scholarly journals Clearance of HIV Type 1 Envelope Recombinant Sendai Virus Depends on CD4+T Cells and Interferon-γ But Not B Cells, CD8+T Cells, or Perforin

2010 ◽  
Vol 26 (7) ◽  
pp. 783-793 ◽  
Author(s):  
Sherri L. Surman ◽  
Scott A. Brown ◽  
Bart G. Jones ◽  
David L. Woodland ◽  
Julia L. Hurwitz
Keyword(s):  
T Cells ◽  
B Cells ◽  
Cd8 T Cells ◽  
Cd4 T Cells ◽  
Sendai Virus ◽  
Interferon Γ ◽  
Hiv Type 1

scholarly journals Interferon-γ Inducible Protein (IP-10) Expression Is Mediated by CD8+ T Cells and Is Regulated by CD4+ T Cells During the Elicitation of Contact Hypersensitivity

1996 ◽  
Vol 107 (3) ◽  
pp. 360-366 ◽  
Author(s):  
Mihoko Abe ◽  
Tsunenori Kondo ◽  
Hui Xu ◽  
Robert L. Fairchild
Keyword(s):  
T Cells ◽  
Cd8 T Cells ◽  
Cd4 T Cells ◽  
Interferon Γ ◽  
Contact Hypersensitivity ◽  
Inducible Protein

scholarly journals TLR2 Signaling Renders Quiescent Naive and Memory CD4+T Cells More Susceptible to Productive Infection with X4 and R5 HIV-Type 1

2007 ◽  
Vol 179 (7) ◽  
pp. 4357-4366 ◽  
Author(s):  
Sandra Thibault ◽  
Mélanie R. Tardif ◽  
Corinne Barat ◽  
Michel J. Tremblay
Keyword(s):  
T Cells ◽  
Cd4 T Cells ◽  
Productive Infection ◽  
Hiv Type 1 ◽  
Memory Cd4 T Cells ◽  
Tlr2 Signaling

A Detailed Phenotypic Analysis Using Six Color Flow Cytometry of Lymphocyte Subsets Mobilized with AMD3100 Compared to G-CSF.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 408-408 ◽  
Author(s):  
Yoshiyuki Takahashi ◽  
S. Chakrabarti ◽  
R. Sriniivasan ◽  
A. Lundqvist ◽  
E.J. Read ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
T Cells ◽  
T Cell ◽  
B Cells ◽  
Cd8 T Cells ◽  
Cd4 T Cells ◽  
Lymphocyte Subsets ◽  
Phenotypic Analysis ◽  
Color Flow ◽  
Cd34 Cells

Abstract AMD3100 (AMD) is a bicyclam compound that rapidly mobilizes hematopoietic progenitor cells into circulation by inhibiting stromal cell derived factor-1 binding to its cognate receptor CXCR4 present on CD34+ cells. Preliminary data in healthy donors and cancer patients show large numbers of CD34+ cells are mobilized following a single injection of AMD3100. To determine whether AMD3100 mobilized cells would be suitable for allografting, we performed a detailed phenotypic analysis using 6 color flow cytometry (CYAN Cytometer MLE) of lymphocyte subsets mobilized following the administration of AMD3100, given as a single 240mcg/kg injection either alone (n=4) or in combination with G-CSF (n=2: G-CSF 10 mcg/kg/day x 5: AMD3100 given on day 4). Baseline peripheral blood (PB) was obtained immediately prior to mobilization; in recipients who received both agents, blood was analyzed 4 days following G-CSF administration as well as 12 hours following administration of AMD3100 and a 5th dose of G-CSF. AMD3100 alone significantly increased from baseline the PB WBC count (2.8 fold), Absolute lymphocyte count (ALC: 2.5 fold), absolute monocyte count (AMC: 3.4 fold), and absolute neutrophil count (ANC: 2.8 fold). Subset analysis showed AMD3100 preferentially increased from baseline PB CD34+ progenitor counts (5.8 fold), followed by CD19+ B-cells (3.7 fold), CD14+ monocytes (3.4 fold), CD8+ T-cells (2.5 fold), CD4+ T-cells (1.8 fold), with a smaller increase in CD3−/CD16+ or CD56+ NK cell counts (1.6 fold). There was no change from baseline in the % of CD4+ or CD8+ T-cell expressing CD45RA, CD45RO, or CD56, CD57, CD27, CD71 or HLA-DR. In contrast, there was a decline compared to baseline in the mean percentage of CD3+/CD4+ T-cells expressing CD25 (5.5% vs 14.8%), CD62L (12.1% vs 41.1%), CCR7 (2.1% vs 10.5%) and CXCR4 (0.5% vs 40.9%) after AMD3100 administration; similar declines in expression of the same 4 surface markers were also observed in CD3+/CD8+ T-cells. A synergistic effect on the mobilization of CD34+ progenitors, CD19+ B cells, CD3+ T-cells and CD14+ monocytes occurred when AMD3100 was combined with G-CSF (Figure). In those receiving both AMD3100 and G-CSF, a fall in the % of T-cells expressing CCR7 and CXCR4 occurred 12 hours after the administration of AMD3100 compared to PB collected after 4 days of G-CSF; no other differences in the expression of a variety activation and/or adhesion molecules on T-cell subsets were observed. Whether differences in lymphocyte subsets mobilized with AMD3100 alone or in combination with G-CSF will impact immune reconstitution or other either immune sequela (i.e. GVHD, graft-vs-tumor) associated with allogeneic HCT is currently being assessed in an animal model of allogeneic transplantation.

