostaglandin E1 and antigen-presenting moieties, which then determine the direction of the immune response.