Class II-Independent Generation of CD4 Memory T Cells from Effectors

Swain, Susan L.; Hu, Hui; Huston, Gail E.

doi:10.1126/science.286.5443.1381

Cited by 384 publications

(317 citation statements)

References 22 publications

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“…This implies, with respect to the reported kinetics of BFL1/A1 expression with return to basal levels at about 48 h after TCR stimulation [22], that at least a fraction of the CD31 -central naive T cells have recently been stimulated via their TCR. The observation that in all samples analyzed BFL-1/A1 expression was not enhanced in CD45RO + memory as compared to CD31 -central naive CD4 + T cells is consistent with the observation that memory CD4 + T cell maintenance is independent of MHC-II [28][29][30][31]. On the other hand the inconsistent up- regulation of BFL-1/A1 in memory as compared to CD31 + thymic naive CD4 + T cells could easily be explained by varying numbers of cells that have recently been activated in the course of foreign antigen encounter.…”

Section: Discussionsupporting

confidence: 89%

Post-thymic in vivo proliferation of naive CD4+ T cells constrains the TCR repertoire in healthy human adults

et al. 2005

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In spite of thymic involution early in life, the numbers of naive CD4 + T cells only slowly decline in ageing humans implying peripheral post-thymic naive CD4 + T cell expansion. This proliferation may compensate for continuous activation and death of naive CD4 + T cells but may also have negative consequences for protective immunity. Here we show that naive CD4 + T cells that have proliferated in the periphery are characterized by a highly restricted oligoclonal TCR repertoire. Additionally these cells, which constitute the majority of naive CD4 + T cells in the elderly, display signatures of recent TCR engagement. Our results demonstrate for the first time that peripheral post-thymic proliferation of naive CD4 + T cells in healthy human individuals causes a significant contraction of the peripheral TCR repertoire. This age-dependent deterioration of CD4 + T cell immunity could entail ageing-associated autoimmunity, increased susceptibility to infection or cancer and decreased efficiency of vaccination.

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Section: Discussionsupporting

confidence: 89%

Post-thymic in vivo proliferation of naive CD4+ T cells constrains the TCR repertoire in healthy human adults

et al. 2005

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“…T‐cell receptor signaling seems not to be important for the maintenance of CD4 + memory T cells. CD4 + memory T cells persist when their TCR is ablated,98 and also in MHC class II‐deficient hosts 99. For CD8 + memory T cells, the situation is less clear.…”

Section: The Lifestyle Of Circulating Memory T Lymphocytesmentioning

confidence: 99%

Immunological memories of the bone marrow

Chang

Tokoyoda

Radbruch

2018

Immunological Reviews

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SummaryMemory for antigens once encountered is a hallmark of the immune system of vertebrates, providing us with an immunity adapted to pathogens of our environment. Despite its fundamental relevance, the cells and genes representing immunological memory are still poorly understood. Here we discuss the concept of a circulating, proliferating, and ubiquitous population of effector lymphocytes vs concepts of resting and dormant populations of dedicated memory lymphocytes, distinct from effector lymphocytes and residing in defined tissues, particularly in barrier tissues and in the bone marrow. The lifestyle of memory plasma cells of the bone marrow may serve as a paradigm, showing that persistence of memory lymphocytes is not defined by intrinsic “half‐lives”, but rather conditional on distinct survival signals provided by dedicated niches. These niches are organized by individual mesenchymal stromal cells. They define the capacity of immunological memory and regulate its homeostasis.

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“…Different models were proposed to explain the longevity of memory cells. Maintenance of memory CD4 and CD8 cells seems to be independent of antigen or MHC class II and I molecules, respectively [20,21]. The generation of efficient CD8 memory T cells requires the presence of CD4 T cells [22][23][24][25].…”

Section: Introductionmentioning

confidence: 99%

In vitro generated human memory‐like T cells are CD95 type II cells and resistant towards CD95‐mediated apoptosis

et al. 2006

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An adaptive immune response implies expansion of activated T cells and subsequent elimination to maintain homeostasis in a process called activation-induced cell death. Some cells, however, differentiate into memory cells and ensure a strong secondary immune response. To analyze the apoptosis phenotype of memory T cells on a cellular and molecular level, we have established an in vitro model of T cell activation and generation of cells phenotypically and functionally similar to memory cells. These longterm cultured T cells show a CD95-resistant phenotype, although they are still sensitive towards TCR/CD3-mediated apoptosis. Biochemical analysis revealed that these cells shift from CD95 type I (direct signaling from the receptor) during the effector phase to CD95 type II cells (dependent on the mitochondrial amplification loop). Moreover, their mitochondria are protected, probably due to high expression levels of Bcl-x L and Bcl-2. Thus, our data suggest a mechanism how memory T cells acquire resistance towards bystander cell death via the CD95 system.

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Class II-Independent Generation of CD4 Memory T Cells from Effectors

Cited by 384 publications

References 22 publications

Post-thymic in vivo proliferation of naive CD4+ T cells constrains the TCR repertoire in healthy human adults

Post-thymic in vivo proliferation of naive CD4+ T cells constrains the TCR repertoire in healthy human adults

Immunological memories of the bone marrow

In vitro generated human memory‐like T cells are CD95 type II cells and resistant towards CD95‐mediated apoptosis

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