scholarly journals CD25+CD8+, CLA+CD4+, CD11a+ CD4+, and CD11a+ CD8+ T Cell Counts Are Elevated in the Blood of Brazilian Patients With Chronic Plaque Psoriasis

2011 ◽  
Vol 102 (5) ◽  
pp. 388-390 ◽  
Author(s):  
C. Porto Ferreira ◽  
A. Gomes da Silva ◽  
C.J. Martins ◽  
A.M. Da-Cruz
Keyword(s):  
T Cell ◽  
Plaque Psoriasis ◽  
Cd8 T Cell ◽  
Chronic Plaque Psoriasis ◽  
Cell Counts

scholarly journals Lymphocyte subset analysis to evaluate the prognosis of HIV-negative patients with pneumocystis pneumonia

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Fan Jin ◽  
Jing Xie ◽  
Huan-ling Wang
Keyword(s):  
T Cell ◽  
Cell Count ◽  
Lymphocyte Subsets ◽  
Nk Cell ◽  
Cd8 T Cell ◽  
Pneumocystis Pneumonia ◽  
Lymphocyte Subset ◽  
Cd4 T Cell ◽  
Cell Counts ◽  
Hiv Negative

Abstract Objectives We analysed the peripheral blood lymphocyte subsets of human immunodeficiency virus (HIV)-negative patients infected with pneumocystis pneumonia (PCP) to determine the relationships between the levels of different types of lymphocytes and the prognosis of patients. Methods We retrospectively reviewed HIV-negative patients with PCP diagnosed in our department. All the eligible patients underwent lymphocyte subset analysis on admission. Results A total of 88 HIV-negative PCP patients were enrolled in the study. In univariate analyses, low CD4+ T cell count, low CD8+ T cell count, and low natural killer cell (NK cell) count were associated with higher in-hospital mortality. CD8+ T cell count ≤300/μL was found to be an independent risk factor for poor prognosis in multivariate logistical regression analysis (p = 0.015, OR = 11.526, 95% CI = 1.597–83.158). Although low CD4+ T cell and NK cell counts were not independent risk factors, the mortality rates of PCP patients decreased as the CD4+ T cell and NK cell counts increased. Conclusion The immune process of Pneumocystis jirovecii infection is complex but important. We propose that lymphocyte subsets could give clinicians a better understanding of patient immune status, helping with the early identification of potentially lethal infections and treatment decision making, such as adjusting the immunosuppressive regimen and choosing an appropriate patient monitoring level.

Evaluation of a New Fluorescence Immunoassay for CD4+ and CD8+ T Cell Counts in Clinical Samples

Vox Sanguinis ◽  
1994 ◽  
Vol 67 (1) ◽  
pp. 86-87 ◽  
Author(s):  
M. Jose Saez ◽  
M. de Frutos ◽  
P. Martinez ◽  
V. Soriano
Keyword(s):  
T Cell ◽  
Cd8 T Cell ◽  
Clinical Samples ◽  
Fluorescence Immunoassay ◽  
Cell Counts

scholarly journals Cortisol and epinephrine control opposing circadian rhythms in T cell subsets

Blood ◽  
2009 ◽  
Vol 113 (21) ◽  
pp. 5134-5143 ◽  
Author(s):  
Stoyan Dimitrov ◽  
Christian Benedict ◽  
Dennis Heutling ◽  
Jürgen Westermann ◽  
Jan Born ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Circadian Rhythms ◽  
Cd8 T Cells ◽  
Low Dose ◽  
Cd8 T Cell ◽  
T Cell Subsets ◽  
Naive T Cells ◽  
Naïve T Cells ◽  
Cell Counts

Abstract Pronounced circadian rhythms in numbers of circulating T cells reflect a systemic control of adaptive immunity whose mechanisms are obscure. Here, we show that circadian variations in T cell subpopulations in human blood are differentially regulated via release of cortisol and catecholamines. Within the CD4+ and CD8+ T cell subsets, naive cells show pronounced circadian rhythms with a daytime nadir, whereas (terminally differentiated) effector CD8+ T cell counts peak during daytime. Naive T cells were negatively correlated with cortisol rhythms, decreased after low-dose cortisol infusion, and showed highest expression of CXCR4, which was up-regulated by cortisol. Effector CD8+ T cells were positively correlated with epinephrine rhythms, increased after low-dose epinephrine infusion, and showed highest expression of β-adrenergic and fractalkine receptors (CX3CR1). Daytime increases in cortisol via CXCR4 probably act to redistribute naive T cells to bone marrow, whereas daytime increases in catecholamines via β-adrenoceptors and, possibly, a suppression of fractalkine signaling promote mobilization of effector CD8+ T cells from the marginal pool. Thus, activation of the major stress hormones during daytime favor immediate effector defense but diminish capabilities for initiating adaptive immune responses.

