Relapse markers in multiple sclerosis: are in vitro cytokine production changes reflected by circulatory T-cell phenotype alterations?

1998 ◽  
Vol 4 (3) ◽  
pp. 193-197 ◽  
Author(s):  
Jan Debruyne ◽  
Jan Philippé ◽  
Jacques Dereuck ◽  
Annick Willems ◽  
Geert Leroux-Roels
Keyword(s):  
T Cell ◽  
T Lymphocyte ◽  
Interleukin 2 ◽  
Lymphocyte Subpopulations ◽  
T Cell Subsets ◽  
Cell Phenotype ◽  
Monocyte Count ◽  
Serum Neopterin ◽  
T Lymphocyte Subpopulations

In vitro tumor necrosis factor-a (TNF-a), interferon-g (IFN-g) and interleukin-2 (IL-2) production, serum neopterin levels, and T-lymphocyte subpopulations were determined on a monthly basis in 22 MS patients. We found increased in vitro TNF-a production from 4 weeks on prior to the day of an exacerbation. There was a significant correlation with in vitro IFN-g release, the absolute blood monocyte count and the serum neopterin levels, suggesting that monocytes stimulated by IFN-g play an important role in the TNF-a production. Serial analysis of in vitro TNF-a production proved to be a helpful tool in predicting relapses in MS patients. Furthermore, elevated levels of IFN-g and IL-2 after stimulation with OKT3 during exacerbations were demonstrated. These increases were not reflected by changes in T-lymphocyte subpopulations. However, significant differences in T-cell subsets were observed between controls and relapsing progressive patients.

scholarly journals Maturation of acute T-lymphoblastic leukemia cells after CD2 ligation and subsequent treatment with interleukin-2

Blood ◽  
1994 ◽  
Vol 84 (4) ◽  
pp. 1182-1192 ◽  
Author(s):  
F Mentz ◽  
F Ouaaz ◽  
A Michel ◽  
C Blanc ◽  
P Herve ◽  
...  
Keyword(s):  
T Cell ◽  
Tyrosine Phosphorylation ◽  
Lymphoblastic Leukemia ◽  
Interleukin 1 ◽  
Interleukin 2 ◽  
Subsequent Treatment ◽  
Leukemic Cells ◽  
Cell Phenotype ◽  
Cell Functions

Abstract In this study, we have investigated the ability of various cytokines to induce the maturation of acute lymphoblastic leukemia (T-ALL) cells with early T-cell phenotype. Leukemic blasts from 17 untreated T-ALL patients were assayed for their ability to acquire mature T-cell markers, CD3/T-cell receptor (TCR) in particular, after incubation with one or a combination of recombinant human interleukin-1 (IL-1), IL-2, IL-4, IL-7, and CD2-specific monoclonal antibody (MoAb). IL-7 or IL-2 induced the proliferation of some leukemic cells, whereas sequential cell treatment with CD2-MoAb and then IL-2 promoted CD3/TCR expression on nearly all CD2+ cells (15 of 16), except for 1 T-ALL that developed into CD3-CD16+CD56+ cells. Differentiation of T-ALL cells was also evidenced through the downregulation of CD34 precursor cell antigen, the generation of CD4+ and CD8+ cells from CD4+ CD8+ precursors, and the acquisition of mature T-cell functions. CD2 ligation induced a progressive increase of surface expression of IL-2 receptor alpha (IL- 2R alpha) and IL-2R beta and an accelerated in vitro death of leukemic cells. The ligation of IL-2R by IL-2 rescued T-ALL cells from death and promoted their progression toward more mature cells expressing extracellular CD3/TCR alpha beta complexes. Intracellular analysis indicates that TCR alpha transcription and membrane translocation of both TCR alpha and TCR beta were promoted in these conditions. Analysis of intracellular signals transduced during T-ALL differentiation indicated that CD2-ligation induced Ca2+ influx and that the ligation of CD2 and IL-2R induced distinct tyrosine phosphorylation patterns. The addition of inhibitors of tyrosine phosphorylation abolished T-ALL cell differentiation, which suggests the involvement of tyrosine kinases in this phenomenon. Together, we showed the constant maturation of leukemic early T cells after stimulation of surface CD2 and the high- affinity IL-2R.

scholarly journals T-cell receptor Vβ repertoire of CD8+ T-lymphocyte subpopulations in cutaneous leishmaniasis patients from the state of Rio de Janeiro, Brazil

