Lower percentage of CD8high+CD152+ but not CD8high+CD28+ T lymphocytes in the elderly may be reverted by interleukin 2 in vitro

2002 ◽  
Vol 123 (9) ◽  
pp. 1283-1293 ◽  
Author(s):  
Piotr Trzonkowski ◽  
Jolanta Myśliwska ◽  
Ewa Szmit ◽  
Małgorzata Żak ◽  
Jerzy Foerster ◽  
...  
Keyword(s):  
T Lymphocytes ◽  
Interleukin 2 ◽  
The Elderly ◽  
Lower Percentage

scholarly journals The regulatory role of interleukin 2-responsive T lymphocytes on early and mature erythroid progenitor proliferation

Blood ◽  
1986 ◽  
Vol 67 (6) ◽  
pp. 1607-1610
Author(s):  
Z Estrov ◽  
C Roifman ◽  
YP Wang ◽  
T Grunberger ◽  
EW Gelfand ◽  
...  
Keyword(s):  
T Lymphocytes ◽  
Colony Formation ◽  
Interleukin 2 ◽  
Erythroid Differentiation ◽  
Colony Growth ◽  
Dependent Manner ◽  
Erythroid Progenitor ◽  
Recombinant Interleukin 2

To analyze the role of T lymphocytes in human erythropoiesis, we evaluated the effect of recombinant interleukin 2 (IL 2) on marrow CFU- E and BFU-E colony formation in vitro. IL 2 resulted in an increase in CFU-E and BFU-E colony numbers in a dose-dependent manner. This increase could be prevented by anti-Tac, a monoclonal antibody to the IL 2 receptor. Moreover, anti-Tac on its own resulted in an overall decrease in colony numbers. Depletion of marrow adherent cells did not alter the effect of either IL 2 or anti-Tac on colony growth. Following the removal of marrow T lymphocytes, CFU-E and BFU-E colony formation proceeded normally; however, the effects of IL 2 and anti-Tac were markedly diminished. Readdition of T lymphocytes to the cultures restored the IL 2 effect. Although T lymphocytes were not themselves essential for in vitro erythropoiesis, our studies suggest that IL 2 and IL 2-responsive T cells can regulate both early and mature stages of erythroid differentiation.

Recipient immune-competent T lymphocytes can survive intensive conditioning for bone marrow transplantation

Blood ◽  
1986 ◽  
Vol 68 (4) ◽  
pp. 954-956 ◽  
Author(s):  
A Butturini ◽  
RC Seeger ◽  
RP Gale
Keyword(s):  
Bone Marrow ◽  
Bone Marrow Transplantation ◽  
T Lymphocytes ◽  
Graft Rejection ◽  
Marrow Transplantation ◽  
Interleukin 2 ◽  
Marrow Transplant ◽  
Effector Cells ◽  
And Function

Abstract Bone marrow transplantation is usually preceded by intensive chemotherapy and radiation therapy designed to completely eliminate recipient immune-competent cells that might reject the donor bone marrow. We show that seven of 14 bone marrow transplant recipients who received intensive conditioning retained circulating T lymphocytes that proliferate after incubation with interleukin 2 and phytohemagglutinin and function as effector cells in an in vitro model of graft rejection. These T cells may mediate graft rejection.

scholarly journals BCL-6 expression during B-cell activation

Blood ◽  
1996 ◽  
Vol 87 (12) ◽  
pp. 5257-5268 ◽  
Author(s):  
D Allman ◽  
A Jain ◽  
A Dent ◽  
RR Maile ◽  
T Selvaggi ◽  
...  
Keyword(s):  
B Cells ◽  
T Lymphocytes ◽  
Germinal Center ◽  
Cell Activation ◽  
Interleukin 2 ◽  
Large Cell ◽  
Cd40 Ligand ◽  
Mrna Levels ◽  
Coding Region