Ex-Vivo Reduction of Allograft T Cell Dose Does Not Prevent Acute Graft-vs-Host Disease after Reduced-Intensity Hematopoietic Stem Cell Transplantation.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 2871-2871
Author(s):  
Nancy M. Hardy ◽  
Frances Hakim ◽  
Seth Steinberg ◽  
Michael Krumlauf ◽  
Rebecca Babb ◽  
...  
Keyword(s):  
Stem Cell ◽  
T Cell ◽  
Stem Cell Transplantation ◽  
Cell Transplantation ◽  
Cd8 T Cell ◽  
Hematopoietic Stem ◽  
Cell Counts ◽  
Cell Engraftment ◽  
Graft Vs Host Disease ◽  
Reduced Intensity

Abstract Allograft T cell depletion (TCD) reduces acute graft-vs. host disease (aGVHD) after myeloablative hematopoietic stem cell transplantation (HSCT). Lower incidences of aGVHD reported after reduced-intensity stem cell transplantation (RIST) may reflect delayed donor T cell engraftment. We compared the incidence of aGVHD following RIST with TCD (19 patients (pts) vs. T cell replete (TCR) allografts (20 pts)(Table). There was no difference in the incidence aGVHD, occurring in 71% of TCD recipients (median onset Day 47) and 70% of TCR recipients (median onset Day 25). After TCD, 100% of those who engrafted prior to any DLI developed aGVHD compared with 56% of those who engrafted after DLI, including two pts who developed “late-acute” aGVHD after Day 100, upon completion of donor T cell engraftment. T cell engraftment after TCD was uneven: engraftment kinetics were associated with residual host circulating CD8+ T cell counts after immune depletion; and aGVHD did not occur in the setting of mixed T cell chimerism (Figure). These observations demonstrate that aGVHD can occur with very low doses (105/kg) of allograft T cells after RIST. Protection from aGVHD conferred by mixed T cell chimerism may be lost with full donor T cell engraftment. With limited donor T cell numbers, host T cells appear to determine kinetics of engraftment and of aGVHD after RIST. Figure: Post-induction circulating CD8+ T cell counts in TCD recipients with delayed donor T cell engraftment. After TCD, all subjects who developed aGVHD did so at or after the establishment of T cell full donor T cell chimerism, and occasionally prior to any DLI. Shaded triangle represents the theoretical area in which values would fall if subjects developed aGVHD prior to complete donor T cell engraftment. Arrows: DLI. Patient and Transplant Characteristics and Outcomes Protocol TCD TCR Flu/Cy: Fludarabine and cyclophosphamide; EPOCH-F: Etoposide, doxorubicin, vincristine, cyclophosphamide, prednisone and fludarabine; FDC: Full donor chimerism. Median (range) Median (range) Recipient Age 43 years (32 – 56) 44 (19 – 67) CMV Risk 14/19 16/20 Pretransplant Immune Depletion Flu/Cy EPOCH-F Conditioning Regimen Flu/Cy Flu/Cy Pre-conditioning Host Cell Counts: CD3 86 (1 – 701) 140 (21 – 441) CD4, p=0.017 44 (1 – 156) 71 (12 – 191) CD8 34 (0 – 555) 55 (2 – 309) NK 58 (0 – 376) 88 (3 – 467) Day 0 CD3 Cell Count 1 (1 – 6) 5 (0 – 42) Allograft CD34+ cells/kg 7.75 x 106 (5.1 – 12.9) 7.68 x 106 (4.6–18.4) Allograft CD3+ cells/kg 1.0 x 105 (preset) 3.63 x 108 (1.5 – 8.3) Donor T cell engraftment Day +70 (14 – 180) 14 (14 – 100) Figure Figure

