Interleukin-2: Inception, Impact, and Implications

Smith, Kendall A.

doi:10.1126/science.3131876

Cited by 2,019 publications

(965 citation statements)

References 89 publications

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“…Growth factors, including members of the common cytokine receptor c-chain cytokine family, support T cell viability in vivo [20][21][22][23][24]. A similar need for trophic support also occurs in vitro [25][26][27]. Cell death is readily evident when T cells are cultured in media devoid of growth factors such as IL-2 [28][29][30].…”

Section: Resultsmentioning

confidence: 99%

c‐Maf interacts with c‐Myb to down‐regulate Bcl‐2 expression and increase apoptosis in peripheral CD4 cells

et al. 2007

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The transcription factor c‐Maf is critical for IL‐4 production and the development of Th2 cells, which promote humoral immunity and protect against extracellular parasites. Yet, little else is known of c‐Maf function in CD4 cells. Here, we identify a novel role for c‐Maf in regulating susceptibility to apoptosis. Overexpression of c‐Maf results in increased susceptibility of CD4 cells to apoptosis induced by multiple stimuli, including growth factor withdrawal, dexamethasone, irradiation, and TCR engagement. This effect is independent of Fas or p53; however, Bcl‐2 expression is reduced in c‐Maf Tg CD4 cells. Immunoprecipitation and Western blot analyses demonstrate that c‐Maf–c‐Myb complex formation is enhanced among T cells from c‐Maf Tg mice compared to non‐Tg littermates following TCR engagement. Unlike non‐Tg T cells, c‐Myb binding to the Bcl‐2 promoter is not detectable in c‐Maf Tg T cells by chromatin immunoprecipitation. In reporter assays, Bcl‐2 promoter activity is reduced by c‐Maf in a dose‐dependent manner. Furthermore, transgene‐mediated Bcl‐2 expression corrects the apoptosis defect observed among c‐Maf Tg CD4 cells. These data suggest that c‐Maf can interact with c‐Myb to reduce Bcl‐2 expression, thereby limiting CD4 cell survival following TCR engagement.

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Section: Resultsmentioning

confidence: 99%

c‐Maf interacts with c‐Myb to down‐regulate Bcl‐2 expression and increase apoptosis in peripheral CD4 cells

et al. 2007

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“…In the present study, the ratio of IL-2R + cells to CD2 + cells did not change significantly throughout the course of CR-EAE. IL-2R expression occurs early and transiently after T cell activation (Smith, 1988). The IL-2R population may include the encephalitogenic T cells (Sedgwick et al, 1987).…”

Section: Discussionmentioning

confidence: 99%

Inflammatory cells, microglia and MHC class II antigen-positive cells in the spinal cord of Lewis rats with acute and chronic relapsing experimental autoimmune encephalomyelitis

McCombe

Jersey

Pender

1994

Journal of Neuroimmunology

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Chronic relapsing experimental autoimmune encephalomyelitis (CR-EAE) was induced in Lewis rats by inoculation with guinea pig spinal cord and adjuvants and treatment with low dose cyclosporin A (CsA). Acute EAE was induced by the same method without CsA treatment. Immunocytochemistry and flow cytometry were used to assess inflammatory cells and MHC class II (Ia) antigen expression in the central nervous system of these rats. The inflammatory infiltrate was composed mainly of CD4 + T cells and macrophages, and αβ T cells constituted about 65% of the CD2 + T cells. After recovery from acute EAE and during the first remission of CR-EAE, the number of T cells was significantly less than in the preceding episodes. The number of T cells was higher in the second episode of CR-EAE than in the first remission. Throughout the course of CR-EAE, the majority of the CD2 + T cells were CD45RC −. The ratio of IL-2R + cells to CD2 + cells ranged from 10.5 to 24.0%. The ratio of CD4 + T cells to B cells was lower in the later episodes of CR-EAE than in the first episode. Ia antigen was expressed on infiltrating round cells at all stages of CR-EAE and on microglial cells (identified by dendritic morphology) with increasing intensity throughout the course of CR-EAE. With flow cytometry, the number of Ia + cells obtained from the spinal cord rose throughout the course of CR-EAE. The number of FSC low OX1 low cells, which we consider represent microglia, also increased during the course of CR-EAE.

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“…27 We therefore asked whether the first step in this cascade, the transcriptional activation of the IL-2 gene, could be blocked by PGE 2 . Indeed, PGE 2 treatment efficiently inhibited IL-2 and IFNG gene expression induced by CD3/CD28 crosslinking ( Figure 7E).…”

Section: Accepted Manuscriptmentioning

confidence: 99%

Prostaglandin E2 Prevents Helicobacter-Induced Gastric Preneoplasia and Facilitates Persistent Infection in a Mouse Model

et al. 2010

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Interleukin-2: Inception, Impact, and Implications

Cited by 2,019 publications

References 89 publications

c‐Maf interacts with c‐Myb to down‐regulate Bcl‐2 expression and increase apoptosis in peripheral CD4 cells

c‐Maf interacts with c‐Myb to down‐regulate Bcl‐2 expression and increase apoptosis in peripheral CD4 cells

Inflammatory cells, microglia and MHC class II antigen-positive cells in the spinal cord of Lewis rats with acute and chronic relapsing experimental autoimmune encephalomyelitis

Prostaglandin E2 Prevents Helicobacter-Induced Gastric Preneoplasia and Facilitates Persistent Infection in a Mouse Model

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