2015 ◽  
Vol 110 (5) ◽  
pp. 596-605 ◽  
Author(s):  
Raquel Ferraz ◽  
Clarissa Ferreira Cunha ◽  
Maria Inês Pimentel ◽  
Marcelo Rosandiski Lyra ◽  
Armando Oliveira Schubach ◽  
...  
Keyword(s):  
T Cell ◽  
Cutaneous Leishmaniasis ◽  
T Cell Receptor ◽  
T Lymphocyte ◽  
Cell Receptor ◽  
Lymphocyte Subpopulations ◽  
The State ◽  
T Lymphocyte Subpopulations ◽  
Cd8 T Lymphocyte ◽  
T Cell Receptor Vβ

scholarly journals Multiple In Vitro and In Vivo Regulatory Effects of Budesonide in CD4+ T Lymphocyte Subpopulations of Allergic Asthmatics

PLoS ONE ◽  
2012 ◽  
Vol 7 (12) ◽  
pp. e48816 ◽  
Author(s):  
Elisabetta Pace ◽  
Caterina Di Sano ◽  
Stefania La Grutta ◽  
Maria Ferraro ◽  
Giuseppe Albeggiani ◽  
...  
Keyword(s):  
T Lymphocyte ◽  
Lymphocyte Subpopulations ◽  
T Lymphocyte Subpopulations ◽  
Regulatory Effects

scholarly journals Primary CLL Xenograft: A Model System to Study the Role of T-Cells in CLL Biology and Therapeutic Response

Blood ◽  
2014 ◽  
Vol 124 (21) ◽  
pp. 3284-3284
Author(s):  
Ceri E Oldreive ◽  
Anna Skowronska ◽  
Angelo Agathanggelou ◽  
Helen M Parry ◽  
Sergey Krysov ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Cell Function ◽  
Conflicts Of Interest ◽  
Xenograft Model ◽  
Cell Number ◽  
Biological Properties ◽  
T Cell Subsets ◽  
Cell Phenotype

Abstract The interaction between chronic lymphocytic leukaemia (CLL) cells and T-cells is an important aspect of CLL biology. CLL cells require T-cell support for their proliferation and in addition induce proliferation of regulatory and cytotoxic (CD8+) T-cells. T-cell number and repertoire are both markedly affected by CLL therapy and there is considerable interest in how current treatments modulate the interaction between T-cells and the tumour clone. In this study we investigated whether this relationship was maintained in a xenotransplantation model. CLL engraftment in NOG mice was facilitated by humanisation of the murine microenvironment by allogeneic CD34+ umbilical cord cells or CD14+ monocytes. Accelerated engraftment of both CLL and T-cell compartments was observed in xenografts derived from patients with progressive CLL, suggesting that the biological properties of both subsets are maintained in the murine model. Furthermore, the distribution of helper (CD4+), cytotoxic (CD8+) and regulatory (CD4+CD25+FoxP3+) T-cells was maintained within the xenografts, including retention of the CD4:CD8 ratio. Interestingly, the anergic PD-1+CD160+CD244+TIM3+ T-cell phenotype reported in CLL patients was also evident in T-cells expanded in xenograft models. Consistent with an anergic T-cell phenotype, T-cells from CLL xenografts lacked anti-tumour activity in vitro. Importantly, such anergic cells were observed when T-cells were reconstituted from allogeneic cord blood cells as well as autologous cells, suggesting that CLL cells have the ability to shape T-cell populations of different origin in diverse microenvironments. Finally, to investigate the interaction between specific T-cell subsets and engrafted CLL cells, CD4+, CD8+, and CD25+ T-cells were depleted prior to generation of xenografts. CD8+ T-cell depletion significantly prolonged CLL engraftment (p≤0.01) whereas neither depletion of CD4+ nor CD25+cells had a significant impact. In summary, our results demonstrate that the relationship between CLL tumour cells and reactive T-cells is accurately maintained in a murine xenograft model. Such models will be of great value for investigation of aspects of T-cell function in CLL biology. Disclosures No relevant conflicts of interest to declare.

scholarly journals T lymphocyte colony assay in hemophiliacs

Blood ◽  
1984 ◽  
Vol 64 (1) ◽  
pp. 105-109
Author(s):  
MV Ragni ◽  
A Winkelstein ◽  
TL Evans ◽  
JH Lewis ◽  
FA Bontempo ◽  
...  
Keyword(s):  
T Cell ◽  
T Lymphocyte ◽  
Interleukin 2 ◽  
Immune Deficiency Syndrome ◽  
Risk Groups ◽  
Cell Contact ◽  
Cell Mediated Immunity ◽  
Minimal Cell ◽  
Colony Assay