T Cell Responses during Long-Term Continuous Infusion of MT103 (MEDI-538; Anti-CD19 BiTE) in Patients with Relapsed B-NHL: Data from Dose-Escalation Study MT103-104.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 2725-2725 ◽  
Author(s):  
Matthias Klinger ◽  
Peter Kufer ◽  
Petra Kirchinger ◽  
Ralf Lutterbüse ◽  
Eugen Leo ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
T Cell Activation ◽  
Cd8 T Cells ◽  
Dose Escalation ◽  
Cell Expansion ◽  
Cell Activation ◽  
Cd8 T Cell ◽  
Cell Counts ◽  
T Cell Expansion

Abstract MT103 (MEDI-538) is a bispecific single-chain antibody construct directed at CD3 on human T cells and CD19 on human B lymphoma and normal B cells. Transient linkage of B and T cells by MT103 provides T cells with a T cell receptor (TCR)-like signal leading to redirected lysis of B cell targets without apparent need of costimulation and inducing T cells to proliferate, secrete cytokines and upregulate surface activation markers. TCR-like signalling by MT103 is strictly dependent on the presence of target cells. Redirected lysis of CD19-positive cells by MT103 is seen at low picomolar concentrations and at low effector-to-target ratios. The in-vivo half-life of MT103 is approximately two hours. In the ongoing dose escalation study MT103-104, patients with relapsed B-NHL have so far received continuous infusion of MT103 at maintenance flow-rates of 0.5, 1.5, 5 and 15 μg/m2/24h for 4 or 8 weeks following a 3+3 dose escalation design. Serum concentrations of MT103 remained constant over the entire treatment period at a level depending on the respective maintenance flow-rate. Depletion of circulating B (lymphoma) cells could be observed more frequently with increasing dose levels (DL) from DL1 to DL3, and in all evaluable patients at DL4. Three of six evaluable patients at DL4 showed clinical responses (2 PR, 1 CR) according to standardized Cheson criteria, but no patient of DL1-3. The time courses of absolute CD4 and CD8 T cell counts in peripheral blood were determined by flow cytometry. CD8 T lymphocytes were further subdivided for analysis into naïve T cells, TCM (central memory T cells), TEM (effector memory T cells) and TEMRA (non-proliferating terminally differentiated CTL), and CD4 T lymphocytes into naïve T cells, TCM and TEM. Activation of CD4 and CD8 T cell subsets was determined by measuring upregulation of CD69, CD25 and HLA-DR. Serum levels of cytokines were determined as additional biomarkers for T cell activation. In 50% of patients at DL1 to DL3, CD4 and CD8 T cell counts increased during the course of treatment - over pre-treatment levels. The TEM subset from both CD4 and CD8 T cells accounted for most of the observed increases, while the naïve T cell subsets showed no increase but also no signs of apoptosis. The non-proliferative TEMRA subset of CD8 T cells also remained unchanged in most patients. This indicated that the selective increase of proliferation-competent TEM subsets was attributed to MT103-induced T cell proliferation. At DL4, all evaluable patients showed signs of T cell expansion after 2 weeks of MT103 infusion, which was most pronounced in those who developed a partial or complete remission. The increase of CD8 T cell counts was more pronounced than that of CD4 T cells. T cell expansion was accompanied by upregulation of T cell activation markers as well as by increases in serum concentrations of cytokines like IFN-γ. T cell expansion and activation reverted in all cases when the infusion of MT103 was stopped. In summary, MT103 induced a reversible secondary T cell response involving T cell activation and proliferation as well as T cell cytotoxicity against circulating B cells and lymphoma tissue. The dose-dependent T cell expansion observed during long-term infusion of MT103, particularly within the cytotoxic TEM subset of CD8 T cells, appears to play a key role for clinical activity.

