scholarly journals In vitro T lymphocyte proliferation by carboxyfluorescein diacetate succinimidyl ester method is helpful in diagnosing and managing primary immunodeficiencies

2017 ◽  
Vol 32 (1) ◽  
pp. e22216 ◽  
Author(s):  
Elif Azarsiz ◽  
Neslihan Karaca ◽  
Birgul Ergun ◽  
Mehmet Durmuscan ◽  
Necil Kutukculer ◽  
...  
Keyword(s):  
T Lymphocyte ◽  
Lymphocyte Proliferation ◽  
Primary Immunodeficiencies ◽  
T Lymphocyte Proliferation ◽  
Ester Method ◽  
Succinimidyl Ester ◽  
Diacetate Succinimidyl

scholarly journals LASER MODULATION OF T-LYMPHOCYTE PROLIFERATION IN VITRO

LASER THERAPY ◽  
1998 ◽  
Vol 10 (4) ◽  
pp. 153-158 ◽  
Author(s):  
Atif Agaiby ◽  
Lucy Ghali ◽  
Mary Dyson
Keyword(s):  
T Lymphocyte ◽  
Lymphocyte Proliferation ◽  
Laser Modulation ◽  
T Lymphocyte Proliferation ◽  
Proliferation In Vitro

Ganciclovir Suppresses Human T Lymphocyte Proliferation In Vitro.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 5378-5378
Author(s):  
Minoo Battiwalla ◽  
Yiyuan Wu ◽  
Ryotaro Nakamura ◽  
Marija Radovic ◽  
Rajinder P.S. Bajwa ◽  
...  
Keyword(s):  
Dna Synthesis ◽  
T Lymphocyte ◽  
Lymphocyte Proliferation ◽  
Brdu Incorporation ◽  
Human Pbmcs ◽  
Post Transplant ◽  
T Lymphocyte Proliferation ◽  
Proliferation In Vitro ◽  
Cmv Reactivation

Abstract Clinically significant cytomegalovirus (CMV) infection in allogeneic blood or marrow transplant recipients has dramatically declined in recent years by the strategy of early detection of reactivation and pre-emptive therapy with Ganciclovir (GCV). We have previously shown that even in the absence of overt CMV disease, persisting post-transplant antigenemia predicts for increased late relapse and treatment failure. (Nakamura, et al BBMT 2004) In other words, frequent CMV reactivation serves as a surrogate for impaired post-transplant immune reconstitution. To explain the observed association between CMV reactivation and relapse we also raised the possibility that several weeks of GCV therapy could exert a deleterious effect on a fragile immune system. Clinical association between GCV administration and impaired lymphocyte function has not received attention previously; perhaps because of confounding effects from the underlying conditions (HIV or post-transplant) that induce CMV reactivation. We examined the effect of GCV in vitro on normal human PBMCs. Human PBMCs were extracted from normal volunteers and subjected to mitogenic stimulation (PHA) in the absence or presence of varying concentrations of GCV. PHA-induced proliferation, measured by uptake of 3[H]-thymidine after 5 days incubation in RPMI-10% AB serum, was reduced by 35% at peak therapeutic concentrations (10mg/ml) of GCV as opposed to 73% by Tacrolimus (10ng/ml). GCV did not induce lymphocyte apoptosis in the presence or absence of stimulation. Flow cytometry-based BrdU incorporation assays show that GCV exerts a time-dependent impairment of DNA synthesis in lymphocytes. Collectively, these results show that GCV suppresses T-lymphocyte proliferation in vitro at therapeutic concentrations and the likely mechanism of action is inhibition of DNA synthesis. Further work is ongoing to evaluate the effect of GCV on proliferative responses to specific antigens and to confirm these effects in comparison to other drugs used in the transplant setting. Figure Figure

scholarly journals H-2D control of recovery from Friend virus leukemia: H-2D region influences the kinetics of the T lymphocyte response to Friend virus.

1983 ◽  
Vol 157 (6) ◽  
pp. 1736-1745 ◽  
Author(s):  
W J Britt ◽  
B Chesebro
Keyword(s):  
T Lymphocyte ◽  
Lymphocyte Proliferation ◽  
Lymphocyte Proliferation Assay ◽  
Friend Virus ◽  
Proliferation Assay ◽  
Lymphocyte Response ◽  
T Lymphocyte Proliferation ◽  
Virus Dose ◽  
Kinetics Of

A Friend virus (FV)-specific T lymphocyte proliferation assay was used to compare the T lymphocyte responses of H-2 congenic mice that differed in their ability to recover from FV leukemia after inoculation of high virus doses. Gene(s) of the H-2D region influenced the kinetics of this response such that H-2Db/b homozygous mice were positive 6-8 d earlier than H-2Dd/b mice. This correlated with the Rfv-1, H-2D-linked influence on recovery from FV by these mice, and also appeared to explain the prominent effect of virus dose on recovery incidence. These findings were supported by the ability of passively transferred immune splenic T lymphocytes to induce recovery from leukemia at 6 d after FV inoculation, but not at 16 d. H-2a/a mice were found to be unresponsive in the FV-specific T lymphocyte proliferation assay. This effect mapped to the left of H-2D, possibly in the H-2I region, and may be an in vitro manifestation of the Rfv-2 gene. No evidence for nonspecific immunosuppression of the T lymphocyte response to concanavalin A was observed in any of the H-2 congenic F1 mice studied.

scholarly journals Surfactant protein A inhibits T cell proliferation via its collagen-like tail and a 210-kDa receptor

1998 ◽  
Vol 275 (4) ◽  
pp. L679-L686 ◽  
Author(s):  
Paul Borron ◽  
Francis X. McCormack ◽  
Baher M. Elhalwagi ◽  
Zissis C. Chroneos ◽  
James F. Lewis ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
T Cell ◽  
T Lymphocyte ◽  
Lymphocyte Proliferation ◽  
Pulmonary Surfactant ◽  
Protein A ◽  
T Cell Proliferation ◽  
T Lymphocyte Proliferation ◽  
Human T Lymphocyte

Investigation of possible mechanisms to describe the hyporesponsiveness of pulmonary leukocytes has led to the study of pulmonary surfactant and its constituents as immune suppressive agents. Pulmonary surfactant is a phospholipid-protein mixture that reduces surface tension in the lung and prevents collapse of the alveoli. The most abundant protein in this mixture is a hydrophilic molecule termed surfactant-associated protein A (SP-A). Previously, we showed that bovine (b) SP-A can inhibit human T lymphocyte proliferation and interleukin-2 production in vitro. Results presented in this investigation showed that different sources of human SP-A and bSP-A as well as recombinant rat SP-A inhibited human T lymphocyte proliferation in a dose-dependent manner. A structurally similar collagenous protein, C1q, did not block the in vitro inhibitory action of SP-A. The addition of large concentrations of mannan to SP-A-treated cultures also did not disrupt inhibition, suggesting that the effect is not mediated by the carbohydrate recognition domain of SP-A. Use of recombinant mutant SP-As revealed that a 36-amino acid Arg-Gly-Asp (RGD) motif-containing span of the collagen-like domain was responsible for the inhibition of T cell proliferation. A polyclonal antiserum directed against an SP-A receptor (SP-R210) completely blocked the inhibition of T cell proliferation by SP-A. These results emphasize a potential role for SP-A in dampening lymphocyte responses to exogenous stimuli. The data also provide further support for the concept that SP-A maintains a balance between the clearance of inhaled pathogens and protection against collateral immune-mediated damage.

Sign in / Sign up

Export Citation Format

Share Document