Unexplained lymphadenopathy, with or without accompanying symptoms, known as the “lymphadenopathy syndrome,” has been recognized in groups at risk for acquired immune deficiency syndrome (AIDS), namely, homosexuals and hemophiliacs. To date, however, no test has been defined that discriminates between asymptomatic individuals and those with adenopathy in these high-risk groups. The T colony assay, which measures T lymphocyte growth in soft agar and which allows selective T cell proliferation with minimal cell-cell contact, was evaluated in asymptomatic hemophiliacs. Significantly lower mean colony counts were found in eight hemophiliacs with adenopathy (HA), 763 +/- 348 (+/- SEM), than in 16 healthy hemophiliacs (HH) 3,044 +/- 661 (P less than .005), or than in 24 heterosexual control subjects, 3,964 +/- 395 (P less than .005). The in vitro addition of exogenous interleukin-2 (IL- 2) restored normal colony growth in the HA population. These results indicate that the T colony assay can detect abnormal cell-mediated immunity among hemophiliacs and specifically discriminates between asymptomatic hemophiliacs (HH) and those with adenopathy (HA). In addition, IL-2 may be of potential benefit in improving T cell defects in AIDS or the “lymphadenopathy syndrome”; however, this remains to be proven.

T Lymphocyte Subpopulations in High-Risk Infants: Influence of Age and Blood Transfusions

PEDIATRICS ◽  
1985 ◽  
Vol 76 (6) ◽  
pp. 914-917
Author(s):  
Savita Pahwa ◽  
Concepcion Sia ◽  
Rita Harper ◽  
Rajendra Pahwa
Keyword(s):  
T Cell ◽  
High Risk ◽  
Neonatal Period ◽  
Lymphocyte Subpopulations ◽  
T Cell Subsets ◽  
Lower Percentage ◽  
Blood Transfusions ◽  
T Lymphocyte Subpopulations ◽  
Per Se ◽  
High Risk Infants

Methodology was established to analyze T lymphocytes and T cell subsets with monoclonal antibodies on microsamples of blood obtained by heel puncture in infants. Results in 39 high-risk infants indicated that during the early neonatal period they had a higher percentage of T4-bearing cells and a lower percentage of T8 antigen-positive cells as compared with adults. These values progressively approached adult values, and at 3 to 7 months the T cell subsets and the T4/T8 ratios were within the adult range. A significant inverse relationship was noted between the number of blood transfusions given to the infants between 2 and 12 weeks of age and the corresponding T4/T8 ratio. These findings suggest that interpretation of T cell subsets in frequently transfused infants should take into consideration not only the age of the infant but also the possible influence of transfusions per se on the distribution of T cell subsets in the peripheral blood.

Growth, interleukin-2 production, and responsiveness to IL-2 in T4- positive T Lymphocyte populations from malignant cutaneous T cell lymphoma (Sezary's syndrome): the effect of cyclosporin A

Blood ◽  
1984 ◽  
Vol 64 (5) ◽  
pp. 1022-1027
Author(s):  
W Solbach ◽  
CE Lange ◽  
M Rollinghoff ◽  
H Wagner
Keyword(s):  
T Cell ◽  
T Lymphocyte ◽  
Peripheral Blood ◽  
Interleukin 2 ◽  
Immunosuppressive Drug ◽  
Blood Monocytes ◽  
Normal Individuals ◽  
Biologic Function ◽  
Lymphocyte Populations

Functional analysis and surface phenotyping using monoclonal antibodies have revealed that malignant T lymphocyte populations in the peripheral blood of patients with Sezary's syndrome resemble the T helper cell populations from normal individuals. In this article we have studied the effects of the immunosuppressive drug cyclosporine A (CsA) on growth, interleukin-2 (IL-2) production, and the induction of IL-2 responsiveness of peripheral blood monocytes (PBMs) from five patients with Sezary's syndrome in vitro, using the lectin phytohemagglutinin (PHA) and the phorbol ester phorbol myristate acetate (PMA) as stimuli. The following results were obtained: PHA-induced cell proliferation was significantly more sensitive to inhibition by CsA than that induced by PMA or a combination of PMA and PHA (P less than .005). Sezary PBMs produced only small amounts of IL-2 in response to PHA. Stimulation with PMA, however, resulted in significant IL-2 production. PMA and PHA, when given in combination, acted synergistically. The low levels of IL-2 production induced by PHA or PMA were more sensitive to CsA- mediated suppression than those induced by a combination of PHA and PMA (75% and 55% suppression, respectively). CsA-mediated growth suppression could be overcome if the cultures were supplemented with appropriate amounts of exogenous IL-2. We conclude from our data, that CsA in Sezary PBMs inhibits T cell growth indirectly as a consequence of suppression of IL-2 growth indirectly as a consequence of suppression of IL-2 production. Moreover, like normal T lymphocytes, Sezary PBMs do not express the IL-2 receptor spontaneously, but can be induced to do so. CsA does not interfere with intracellular events leading to the expression and the biologic function of the IL-2 receptor.

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