scholarly journals Caspase Inhibitors Attenuate Superantigen-Induced Inflammatory Cytokines, Chemokines, and T-Cell Proliferation

2004 ◽  
Vol 11 (3) ◽  
pp. 621-624 ◽  
Author(s):  
Teresa Krakauer
Keyword(s):  
Cell Proliferation ◽  
T Cell ◽  
Mononuclear Cells ◽  
Human Peripheral Blood ◽  
Therapeutic Modality ◽  
T Cell Proliferation ◽  
Toxic Shock ◽  
Peripheral Blood Mononuclear ◽  
Caspase Inhibitors ◽  
Cytokines And Chemokines

ABSTRACT Proinflammatory cytokines mediate the toxic effect of superantigenic staphylococcal exotoxins (SE). A pan-caspase inhibitor suppressed SE-stimulated T-cell proliferation and the production of cytokines and chemokines by human peripheral blood mononuclear cells. These data suggest that caspase inhibitors may represent a novel therapeutic modality for treating SE-induced toxic shock.

scholarly journals Doxycycline Is Anti-Inflammatory and Inhibits Staphylococcal Exotoxin-Induced Cytokines and Chemokines

2003 ◽  
Vol 47 (11) ◽  
pp. 3630-3633 ◽  
Author(s):  
Teresa Krakauer ◽  
Marilyn Buckley
Keyword(s):  
Cell Proliferation ◽  
Proinflammatory Cytokines ◽  
Mononuclear Cells ◽  
Human Peripheral Blood ◽  
T Cell Proliferation ◽  
Peripheral Blood Mononuclear ◽  
Cytokines And Chemokines ◽  
Blood Mononuclear Cells ◽  
Anti Inflammatory ◽  
Pathogenic Effects

ABSTRACT Proinflammatory cytokines mediate the toxic effect of superantigenic staphylococcal exotoxins (SE). Doxycycline inhibited SE-stimulated T-cell proliferation and production of cytokines and chemokines by human peripheral blood mononuclear cells. These results suggest that the antibiotic doxycycline has anti-inflammatory effects and is therapeutically useful for mitigating the pathogenic effects of SE.

scholarly journals Coordinate Suppression of Superantigen-Induced Cytokine Production and T-Cell Proliferation by a Small Nonpeptidic Inhibitor of Class II Major Histocompatibility Complex and CD4 Interaction

2000 ◽  
Vol 44 (4) ◽  
pp. 1067-1069 ◽  
Author(s):  
Teresa Krakauer
Keyword(s):  
Cell Proliferation ◽  
Major Histocompatibility Complex ◽  
T Cell ◽  
Mononuclear Cells ◽  
Human Peripheral Blood ◽  
Class Ii ◽  
T Cell Proliferation ◽  
Major Histocompatibility ◽  
Peripheral Blood Mononuclear ◽  
Histocompatibility Complex

ABSTRACT Proinflammatory cytokines mediate the toxic effect of superantigenic staphylococcal exotoxins (SE). TJU103, a small nonpeptidic molecule that blocks the interaction between major histocompatibility complex class II and CD4 molecules inhibited SE-stimulated T-cell proliferation (by 92%) and production of tumor necrosis factor, interleukin 1β, interleukin 6, and gamma interferon (by 66, 56, 76, and 72%, respectively) by human peripheral blood mononuclear cells. These data suggest that TJU103 may be useful for mitigating the pathogenic effects of SE.

Reciprocal role of hBD2 and hBD3 on the adaptive immune response by measuring T lymphocyte proliferation in terms of CD4 and CCR6 expression

2018 ◽  
Vol 35 (3) ◽  
Author(s):  
Nima Taefehshokr ◽  
Alireza Isazadeh ◽  
Amin Oveisi ◽  
Yashar Azari Key ◽  
Sina Taefehshokr
Keyword(s):  
Cell Proliferation ◽  
T Cells ◽  
T Cell ◽  
Mononuclear Cells ◽  
Adaptive Immune Response ◽  
T Cell Proliferation ◽  
Peripheral Blood Mononuclear ◽  
Adaptive Immune ◽  
T Lymphocyte Proliferation

Abstract Background Human β-defensins (hBD2 and hBD3) are small cationic antimicrobial peptides of innate immune system which can act as a barrier against the majority of pathogens, contributing to the host immune defence. Objective The aim of study is to determine whether hBD2 and hBD3 play a role in development and proliferation of human effector CD4 T cells or not. Furthermore, if enhanced proliferation is observed in the presence of hBD2 and hBD3, these data will demonstrate whether chemokine receptor type 6 (CCR6) is required to be present for this activity to occur. Methods In this study, we examined the effect of hBD2 and hBD3 on CD4+ T cell proliferation in CCR6+ and CCR6− T cells through co-culture of peripheral blood mononuclear cells with anti-CD3 and anti-CD28 stimulation in the presence or absence of hBD2 and hBD3. Proliferation was assessed using flow cytometry. Results It was demonstrated that, co-culture with hBD2 and hBD3 led to up-regulation of CD4+ T cell proliferation after 72 h whereas, CD4+ T cell proliferation was suppressed after 96 h. On the other hand, CCR6− and CCR6+ T cell proliferation was up-regulated after 72 h. But, CCR6+ only was down-regulated in the second cycle in the presence of hBD3. In contrast, after 96 h CCR6+ and CCR6− T cell proliferation was decreased. Conclusion Collectively, our data indicated that hBD2 and hBD3 play a positive and negative regulatory role in development and proliferation of human effector CD4+ T cells which is essential for optimal adaptive immune responses and the control of immunopathology.

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