INTERFERENCE WITH T CELL ACTIVATION SIGNAL ONE AND SIGNAL TWO WITH A COMBINATION OF ANTI-CD45RB AND ANTI-CD40L MONOCLONAL ANTIBODIES INDUCES LONG-TERM ISLET ALLOGRAFT SURVIVAL IN MICE

1998 ◽  
Vol 66 (8) ◽  
pp. S62
Author(s):  
G P Basadonna ◽  
H-Y Qian ◽  
M. Minozzo ◽  
M Sayegh ◽  
D M Rothstein
Keyword(s):  
Monoclonal Antibodies ◽  
T Cell ◽  
T Cell Activation ◽  
Cell Activation ◽  
Allograft Survival ◽  
Islet Allograft

scholarly journals Prevention of T-cell activation by rhCTLA4-Ig and anti-CD40L monoclonal antibody results in indefinite islet allograft survival

1999 ◽  
Vol 31 (1-2) ◽  
pp. 1242-1243 ◽  
Author(s):  
C Rastellini ◽  
A Salam ◽  
R Kuddus ◽  
A Aitouche ◽  
V Subbotin ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
T Cell ◽  
T Cell Activation ◽  
Cell Activation ◽  
Allograft Survival ◽  
Islet Allograft

scholarly journals Mechanisms of tolerance induction: blockade of co–stimulation

2001 ◽  
Vol 356 (1409) ◽  
pp. 649-657 ◽  
Author(s):  
Fabien Sebille ◽  
Bernard Vanhove ◽  
Jean-Paul Soulillou
Keyword(s):  
T Cell ◽  
T Cell Activation ◽  
Cell Activation ◽  
Biological Effects ◽  
Essential Feature ◽  
Tolerance Induction ◽  
Allograft Survival ◽  
Transplantation Antigens

Induction of tolerance to transplantation antigens is believed to be a promising way to achieve long–term allograft survival without a deleterious immunosuppressive regimen. T–cell activation, which is an essential feature of graft rejection, requires a first signal provided by T–cell receptor (TCR) ligation and a second signal provided by engagement of co–stimulatory molecules with their respective ligands on antigen–presenting cells. The coordinated triggering of these two independent signalling systems ensures the full T–cell activation, including proliferation and acquisition of effector function. TCR occupancy in the absence of co–stimulatory signals leads to a sustained loss of antigen responsiveness called clonal anergy, which could be of major importance in transplantation. In vivo , co–stimulation blockade was indeed shown to allow for long–term allograft survival in several transplantation models. However, the current continuous identification of new co–stimulatory molecules suggests that a functional redundancy of the system exists and that tolerance to transplantation antigens might be achieved more easily through the combined blockade of two or several co–stimulatory signals. In this review, we analyse the biological effects of the disruption of some co–stimulation pathways in vitro and in vivo and discuss their potential interest for tolerance induction.

scholarly journals Changes in Inflammation but Not in T-Cell Activation Precede Non-AIDS-Defining Events in a Case-Control Study of Patients on Long-term Antiretroviral Therapy

2017 ◽  
Vol 218 (2) ◽  
pp. 239-248 ◽  
Author(s):  
Konstantia Angelidou ◽  
Peter W Hunt ◽  
Alan L Landay ◽  
Cara C Wilson ◽  
Benigno Rodriguez ◽  
...  
Keyword(s):  
T Cell ◽  
Antiretroviral Therapy ◽  
T Cell Activation ◽  
Cell Activation ◽  
Case Control Study ◽  
Case Control ◽  
Control Study

scholarly journals Factors Associated With CD8+ T-Cell Activation in HIV-1–Infected Patients on Long-term Antiretroviral Therapy

2014 ◽  
Vol 67 (2) ◽  
pp. 153-160 ◽  
Author(s):  
Lu Zheng ◽  
Babafemi Taiwo ◽  
Rajesh T. Gandhi ◽  
Peter W. Hunt ◽  
Ann C. Collier ◽  
...  
Keyword(s):  
T Cell ◽  
Antiretroviral Therapy ◽  
T Cell Activation ◽  
Cell Activation ◽  
Cd8 T Cell ◽  
Factors Associated ◽  
Hiv 1

T-Cell Activation by Bispecific Monoclonal Antibodies for Lysis of Renal Cell Carcinoma In Vitro