A Phase II Study of the Purine Nucleoside Phosphorylase (PNP) Inhibitor RO5092888 (BCX-4208) in Patients with Moderate to Severe Chronic Plaque Psoriasis: Safety, Tolerability and Lymphocyte Effects

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 2583-2583
Author(s):  
Joseph P Gomes ◽  
Angela Georgy ◽  
Sharon Passe ◽  
Adrienne Farid ◽  
Shanta Bantia ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Plaque Psoriasis ◽  
Apoptotic Cell ◽  
Study Drug ◽  
T Cell Subsets ◽  
Upper Respiratory Tract ◽  
Chronic Plaque Psoriasis ◽  
Double Blind ◽  
Tract Infections

Abstract Introduction: PNP is a purine-metabolizing enzyme that catalyzes the phosphorolysis of 2′-deoxyguanosine [dGuo] to guanine and deoxyribose-1-phosphate. In T-cells, PNP inhibition leads to accumulation of deoxyguanosine triphosphate (dGTP), triggering apoptotic cell death. Chronic-plaque type psoriasis (psoriasis) is an autoimmune disorder, in which T-cells contribute, at least in part, to the manifestations and maintenance of the disease. Therefore, targeting T-cells may be a beneficial treatment strategy. Since for chronic inflammatory diseases the safety of potential immunosuppressive drugs is a major consideration, we conducted this study to investigate safety and tolerability of oral RO5092888 (BCX-4208) in patients with moderate to severe chronic plaque psoriasis. Methods: This was a randomized, double-blind, placebo-controlled, dose-ranging study. Sixty-six patients 18 to 70 years old were randomized into one of three groups: placebo, 20mg/d or 120mg/d. The study was conducted from August 2007 to June 2008. Patients received study drug over six weeks and were observed over an additional 4 weeks. Assessments for safety included tracking of adverse events (AEs) including infections; vital signs; ECGs; chemistry panel; LFTs; hematologic parameters including peripheral blood (PB) lymphocyte subsets CD3+, CD4+, CD8+, CD56+, CD20+; and urinalysis. Results: 65 of the 66 enrolled patients were analyzed. One serious AE was observed in the 20mg/d group, a deep vein thrombosis (DVT) in a patient with a history of DVTs, and was considered unrelated to study drug. The percentage of patients experiencing at least one adverse event (AE) of any grade was placebo: 33% (7/21), 20mg: 41% (9/22), and 120mg: 59% (13/22). During treatment, two infections occurred in the placebo group (influenza and sinusitis), one in the 20mg group (nasopharyngitis), and 4 in the 120mg group (2-upper respiratory tract infections, 1 bronchitis, and 1 otitis externa). Reductions in PB lymphocytes and subsets were observed (Table 1). Nine patients showed decreased levels of CD4+ lymphocytes, below 350 cells/μL (20mg/d, 3; 120mg/d, 6). Conclusion: Daily oral administration of 20 mg or 120 mg of RO5092888 for up to 6 weeks demonstrated adequate safety and tolerability. Reductions in PB T cells, T cell subsets and B cells were observed. Further investigation of RO5092888 is warranted in both T-cell and B-cell diseases. Lymphocyte subpopulation Mean Nadir (% change from baseline) Placebo (n=21) 20 mg (n=22) 120 mg (n=22) CD3+ 24.0 30.6 47.5 CD4+ 23.6 28.9 44.9 CD8+ 26.1 31.8 53.9 CD20+ 37.5 42.6 64.2 CD56+ 40.1 47.7 72.6 Table 1

The effect of androgen deprivation therapy on CD4/CD8 T cells in HIV-negative patients receiving definitive 3D radiation treatment for their prostate carcinoma: Final report of a prospective study

2009 ◽  
Vol 27 (15_suppl) ◽  
pp. 11056-11056
Author(s):  
M. A. Elshaikh ◽  
Z. Abdel Hafeez ◽  
M. Lu ◽  
D. Ibrahim ◽  
T. El Masry ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Cd8 T Cells ◽  
Radiation Treatment ◽  
Cd8 T Cell ◽  
Total Testosterone ◽  
Blood Samples ◽  
Testosterone Levels ◽  
Cell Counts ◽  
Hiv Negative