Anti-GvHD Effect of Antithymocyte Globulin Is Mediated by Antibodies Binding to T Cells and Regulatory NK Cells, and Less So or Not at All by Antibodies Binding to Other Mononuclear Cell Subsets

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 2346-2346
Author(s):  
Mette Hoegh-Petersen ◽  
Minaa Amin ◽  
Yiping Liu ◽  
Alejandra Ugarte-Torres ◽  
Tyler S Williamson ◽  
...  
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
B Cells ◽  
Nk Cells ◽  
Cd8 T Cells ◽  
Cd4 T Cells ◽  
Antithymocyte Globulin ◽  
Chronic Gvhd ◽  
Wilcoxon Test ◽  
Effector Memory

Abstract Abstract 2346 Introduction: Polyclonal rabbit-anti-human T cell globulin may decrease the likelihood of graft-vs-host disease (GVHD) without increasing the likelihood of relapse. We have recently shown that high levels of antithymocyte globulin (ATG) capable of binding to total lymphocytes are associated with a low likelihood of acute GVHD grade 2–4 (aGVHD) as well as chronic GVHD needing systemic therapy (cGVHD) but not increased likelihood of relapse (Podgorny PJ et al, BBMT 16:915, 2010). ATG is polyclonal, composed of antibodies for antigens expressed on multiple cell subsets, including T cells, B cells, NK cells, monocytes and dendritic cells. These cell subsets may play a role in the pathogenesis of GVHD. The anti-GVHD effect of ATG may be mediated through killing/inhibition of one or several of these cell subsets (eg, T cells) or their subsets (eg, naïve T cells as based on mouse experiments naïve T cells are thought to play a major role in the pathogenesis of GVHD). To better understand the mechanism of action of ATG on GVHD, we set out to determine levels of which ATG fraction (capable of binding to which cell subset) are associated with subsequent development of GVHD. Patients and Methods: A total of 121 patients were studied, whose myeloablative conditioning included 4.5 mg/kg ATG (Thymoglobulin). Serum was collected on day 7. Using flow cytometry, levels of the following ATG fractions were determined: capable of binding to 1. naïve B cells, 2. memory B cells, 3. naïve CD4 T cells, 4. central memory (CM) CD4 T cells, 5. effector memory (EM) CD4 T cells, 6. naïve CD8 T cells, 7. CM CD8 T cells, 8. EM CD8 T cells not expressing CD45RA (EMRA-), 9. EM CD8 T cells expressing CD45RA (EMRA+), 10. cytolytic (CD16+CD56+) NK cells, 11. regulatory (CD16-CD56high) NK cells, 12. CD16+CD56− NK cells, 13. monocytes and 14. dendritic cells/dendritic cell precursors (DCs). For each ATG fraction, levels in patients with versus without aGVHD or cGVHD were compared using Mann-Whitney-Wilcoxon test. For each fraction for which the levels appeared to be significantly different (p<0.05), we determined whether patients with high fraction level had a significantly lower likelihood of aGVHD or cGVHD than patients with low fraction level (high/low cutoff level was determined from ROC curve, using the point with maximum sum of sensitivity and specificity). This was done using log-binomial regression models, ie, multivariate analysis adjusting for recipient age (continuous), stem cell source (marrow or cord blood versus blood stem cells), donor type (HLA-matched sibling versus other), donor/recipient sex (M/M versus other) and days of follow up (continuous). Results: In univariate analyses, patients developing aGVHD had significantly lower levels of the following ATG fractions: binding to naïve CD4 T cells, EM CD4 T cells, naïve CD8 T cells and regulatory NK cells. Patients developing cGVHD had significantly lower levels of the following ATG fractions: capable of binding to naïve CD4 T cells, CM CD4 T cells, EM CD4 T cells, naïve CD8 T cells and regulatory NK cells. Patients who did vs did not develop relapse had similar levels of all ATG fractions. In multivariate analyses, high levels of the following ATG fractions were significantly associated with a low likelihood of aGVHD: capable of binding to naïve CD4 T cells (relative risk=.33, p=.001), EM CD4 T cells (RR=.30, p<.001), naïve CD8 T cells (RR=.33, p=.002) and regulatory NK cells (RR=.36, p=.001). High levels of the following ATG fractions were significantly associated with a low likelihood of cGVHD: capable of binding to naïve CD4 T cells (RR=.59, p=.028), CM CD4 T cells (RR=.49, p=.009), EM CD4 T cells (RR=.51, p=.006), naïve CD8 T cells (RR=.46, p=.005) and regulatory NK cells (RR=.55, p=.036). Conclusion: For both aGVHD and cGVHD, the anti-GVHD effect with relapse-neutral effect of ATG appears to be mediated by antibodies to antigens expressed on naïve T cells (both CD4 and CD8), EM CD4 T cells and regulatory NK cells, and to a lesser degree or not at all by antibodies binding to antigens expressed on B cells, cytolytic NK cells, monocytes or DCs. This is the first step towards identifying the antibody(ies) within ATG important for the anti-GVHD effect without impacting relapse. If such antibody(ies) is (are) found in the future, it should be explored whether such antibody(ies) alone or ATG enriched for such antibody(ies) could further decrease GVHD without impacting relapse. Disclosures: No relevant conflicts of interest to declare.

