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Results for “Immunologic Memory”

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At least 253 records · Page 14Linked to original sources
PubMed1976

Relation of antigen-binding cells to immunological memory.

Priming of mice with a conjugate of HSA with sheep red cells induced a high level of memory to HSA, with very little antibody production ("pure priming"). HSA specific antigen binding cells in the spleens of the primed mice were assayed by means of a rosette technique, using HSA conjugated to donkey red cells. Rosette formation was almost completely inhibited by soluble HSA, thus confirming that the RFC were specific for this antigen. Spleens of primed mice contained up to 0.6% RFC, as compared to 0.08% HSA specific RFC in the spleens of non immunized animals. Suspensions enriched in rosettes (containing up to 16% RFC) were prepared by centrifugation on BSA density gradients. Adoptive transfer experiments showed that the rosette rich fraction contained all the memory cells. A marginal level of memory could be transferred to irradiated recipients with 3000 rosettes. A comparable degree of responsiveness to HSA could also be transferred with 70,000 RFC enriched from spleens of non immunized mice, but only when injected together with primed, RFC depleted spleen cells. Kinetic studies showed that the level of memory correlated well with the number of RFC up to two months after priming. The number of RFC decreased at later time intervals (though remaining higher than in controls at all times), without a corresponding decrease in the level of memory. A change in the quality of the memory cell with time is postulated.

Animals↗
PubMed2004

Generation and maintenance of immunological memory.

The key feature of the adaptive immune response is its specificity and the ability to generate and maintain memory. Preexisting antibodies in the circulation and at the mucosa provide the first line of defense against re-infection by extracellular as well as intracellular pathogens. Memory T cells are an important second line of defense against intracellular pathogens, and in particular against microbes that can cause chronic or latent infection. In this article we will review our current understanding of the generation and maintenance of B cell and T cell memory.

Animals↗
PubMed1975

Immunological memory function of the T and B cell types: distribution over mouse spleen and lymph nodes.

Spleens from LAF1 mice injected intravenously with sheep erythrocytes (SE) are relatively rich in memory T cells early in the immune response (1 to 3 days) and rich in memory B cells as the response progresses (2 weeks or more). Marked cooperation for the secondary immune response in vitro was obtained by combining 10(6) spleen cells from LAF1 mice, taken 2 days after intravenous priming with SE, with 10(7) spleen cells from day 14 primed mice. The results indicate relative deficiencies in the spleen for B memory cells on days 1 to 2 and for T memory cells on day 14 after priming. Day -14, but not day -2, immune lymph node (LN) cells could replace the day -2 spleen cells (anti-Thy 1.2 sensitive) in the in vitro cooperation with day -14 immune spleen cells. Immune spleen cells taken 4 to 7 days after priming contain more equivalent numbers of B and T memory cells, but 10 to 7 days after transfer of such immune spleen cells without SE into irradiated recipients the T memory cells were again more prominent in lymph node and the B memory cells in spleen as shown by in vitro cooperation studies. These results suggest that during the second week after intravenous injection of SE relatively more T than B memory cells migrate from spleen to lymph node, resulting in an imbalance in the splenic memory cell population favoring B memory cell function.

Animals↗
PubMed1981

Immunological memory to Listeria monocytogenes in rodents. IV. Studies on origin and fate of tissue-positioned T memory cells.

In this report on memory T cells mediating anti-microbial resistance to Listeria monocytogenes (LM) it was analysed whether memory cells found in tissue during late-phase (e.g. 10-60 days after infection) are long-lived progeny of cells which settled in tissues during early phase (e.g. 4-10 days after infection), or whether they are short lived but constantly replaced from other sources of memory cells. The study provides evidence for both mechanisms. Transfer and parabiosis experiments as well as radiometric and autoradiographic studies suggested that early-phase cells give rise to late-phase memory cells in the extravascular compartment. These memory cells were shown to mediate resistance and respond to antigen in vitro. Mediators of resistance in the unstimulated peritoneal cavity during late-phase are long-lived. On the other hand, parabiosis studies suggested that late-phase resident peritoneal cells which mediate resistance and respond to antigen in vitro have in part arrived after the end of early phase. Such cells are found in low numbers in central lymph during late-phase. The simplest interpretation of these data is that LM-specific lymphoblasts spontaneously extravasate and settle in tissues as long-lived memory cells. Since the numbers of LM-specific lymphoblasts released from lymphoid tissue is highest during early phase, the majority of resident memory cells are progeny of early-phase lymphoblasts.

Animals↗