| Summary: | <p>Abstract</p> <p>Background</p> <p>We previously reported that NKG2A, a key inhibitory ligand for HLA-E, is expressed on activated TH2 but not TH1 cells. Here we measured cytokine expression in human <it>ex vivo </it>TH2 cells upon activation with anti-CD3/28 and challenge with an NKG2A-specific agonist.</p> <p>Methods</p> <p>TH2 cells were purified from healthy volunteers and activated with anti-CD3/28 in the presence and absence of NKG2A-specific agonist. IL-4 was used as a marker of TH2 effector function and measured by flow cytometry.</p> <p>Results</p> <p>Activation of TH2 cells increased NKG2A positivity from (Mean ± SE) 7.3 ± 2.4% to 13.7 ± 3.8%; (p = 0.03). The presence of NKG2A agonist did not significantly alter NKG2A expression, however, the percentage of activated TH2 cells expressing intracellular IL-4 decreased from 25.5 ± 6.8% to 9.3 ± 4.8% (p = 0.001).</p> <p>Conclusion</p> <p>We show that signalling through NKG2A suppresses TH2 effector function. This may provide a means to modulate Th1/Th2 balance in diseases where Th2 cytokines predominate.</p>
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