scholarly journals Both CD31+and CD31−Naive CD4+T Cells Are Persistent HIV Type 1–Infected Reservoirs in Individuals Receiving Antiretroviral Therapy

2010 ◽  
Vol 202 (11) ◽  
pp. 1738-1748 ◽  
Author(s):  
Fiona Wightman ◽  
Ajantha Solomon ◽  
Gabriela Khoury ◽  
Justin A. Green ◽  
Lachlan Gray ◽  
...  
Keyword(s):  
T Cells ◽  
Antiretroviral Therapy ◽  
Cd4 T Cells ◽  
Hiv Type 1

Production Of Interleukin-4, Interleukin-10, And Interferon-γ From CD4+ T Cells And CD8+ T Cells In Patients With Asthma

2010 ◽  
Vol 125 (2) ◽  
pp. AB42
Author(s):  
J. Yoon ◽  
H. Kim ◽  
J. Lee ◽  
H. Lee ◽  
H. Lee ◽  
...  
Keyword(s):  
T Cells ◽  
Cd8 T Cells ◽  
Cd4 T Cells ◽  
Interleukin 10 ◽  
Interferon Γ ◽  
Interleukin 4

scholarly journals CD38 Expression in CD8+T Cells Predicts Virological Failure in HIV Type 1–Infected Children Receiving Antiretroviral Therapy

2004 ◽  
Vol 38 (3) ◽  
pp. 412-417 ◽  
Author(s):  
Salvador Resino ◽  
Jose M. Bellon ◽  
M. Dolores Gurbindo ◽  
M. Angeles Munoz‐Fernandez
Keyword(s):  
T Cells ◽  
Antiretroviral Therapy ◽  
Cd8 T Cells ◽  
Virological Failure ◽  
Cd38 Expression ◽  
Hiv Type 1

T helper type 1 development of naive CD4+ T cells requires the coordinate action of interleukin-12 and interferon-γ and is inhibited by transforming growth factor-β

1994 ◽  
Vol 24 (4) ◽  
pp. 793-798 ◽  
Author(s):  
Edgar Schmitt ◽  
Petra Hoehn ◽  
Christoph Huels ◽  
Sigrid Goedert ◽  
Norbert Palm ◽  
...  
Keyword(s):  
T Cells ◽  
Growth Factor ◽  
Cd4 T Cells ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Interferon Γ ◽  
Interleukin 12 ◽  
T Helper ◽  
Helper Type

scholarly journals Epigenetic Repression of Interleukin 2 Expression in Senescent CD4+T Cells During Chronic HIV Type 1 Infection

2014 ◽  
Vol 211 (1) ◽  
pp. 28-39 ◽  
Author(s):  
Kaori Nakayama-Hosoya ◽  
Takaomi Ishida ◽  
Ben Youngblood ◽  
Hitomi Nakamura ◽  
Noriaki Hosoya ◽  
...  
Keyword(s):  
T Cells ◽  
Cd4 T Cells ◽  
Interleukin 2 ◽  
Hiv Type 1 ◽  
Epigenetic Repression

Increased Expression of TLR7 in CD8+T Cells Leads to TLR7-Mediated Activation and Accessory Cell-Dependent IFN-γ Production in HIV Type 1 Infection

2009 ◽  
Vol 25 (12) ◽  
pp. 1287-1295 ◽  
Author(s):  
Yang Song ◽  
Yan Zhuang ◽  
Song Zhai ◽  
Dedong Huang ◽  
Ying Zhang ◽  
...  
Keyword(s):  
T Cells ◽  
Cd8 T Cells ◽  
Accessory Cell ◽  
Ifn Γ ◽  
Hiv Type 1
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