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PubMed1986

Cells involved in the immune response. XXXIV: Suppressor cells in the thymus of the immunized rabbit capable of secreting a factor which can suppress the secretion of antibodies from antibody-forming cells in vitro.

Outbred rabbits were immunized intravenously with 10(9) sheep erythrocytes (SRBC) and/or horse erythrocytes (HRBC) and sacrificed 1 to 60 days later. At the height of the immune response (Day 7 postimmunization), antibody-forming cells identified by their ability to form hemolytic plaques in the plaque-forming cell (PFC) assay were detected only in the spleen. The splenic PFCs were totally inhibited if they were first incubated with the autologous thymus cells (immune thymus suppressor cells or ITSCs) for 4 hr prior to assaying for PFCs. Incubation of the spleen mononuclear cells with cells of any of the other lymphoid organs of the immunized rabbit for up to 6 hr did not inhibit the PFCs to any significant degree. There is no MHC restriction in the suppressor activity of the ITSCs since they could totally suppress the PFCs of autologous and allogeneic 7-day immune spleen cells. Neither thymus cells nor cells of any of the other lymphoid organs of the unimmunized rabbit could inhibit allogeneic 7-day immune splenic PFCs. The ITSCs from rabbits immunized with SRBC could be isolated by rosetting with the immunizing antigen, SRBC, but not with the non-cross-reacting antigens HRBC, human erythrocytes (HuRBC), and rabbit erythrocytes (RRBC), and vice versa, thus demonstrating the antigenic specificity of the suppressor cells. The thymus cells, but not the cells of any of the other lymphoid organs of the SRBC-immunized rabbit, secreted a factor referred to as immune thymus suppressor factor (ITSF) during incubation for 4 hr at 37 degrees C which could, by itself, totally suppress the splenic PFC. ITSF could be absorbed out of solution by incubation with the immunizing antigen, SRBC, but not with the non-cross-reacting antigens HRBC, HuRBC, and RRBC. Similarly, the ITSF secreted by the thymus cells of the HRBC-immunized rabbit could be absorbed out of solution by incubation with the immunizing antigen, HRBC, but not with the SRBC, HuRBC, and RRBC. ITSF is therefore antigen specific as is its parent ITSC. The cells of the lymphoid organs of unimmunized rabbits did not secrete a suppressor factor during incubation in vitro. ITSCs capable of totally inhibiting the PFCs were detected in the immunized rabbits by Day 5 post-primary-immunization; the ITSCs were capable of secreting ITSF which could totally inhibit the PFCs by Day 7 post-primary-immunization. Although the ITSCs were detected in a suppressive state up to Day 40 post-primary-immunization, they lost their capacity to secrete ITSF by Day 21 post-primary-immunization.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2001

Man the barrier! Strategic defences in the intestinal mucosa.

Immunologists typically study the immune responses induced in the spleen or peripheral lymph nodes after parenteral immunization with antigen and poorly defined experimental adjuvants. However, most antigens enter the body through mucosal surfaces. It is now clear that the microenvironment in these mucosal barriers has a marked influence on the immune response that ultimately ensues. Nowhere is the microenvironment more influential than in the gut-associated lymphoid tissue (GALT). The GALT must constantly distinguish harmless antigens that are present in food or on commensal bacteria from pathogenic assault by microbes. It is perhaps not surprising, then, that the GALT contains more lymphocytes than all of the secondary lymphoid organs combined.

Animals↗
PubMed2006

Regulation of Th2 differentiation and Il4 locus accessibility.

Helper T cells coordinate immune responses through the production of cytokines. Th2 cells express the closely linked Il4, Il13, and Il5 cytokine genes, whereas these same genes are silenced in the Th1 lineage. The Th1/Th2 lineage choice has become a textbook example for the regulation of cell differentiation, and recent discoveries have further refined and expanded our understanding of how Th2 differentiation is initiated and reinforced by signals from antigen-presenting cells and cytokine-driven feedback loops. Epigenetic changes that stabilize the active or silent state of the Il4 locus in differentiating helper T cells have been a major focus of recent research. Overall, the field is progressing toward an integrated model of the signaling and transcription factor networks, cis-regulatory elements, epigenetic modifications, and RNA interference mechanisms that converge to determine the lineage fate and gene expression patterns of differentiating helper T cells.

