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Results for “Lymphopenia”

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At least 271 records · Page 15Linked to original sources
PubMed2005

MHC class I-positive dendritic cells (DC) control CD8 T cell homeostasis in vivo: T cell lymphopenia as a prerequisite for DC-mediated homeostatic proliferation of naive CD8 T cells.

The sizes of peripheral T cell pools are regulated by competition for environmental signals within a given ecological T cell niche. Cytokines and MHC molecules have been identified as resources for which naive T cells compete to proliferate homeostatically in lymphopenic hosts to fill up their respective compartments. However, it still remains unclear to what extent CD4 and CD8 T cells intercompete for these resources and which role dendritic cells (DC) play in this scenario. Using transgenic mice in which only DC express MHC class I, we demonstrate that this type of APC is sufficient to trigger complete homeostatic proliferation of CD8 T cells in vivo. However, normal numbers of endogenous naive CD4 T cells, but not CD25(+)CD4(+) T regulatory cells, efficiently suppress this expansion in vivo. These findings identify DC as a major resource and a possible target for homeostatic competition between naive CD4 and CD8 T cells.

Animals↗
PubMed2006

CD25+Foxp3+ regulatory T cells facilitate CD4+ T cell clonal anergy induction during the recovery from lymphopenia.

T cell clonal anergy induction in lymphopenic nu/nu mice was found to be ineffective. Exposure to a tolerizing peptide Ag regimen instead induced aggressive CD4(+) cell cycle progression and increased Ag responsiveness (priming). Reconstitution of T cell-deficient mice by an adoptive transfer of mature peripheral lymphocytes was accompanied by the development of a CD25(+)Foxp3(+)CTLA-4(+)CD4(+) regulatory T cell population that acted to dampen Ag-driven cell cycle progression and facilitate the induction of clonal anergy in nearby responder CD25(-)CD4(+) T cells. Thus, an early recovery of CD25(+) regulatory T cells following a lymphopenic event can prevent exuberant Ag-stimulated CD4(+) cell cycle progression and promote the development of clonal anergy.

Adoptive Transfer↗
PubMed2006

Peripheral T cell lymphopenia and concomitant enrichment in naturally arising regulatory T cells: the case of the pre-Talpha gene-deleted mouse.

In pre-Talpha (pTalpha) gene-deleted mice, the positively selectable CD4+ CD8+ double-positive thymocyte pool is only 1% that in wild-type mice. Consequently, their peripheral T cell compartment is severely lymphopenic with a concomitant increase in proportion of CD25+ FoxP3+ regulatory T cells. Using mixed bone marrow chimeras, where thymic output was 1% normal, the pTalpha(-/-) peripheral T cell phenotype could be reproduced with normal cells. In the pTalpha(-/-) thymus and peripheral lymphoid organs, FoxP3+ CD4+ cells were enriched. Parabiosis experiments showed that many pTalpha(-/-) CD4+ single-positive thymocytes represented recirculating peripheral T cells. Therefore, the enrichment of FoxP3+ CD4+ single-positive thymocytes was not solely due to increased thymic production. Thus, the pTalpha(-/-) mouse serves as a model system with which to study the consequences of chronic decreased thymic T cell production on the physiology of the peripheral T cell compartment.

Animals↗
PubMed1978

Corticosteroid-induced lymphopenia, immunosuppression, and body defense.

The apparent paradox of heightened adrenal corticosteroid levels associated with reduction in the competence of the body's defensive apparatus to cope with exposure to new microbial antigens is considered. The question is asked how this lowered defensive capability, which occurs in the face of a threat to body integrity, is consistent with Cannon's principals of the "wisdom of the body." The suggestion is offered that the immunologic response to self-antigens exposed by disease or trauma may be suppressed by corticosteroid to offset the likelihood of autoimmune attack.

Adrenal Cortex Hormones↗
PubMed2000

[CD4 lymphopenia and postoperative immunosuppression in cardiac surgery].

The diversity and heterogeneity of biologic reactions is a condition sine qua non for the adaptation of live organisms to changes of external environment. Reactions of the immune system enable survival even in extreme conditions. Modern medicine often reaches situations never met by the organism in phylogenesis. Thanks to up-to-date therapeutical approaches many patients survive with grave symptoms such as multiple organ failure and extensive forms of injury. New infectious diseases are emerging, e.g. HIV/AIDS. Notwithstanding the broad array of external insults, it becomes obvious that organisms mobilize defence reactions according to a general scheme. Likewise, exhaustion of the immune potential occurs according to an archetypal pattern. In the case of cell-mediated immunity the faultless course of which is of critical importance for organisms in extreme conditions, the loss begins with the absence of reactivity of T-cells to specific antigens to end with the absence of their reactivity to polyclonal mitogens. The article deals with pathogenic mechanisms underlying the onset of immunodeficiencies caused by both infectious and non-infectious stimuli with special regard being focused on cardiac surgery in extracorporeal circuit.

CD4-Positive T-Lymphocytes↗