Redistribution of H-2 antigens on mouse lymphocytes induced by specific antibodies. The effect of tissue extracts, sera and anaesthetics [proceedings].
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Biomedical subjects
Publications and source records attributed to I Hilgert.
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The comparisons of immune responses to tumour allografts in male and female mice showed the following intersex differences: 1. Production of humoral antibodies is, in general, higher in females; since, however, the time course of titres differs for haemagglutinating and cytotoxic antibodies as well as with the sex, the titre of the same antibody may be higher in males at certain time intervals when the peak is delayed and the production in females is already declining. 2. In recipients specifically presensitized with spleen extract as well as in controls, the growth of allogeneic tumour (SaI) exhibits quantitative intersex differences being reduced in females. In the initial phase of growth, following the spleen extract, the facilitation (enhancement) of the tumour allograft is apparent olny in males, whereas in females it is delayed. 3. The facilitating effect of antibodies passively transferred from males or females corresponds mainly to the sex and strain of the recipient, only rarely to the sex of the producer. 4. In CBA strain mice, females are more resistant to the growth of SaI and also mortality from the primary tumour is lower in females; in contrast, the frequency of metastases in females is higher. 5. In the IC strain, where the sex effect on tumour growth is particularly pronounced, the consequences of castration were concordant with the inferred hormonal control of the allograft response: in males, the relatively high percentage of lethal spontaneous takes (60%) was reduced following castration (to 13%), whereas the opposite trend was observed in females, namely an increase from 0% in sham-operated controls to 23% in the castrated group.
Immunogenic versus tolerogenic capacity of mouse alloantigens from ischaemic liver was tested in two different congenic strain combinations (H-2 compatible, non-H-2 incompatible). The recipients of test skin allografts were pretreated with tissue homogenate or particulate fraction and the survival pattern of the skin allografts was used as the criterion of the induced status. The results showed a difference in the immunogenicity of antigenic extracts from normal (healthy) and ischaemic liver. Following a single dose, alloantigens from ischaemic liver had an increased immunogenicity (which could be reduced through perfusion) as compared to control (extracts from healthy liver). Following three larger doses of ischaemic liver extracts, the effect was tolerogenic. Possible mechanism of the altered immunogenicity of alloantigens due to ischaemization of the liver tissue and the effect of perfusion are discussed.
Cell-free spleen and liver extracts were used for attempted induction of allograft tolerance across a restricted H-2 barrier due to a chemically induced mutation in the B10.D2 mouse strain. When using mice of the latter strain as donors and the new congenic strain carrying the mutant H-2 hyaplotype as recipients, and with long-term administration of the cell-free antigens in adult life up to 100% yields (according to the dose of antigen) of permanently tolerant animals (particularly males) was obtained with spleen extract, but not with liver extract. This contrasts with a higher tolerance-inducing efficiency of liver extracts in various non-H-2 incompatibilities. In the reversed donor-recipient combination, neither spleen nor liver extracts gave positive results. The immune status of the permanently tolerant animals was analyzed and it was shown that with their bone marrow normal responsiveness can be conferred upon lethally irradiated syngeneic hosts whereas the specific allograft tolerance can be adoptively transferred to sublethally irradiated recipients by means of spleen or lymph node cells. It is concluded that in the present system the state of allograft tolerance is maintained by an immunologically active process of peripheral lymphocytes.
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