Animals↗
PubMed2006

Intestinal and pulmonary mucosal T cells: local heroes fight to maintain the status quo.

Mucosal immunity in the lung and intestine is controlled by complex multifaceted systems. While mucosal T cells are essential for protection against invading pathogens owing to their proximity to the outside world, powerful systems must also be in place to harness ongoing inflammatory processes. In each site, distinct anatomical structures play key roles in mounting and executing both protective and deleterious mucosal T cell responses. Although analogies can be drawn regarding the immune systems of these two organs, there are substantial dissimilarities necessitated by unique physiologic constraints. Here, we discuss how T cell activation and effector function are generated in the mucosae.

Antigen Presentation↗
PubMed2001

Is tumor expression of the major histocompatibility complex antigen required for T cell immune surveillance?

Tumor expression of major histocompatibility complex antigen (MHC) class I and class II is not essential for the induction of memory T cells. However, induction of MHC class I-restricted effector cytotoxic T cells (CTL) appears dependent on MHC class I expression on tumors. Moreover, the effector function of tumor-specific CTL requires direct recognition of the tumor. In contrast, both the inductive and the effector phases of MHC class II-restricted T cells are independent of MHC class II expression on tumors.

Histocompatibility Antigens Class I↗
PubMed2004

Dynamic optimization of host defense, immune memory, and post-infection pathogen levels in mammals.

When attacked by pathogens, higher vertebrates produce specific immune cells that fight against them. We here studied the host's optimal schedule of specific immune cell production. The damage caused by the pathogen increases with the pathogen amount in the host integrated over time. On the other hand, there is also a cost incurred by the production of specific immune cells, not only in terms of the energy needed to produce and maintain the cells, but also with respect to damages sustained by the host's body as a result of immune activity. The optimal strategy of the host is the one that minimizes the total cost, defined as a weighted sum of the damage caused by pathogens and the costs caused by the specific immune cells. The problem is solved by using Pontryagin's maximum principle and dynamic programming. The optimal defense schedule is typically as follows: In the initial phase after infection, immune cells are produced at the fastest possible rate. The amount of pathogen increases temporarily but is eventually suppressed. When the pathogen amount is suppressed to a sufficiently low level, the immune cell number decreases and converges to a low steady level, which is maintained by alternately switching between fastest production and no production. We examine the effect of time delay required to have fully active immune cells by comparing cases with different number of rate limiting steps before producing immune cells. We examine the effect of the duration of time (time delay) required before full-scale production of active immune cells by comparing cases with different numbers of rate-limiting steps before immune-cell production. We also discuss the role of immune memory based on the results of the optimal immune reaction.

Animals↗
PubMedDate not supplied

A mathematical model for the immunosenescence.

We propose a model for the dynamics of the immune system by considering the subpopulations of virgin and memory T lymphocytes on a time scale corresponding to the human life span. In the deterministic balance equation we introduce a fluctuating term in order to take into account the chronic antigenic stress. Starting from the hypothesis that the depletion of virgin cells with cytotoxic properties (CD8+) is a mortality marker, the model provides survival curves quite similar to the demographic curves.

Aging↗
PubMed1995

Environmental antigens and atopic disease: underlying mechanisms and prospects for therapy and prophylaxis.

Natural exposure to non-pathogenic antigens, the so-called 'environmental antigens', experimentally elicits a characteristic pattern of T-cell immunity, involving selective suppression of the T-cell-dependent IgE responses that trigger allergic reactions. This 'immune deviation' results in the generation of long-lived T-cell memory, which confers active protection against allergic sensitization. Corresponding primary immune responses to environmental antigens in humans occur most frequently during infancy, and the development of allergic sensitization can be viewed as a failure of this natural immune-deviation process. In this article, potential strategies for primary prevention of allergic disease in infants involving, in particular, the exploitation of oral and mucosal tolerance to stimulate protective CD8+ T-cell-mediated immune deviation, are discussed.

Allergens↗