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(Journal of Leukocyte Biology. 2001;70:219-224.)
© 2001 by Society for Leukocyte Biology

Expression of CD94 and NKG2 molecules on human CD4⁺ T cells in response to CD3-mediated stimulation

Pilar Romero^*, Consuelo Ortega^*, Agustín Palma^*, Ignacio J. Molina, José Peña^* and Manuel Santamaría^*

^* Departamento de Inmunología, Facultad de Medicina, Hospital Universitario "Reina Sofía," Universidad de Córdoba, Córdoba, Spain, and
Unidad de Inmunología, Facultad de Medicina, Universidad de Granada, Granada, Spain

Correspondence: Dr. Manuel Santamaría, Servicio de Inmunología, Hospital Universitario Reina Sofía, Avenida Menendez Pidal s/n, E-14004 Córdoba, Spain. E-mail: msantamaria{at}uco.es

We investigated the ability of human peripheral CD4⁺ cells to express CD94 and NKG2 molecules as a consequence of CD3-mediated activation. Using highly purified peripheral CD4⁺ T cells, we found expression of both CD94 and NKG2A 15 days after CD3-mediated stimulation of cells. We also determined by reverse transcriptase-PCR that all gene members of NKG2 family—namely, NKG2A, -C, -D, and -E—are sequentially expressed on CD4⁺ cells. We found that this expression is tightly regulated by cytokines, and we identified transforming growth factor-ß1 and interleukin-10 as the main factors that, on CD3-dependent stimulation, positively contribute to the expression of CD94 and NKG2A on CD4⁺ cells. We also investigated the functional role of NKG2A and found that coligation of CD3 and NKG2A by specific monoclonal antibodies results in significant inhibition of interferon and tumor necrosis factor production by stimulated CD4⁺ cells. The presence and function of these receptors on CD4⁺ lymphocytes support a more general role for NKG2 molecules, whose functions were originally thought to be confined to cytotoxic cells, in the immune system.

Key Words: C-type lectin receptors • cytokine regulation • TNF- • IFN-

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