11056 Background: CD4 and CD8 T cells play critical roles in human immunity. The aim of this prospective study is to explore the correlation of the absolute CD4/CD8 T cell counts and total testosterone in patients receiving androgen deprivation therapy (ADT) with goserelin acetate and definitive radiation treatment (RT) for their prostate cancer. Methods: Thirty-four HIV-negative patients were included in this study between June 2006 and January 2007. All patients had a baseline total testosterone level (T), PSA, CD4 and CD8 T cell counts. CD4/8 T cells count was measured using flow cytometry. All patients received 6 months of ADT prior to (baseline) and during RT to the prostate. Subsequent blood samples were taken at 2, 8, 12 and 24 months. Blood samples were taken between 8–10 am to control for diurnal variations in CD4/CD8 T cell counts and T levels. To study the correlation of T with CD4/8 T cell changes, the Spearman correlation coefficient was calculated. The study was approved by the appropriate Ethics Committee. Results: Median age for the study patients was 68 years. At baseline, median testosterone level was 350 ng/dL, median CD4 T cell count was 1055 mm3, and median CD8 T cell count was 644 mm3. None of the patients received anti-androgens. At two months, testosterone was at the castrate and subnormal levels in 85% and 100% of the patients, respectively. The lower testosterone levels resulted in significant reduction of CD4 and CD8 T cell counts at 2, 8, 12 and 24 months compared to baseline counts. This effect was more pronounced for CD4 T cells at all time points (p=<0.02). At 24 months, when total testosterone levels were increasing, CD4 and CD8 T cell counts were also following these upward trends. The seen correlation between lower testosterone and decline in CD4 and CD8 T cells was only statistically significant in older patients (>65 years) and was not associated with significant decline in total white blood cell counts. Conclusions: CD4/CD8 T cell counts are sensitive to changes in total testosterone levels. Lower testosterone levels negatively affecting CD4/CD8 T cells counts at all study time points. Since CD4/CD8 T cells play major roles in cellular immunity, further studies are warranted No significant financial relationships to disclose.

Prognostic value of an immune score combining intra- and peritumoral T-cell subset density in patients with pancreatic adenocarcinoma.

2013 ◽  
Vol 31 (15_suppl) ◽  
pp. 4060-4060
Author(s):  
Simon Turcotte ◽  
Yannic McNicoll ◽  
Genevieve Soucy ◽  
Louis Gaboury ◽  
Real W. Lapointe ◽  
...  
Keyword(s):  
T Cell ◽  
Cell Count ◽  
Pancreatic Adenocarcinoma ◽  
Prognostic Value ◽  
Cd8 T Cell ◽  
Tnm Staging ◽  
Cd4 T Cell ◽  
Cell Counts ◽  
Immune Score ◽  
Cd4 T Cell Count

4060 Background: Immune scoring based on T-cell subsets and density can add prognostic value to conventional TNM staging for patients with solid tumors, but limited data are available for pancreatic adenocarcinoma. Methods: Using tissue microarrays, CD3, CD4, CD8, CD45RO, and FOXP3 T-cells were quantified by immunohistochemistry in the intratumoral (IT) compartment and peritumoral (PT) parenchyma of 111 consecutively resected specimens. T-cell counts were correlated with patient overall survival, disease-free survival, and time to recurrence (OS, DFS, TTR) by Cox regression, controlling for clinicopathological factors. An immune score (IS) based on IT CD4 T-cell count > median, PT CD8 T-cell count ≤ median, and IT/PT CD3 T-cell ratio >1, grouped patients into high, intermediate, or low categories if all 3, 1 to 2, or none of these immune features were present, respectively. Results: Median follow-up time was 20 months, and 85% of patients either died or recurred during the study period. By univariate analysis, PT CD8 T-cell count was associated with shorter OS (p=0.02), whereas both IT CD4 T-cell count and IT/PT CD3 T-cell ratio were associated with longer OS (p=0.01 and p=0.05, respectively). Alone, none of these immune features predicted TTR. Combined into an IS, patients in the high (n=23), intermediate (n=60), or low (n=23) categories had significantly different OS (respective medians 30, 17, and 13 months, log-rank p=0.01), DFS (28, 16, and 12 months, p=0.01), and TTR (21, 14, and 10 months, p=0.02). By multivariate analysis, the association between IS and clinical outcomes was independent of tumor size, extra-pancreatic invasion, and nodal metastases (TNM staging). The IS discriminated outcomes among patients with nodal metastases (n=80), such that node-positive patients with a high IS had a median survival similar to node-negative patients (30 and 33 months, p=0.7). FOXP3 and CD45RO T-cell counts did not appear to add prognostic value to the IS. Conclusions: An immune score that combines specific T-cell location and density may have prognostic value in patients with resected pancreatic adenocarcinoma, independently from pathologic features currently used for staging.

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