Translocations involving the BCL-6 gene are common in the diffuse large cell subtype of non-Hodgkin's lymphoma. Invariably, the BCL-6 coding region is intact, but its 5′ untranslated region is replaced with sequences from the translocation partner. The present study shows that BCL-6 expression is regulated in lymphocytes during mitogenic stimulation. Resting B and T lymphocytes contain high levels of BCL-6 mRNA. Stimulation of mouse B cells with anti-IgM or IgD antibodies, bacterial lipopolysaccharide, phorbol 12-myristate 13-acetate plus ionomycin, or CD40 ligand led to a five-fold to 35-fold decrease in BCL-6 mRNA levels. Similar downregulation of BCL-6 mRNA was seen in human B cells stimulated with Staphylococcus aureus plus interleukin-2 or anti-IgM antibodies and in human T lymphocytes stimulated with phytohemagglutinin. BCL-6 mRNA levels began to decrease 8 to 16 hours after stimulation, before cells entered S phase. Although polyclonal activation of B cells in vitro invariably decreased BCL-6 MRNA expression, activated B cells from human germinal centers expressed BCL-6 mRNA at levels comparable to the levels in resting B cells. Despite these similar mRNA levels, BCL-6 protein expression was threefold to 34-fold higher in germinal center B cells than in resting B cells, suggesting that BCL-6 protein levels are controlled by translational or posttranslational mechanisms. These observations suggest that the germinal center reaction provides unique activation signals to B cells that allow for continued, high-level BCL-6 expression.

scholarly journals Interleukin-2 (IL-2) Regulates the Accessibility of the IL-2-Responsive Enhancer in the IL-2 Receptor α Gene to Transcription Factors

1999 ◽  
Vol 19 (4) ◽  
pp. 2681-2689 ◽  
Author(s):  
Corinne Rusterholz ◽  
Patricia Corthésy Henrioud ◽  
Markus Nabholz
Keyword(s):  
Transcription Factors ◽  
T Lymphocytes ◽  
Binding Sites ◽  
Interleukin 2 ◽  
Binding Activity ◽  
Micrococcal Nuclease ◽  
Cooperative Binding ◽  
Α Subunit ◽  
Hypersensitive Sites

ABSTRACT Interleukin-2 (IL-2) responsiveness of T lymphocytes is controlled through transcription of the IL-2 receptor (IL-2R) α subunit by antigen and by IL-2 itself. IL-2 induces IL-2Rα transcription via an IL-2-responsive enhancer (IL-2rE), whose activity depends on the cooperative binding of IL-2-induced STAT5 to two sites and of constitutively active Elf-1 to a third one. Here we describe the changes in IL-2rE chromatin that occur in normal T lymphocytes upon activation of IL-2Rα expression. In cells induced to transiently express IL-2Rα with concanavalin A (which mimics antigen), none of the IL-2rE sites is occupied despite the presence of Elf-1 and STAT1, which bind to the IL-2rE in vitro. The two STAT binding sites are occupied rapidly upon IL-2 stimulation, concomitantly with STAT5 activation. Occupation of the Elf-1 binding site is delayed, although Elf-1 concentration and binding activity are not modified by IL-2. Digestion of T-cell chromatin with DNase I and micrococcal nuclease shows that IL-2 induces the appearance of nuclease-hypersensitive sites flanking the IL-2rE. Thus IL-2, in addition to activating STAT5, appears to regulate IL-2Rα transcription by making IL-2Rα chromatin accessible to transcription factors.

In vivo and in vitro evidence that 99mTc-HYNIC-interleukin-2 is able to detect T lymphocytes in vulnerable atherosclerotic plaques of the carotid artery

2014 ◽  
Vol 41 (9) ◽  
pp. 1710-1719 ◽  
Author(s):  
Andor W. J. M. Glaudemans ◽  
Elena Bonanno ◽  
Filippo Galli ◽  
Clark J. Zeebregts ◽  
Erik F. J. de Vries ◽  
...  
Keyword(s):  
T Lymphocytes ◽  
Carotid Artery ◽  
Interleukin 2 ◽  
Atherosclerotic Plaques

scholarly journals Augmentation of the anti-tumor therapeutic efficacy of long-term cultured T lymphocytes by in vivo administration of purified interleukin 2.