1992 ◽  
pp. 156-161
Author(s):  
J. van Dijk ◽  
S. Th. Zegveld ◽  
J. D. H. van Eendenburg ◽  
E. Braakman ◽  
G. J. Fleuren ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Monoclonal Antibodies ◽  
T Cell ◽  
Cell Carcinoma ◽  
T Cell Activation ◽  
Renal Cell ◽  
Cell Activation

scholarly journals HIV-specific T-cell Responses and Generalized Activation in HIV-1 Infected Long-term Non-progressors and Progressors from South India

2019 ◽  
Vol 16 (4) ◽  
pp. 302-314
Author(s):  
Chinnambedu Ravichandran Swathirajan ◽  
Ramachandran Vignesh ◽  
Greer Waldrop ◽  
Uma Shanmugasundaram ◽  
Pannerselvam Nandagopal ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
T Cell Activation ◽  
Cell Activation ◽  
Cd4 T Cell ◽  
Cell Responses ◽  
Activation Rates ◽  
Hiv 1

Background:Anti-viral cytokine expressions by cytotoxic T-cells and lower activation rates have been reported to correlate with suppressed HIV replication in long-term non-progressors (LTNP). Immune mechanisms underlying disease non-progression in LTNP might vary with HIV-1 subtype and geographical locations.Objective:This study evaluates cytokine expression and T-cells activation in relation to disease non-progression in LTNP.Methods:HIV-1 Subtype C infected LTNP (n=20) and progressors (n=15) were enrolled and flowcytometry assays were performed to study HIV-specific CD8 T-cells expressing IL-2, IFN-γ, TNF-α and MIP-1β against gag and env peptides. CD4+ T-cell activation was evaluated by surface expression of HLADR and CD38.Results:Proportions of cytokines studied did not differ significantly between LTNP and progressors, while contrasting correlations with disease progression markers were observed in LTNP. CD4+ T-cell activation rates were significantly lower in LTNP compared to progressors which indicate the potential role of T-cell activation rates in disease non-progression in LTNP.Conclusion:LTNP and progressors showed similar CD8+ T-cell responses, but final conclusions can be drawn only by comparing multiple immune factors in larger LTNP cohort with HIV-1 infected individuals at various levels of disease progression. A possible role of HIV-1 subtype variation and ethnic differences in addition to host-genetic and viral factors cannot be ruled out.

scholarly journals Inhibition of T cell activation in vivo with mixtures of monoclonal antibodies specific for I-A and I-A/E molecules.

1981 ◽  
Vol 154 (1) ◽  
pp. 188-192 ◽  
Author(s):  
J Sprent ◽  
E A Lerner ◽  
J Bruce ◽  
F W Symington
Keyword(s):  
T Cells ◽  
Monoclonal Antibodies ◽  
T Cell ◽  
B Cells ◽  
T Cell Activation ◽  
Cell Activation ◽  
Marked Contrast ◽  
Sheep Erythrocytes

(CBA x B6)F1 (Iak x Iab) T cells were activated to sheep erythrocytes in irradiated F1 mice in the presence of various monoclonal anti-Ia reagents and then tested for their capacity to collaborate with B cells from B10.BR (I-Ak, I-Ek) (kk), B10.A(4R) (kb), and B10 (bb) mice. Anti-I-Ak antibodies blocked the generation of help for B10.A(4R) B cells, but not B10.BR or B10 B cells. An anti-I-Ab antibody blocked help for B10 B cells, but not for B10.BR or B10.A(4R) B cells. An antibody (Y-17) specific for I-Ak/Ek and I-Ab/Ek molecules, but not for I-Ak or I-Ab molecules, failed to impair the generation of help for B10.BR, B10.A (4R), or B10 B cells. In marked contrast to injecting each antibody separately, a mixture of anti-I-Ak and anti-I-Ak,b/Ek (Y-17) antibodies virtually abolished the generation of help for B10.BR B cells. A mixture of anti-I-Ak and anti-I-Ab antibodies effectively blocked help for (4R x B10)F1 B cells, i.e., cells expressing hybrid I-A molecules. These two antibodies only marginally impaired help for (CBA x B6)F1 B cells. To block help for (CBA x B6)F1 B cells required selection in the presence of a cocktail of anti-I-Ak, anti-I-Ab, and anti-I-Ak,b/Ek antibodies. The implications of these findings are discussed.

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