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A Method to Assess Fc-mediated Effector Functions Induced by Influenza Hemagglutinin Specific Antibodies
Published on: February 23, 2018
Efalizumab modulates T cell function both in vivo and in vitro
Frieder Koszik1, Georg Stary, Nicole Selenko-Gebauer
1Department of Dermatology, Medical University of Vienna, Austria.
Journal of Dermatological Science
|November 4, 2010
Summary
Efalizumab treatment in psoriasis patients induces T cell hyporesponsiveness, explaining its efficacy in stable disease but failure in flares. Prolonged use may increase immunosuppression risk.
Area of Science:
- Immunology
- Dermatology
- Cell Biology
Background:
- Efalizumab, an anti-CD11a mAb, treats moderate to severe psoriasis by targeting LFA-1 on leukocytes.
- Its mechanism is thought to involve T cell migration and immunological synapse interference.
Purpose of the Study:
- To investigate if efalizumab interferes with T cell proliferation.
- To assess T cell response to varied stimuli in the presence of efalizumab.
Main Methods:
- Peripheral blood mononuclear cells (PBMCs) from healthy and psoriatic individuals were stimulated with anti-CD3, PHA, or allogeneic PBMCs.
- PBMCs were treated with efalizumab, with or without prior incubation and removal.
Main Results:
- Efalizumab-treated psoriatic PBMCs showed normal response to PHA but reduced reactivity to anti-CD3 and allogeneic cells.
- Efalizumab impaired normal PBMC proliferation induced by allogeneic cells and suboptimal anti-CD3 concentrations.
- Crosslinking CD11a with efalizumab reduced T cell reactivity to subsequent anti-CD3 stimulation.
Conclusions:
- Efalizumab induces T cell hyporesponsiveness, explaining its effectiveness in stable psoriasis and limitations in flares.
- Prolonged efalizumab therapy may lead to clinically significant immunosuppression.
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