1982 ◽  
Vol 155 (4) ◽  
pp. 968-980 ◽  
Author(s):  
M A Cheever ◽  
P D Greenberg ◽  
A Fefer ◽  
S Gillis
Keyword(s):  
T Lymphocytes ◽  
Therapeutic Efficacy ◽  
Cultured Cells ◽  
Tumor Therapy ◽  
Interleukin 2 ◽  
Adoptive Therapy ◽  
In Vivo Efficacy

Spleen cells from C57BL/6 mice immunized in vivo with a syngeneic Friend virus-induced leukemia, FBL-3, were specifically activated by culture for 7 d with FBL-3, then nonspecifically induced to proliferate in vitro for 12 d by addition of supernatants from concanavalin A-stimulated lymphocytes containing interleukin 2 (IL-2). Such long-term cultured T lymphocytes have previously been shown to specifically lyse FBL-3 and to mediate specific adoptive therapy of advanced disseminated FBL-3 when used as an adjunct to cyclophosphamide (CY) in adoptive chemoimmunotherapy. Because the cultured cells are dependent upon IL-2 for proliferation and survival in vitro, their efficacy in vivo is potentially limited by the availability of endogenous IL-2. Thus, the aim of the current study was to determine whether exogenously administered purified IL-2 could augment the in vivo efficacy of long-term cultured T lymphocytes. Purified IL-2 alone or as an adjunct to CY as ineffective in tumor therapy. However, IL-2 was extremely effective in augmenting the efficacy of IL-2-dependent long-term cultured T lymphocytes in adoptive chemoimmunotherapy. The mechanism by which IL-2 functions in vivo is presumably by promoting in vivo growth and/or survival of adoptively transferred cells. This assumption was supported by the findings that IL-2 did not enhance the modest therapeutic efficacy of irradiated long-term cultured cells that were incapable of proliferating in the host and was ineffective in augmenting the in vivo efficacy of noncultured immune cells that are not immediately dependent upon exogenous IL-2 for survival.

Dressed to kill? A review of why antiviral CD8 T lymphocytes fail to prevent progressive immunodeficiency in HIV-1 infection

Blood ◽  
2001 ◽  
Vol 98 (6) ◽  
pp. 1667-1677 ◽  
Author(s):  
Judy Lieberman ◽  
Premlata Shankar ◽  
N. Manjunath ◽  
Jan Andersson
Keyword(s):  
T Cells ◽  
T Cell ◽  
T Lymphocytes ◽  
Cd8 T Cells ◽  
Interleukin 2 ◽  
Interferon Γ ◽  
Short Term Exposure ◽  
Infected Cells ◽  
Hiv 1

Abstract CD8 T cells play an important role in protection and control of HIV-1 by direct cytolysis of infected cells and by suppression of viral replication by secreted factors. However, although HIV-1–infected individuals have a high frequency of HIV-1–specific CD8 T cells, viral reservoirs persist and progressive immunodeficiency generally ensues in the absence of continuous potent antiviral drugs. Freshly isolated HIV-specific CD8 T cells are often unable to lyse HIV-1–infected cells. Maturation into competent cytotoxic T lymphocytes may be blocked during the initial encounter with antigen because of defects in antigen presentation by interdigitating dendritic cells or HIV-infected macrophages. The molecular basis for impaired function is multifactorial, due to incomplete T-cell signaling and activation (in part related to CD3ζ and CD28 down-modulation), reduced perforin expression, and inefficient trafficking of HIV-specific CD8 T cells to lymphoid sites of infection. CD8 T-cell dysfunction can partially be corrected in vitro with short-term exposure to interleukin 2, suggesting that impaired HIV-specific CD4 T helper function may play a significant causal or exacerbating role. Functional defects are qualitatively different and more severe with advanced disease, when interferon γ production also becomes compromised.

scholarly journals PROTEIN REKOMBINAN 38 KDA MYCOBAKTERIUM TUBERKULOSIS DAPAT MENGIMBAS PEMBUATAN INTERLEUKIN-2 DAN INTERFERON-γ LIMFOSIT T DI KULTUR SEL MONONUKLEAR DARAH TEPI

2018 ◽  
Vol 22 (2) ◽  
pp. 151
Author(s):  
Maimun Z Arthamin ◽  
Singgih Pujo Wahono ◽  
Antiek Primardianti ◽  
Ati Rastini ◽  
Tri Wahju Astuti ◽  
...  
Keyword(s):  
Immune Response ◽  
T Lymphocytes ◽  
Recombinant Protein ◽  
Vaccine Development ◽  
Interleukin 2 ◽  
Development Program ◽  
In Vitro Study ◽  
Cell Mediated Immunity ◽  
Ifn Γ

Tuberculosis (TB) is caused by Mycobacterium tuberculosis (M.tb) and is one of the significant mortality causes WHO (2012). Theprimary immune response in TB pathogenesis is Cell Mediated Immunity (CMI), roled by T lymphocytes. Interleukin-2 (IL-2) is a growthfactor for T lymphocytes. Gamma Interferon is the key cytokine in M.tb infection control, synthezised by T lymphocytes. An effectivevaccination strategy is achieved by giving vaccine which is able to stimulate T lymphocytes in synthezising cytokines. The 38 kDa M.tbprotein is potential in the vaccine development program, because it has specific epitopes for T lymphocytes. The aim of this study was toknow how to determine that the 38 kDa recombinant protein of M.tb Malang strain could induce cellular immune response by IL-2 andIFN-γ synthezised by T lymphocytes. The study was carried out by an experimental in vitro study on PBMC from healthy endemic subjects,those having TB contact, and the TB patients themselves. PBMC from subjects was cultured with 38 kDa recombinant protein of M.tbMalang strain, with PPD and without any protein. The analysis of IL-2 and IFN-γ used flowcytometry. The result showed that the highestpercentage of IL-2 was found in the culture with 38 kDa recombinant protein of M.tb Malang strain, in healthy endemic (p=0.000)and in those who had TB contact (p=0.000). the highest percentage of IFN-γ was found in the culture with 38 kDa recombinant proteinof M.tb Malang strain, in healthy endemic (p=0.007) and those who had TB contact (p = 0.105). The 38 kDa recombinant proteinof M.tb Malang strain was able to induce IL-2 and IFN-γ synthezised by TCD3+ lymphocytes from healthy endemic subjects and thosewho had TB contact.

scholarly journals Co-expression of cytokine and suicide genes to enhance the activity and safety of tumor-specific cytotoxic T lymphocytes

Blood ◽  
2007 ◽  
Vol 110 (8) ◽  
pp. 2793-2802 ◽  
Author(s):  
Concetta Quintarelli ◽  
Juan F. Vera ◽  
Barbara Savoldo ◽  
Greta M. P. Giordano Attianese ◽  
Martin Pule ◽  
...  
Keyword(s):  
T Lymphocytes ◽  
Cytotoxic T Lymphocytes ◽  
Severe Combined Immunodeficiency ◽  
Interleukin 2 ◽  
Suicide Gene ◽  
Clinical Value ◽  
Transgenic Expression ◽  
Barr Virus

Abstract The antitumor effect of adoptively transferred tumor-specific cytotoxic T lymphocytes (CTLs) is impaired by the limited capacity of these cells to expand within the tumor microenvironment. Administration of interleukin 2 (IL-2) has been used to overcome this limitation, but the systemic toxicity and the expansion of unwanted cells, including regulatory T cells, limit the clinical value of this strategy. To discover whether transgenic expression of lymphokines by the CTLs themselves might overcome these limitations, we evaluated the effects of transgenic expression of IL-2 and IL-15 in our model of Epstein Barr Virus–specific CTLs (EBV-CTLs). We found that transgenic expression of IL-2 or IL-15 increased the expansion of EBV-CTLs both in vitro and in vivo in a severe combined immunodeficiency disease (SCID) mouse model and enhanced antitumor activity. Although the proliferation of these cytokine genes transduced CTLs remained strictly antigen dependent, clinical application of this approach likely requires the inclusion of a suicide gene to deal with the potential development of T-cell mutants with autonomous growth. We found that the incorporation of an inducible caspase-9 suicide gene allowed efficient elimination of transgenic CTLs after exposure to a chemical inducer of dimerization, thereby increasing the safety and feasibility of the approach.

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