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This article is part of the Research Topic Biology of NK cells and NK cell receptors

Mini Review ARTICLE

Front. Immunol., 11 December 2012 |

Evolving role of 2B4/CD244 in T and NK cell responses during virus infection

Stephen N. Waggoner1,2* and Vinay Kumar3
  • 1Department of Pathology, University of Massachusetts Medical School, Worcester, MA, USA
  • 2Program in Immunology and Virology, University of Massachusetts Medical School, Worcester, MA, USA
  • 3Department of Pathology, University of Chicago, Chicago, IL, USA

The signaling lymphocyte activation molecule (SLAM) family receptor, 2B4/CD244, was first implicated in anti-viral immunity by the discovery that mutations of the SLAM-associated protein, SAP/SH2D1A, impaired 2B4-dependent stimulation of T and natural killer (NK) cell anti-viral functions in X-linked lymphoproliferative syndrome patients with uncontrolled Epstein–Barr virus infections. Engagement of 2B4 has been variably shown to either activate or inhibit lymphocytes which express this receptor. While SAP expression is required for stimulatory functions of 2B4 on lymphocytes, it remains unclear whether inhibitory signals derived from 2B4 can predominate even in the presence of SAP. Regardless, mounting evidence suggests that 2B4 expression by NK and CD8 T cells is altered by virus infection in mice as well as in humans, and 2B4-mediated signaling may be an important determinant of effective immune control of chronic virus infections. In this review, recent findings regarding the expression and function of 2B4 as well as SAP on T and NK cells during virus infection is discussed, with a focus on the role of 2B4–CD48 interactions in crosstalk between innate and adaptive immunity.

Keywords: NK cells, T cells, virus infection, XLP, SLAM receptors, 2B4

Citation: Waggoner SN and Kumar V (2012) Evolving role of 2B4/CD244 in T and NK cell responses during virus infection. Front. Immun. 3:377. doi: 10.3389/fimmu.2012.00377

Received: 28 September 2012; Paper pending published: 19 October 2012;
Accepted: 26 November 2012; Published online: 11 December 2012.

Edited by:

Eric Vivier, Centre d’Immunologie de Marseille-Luminy, France

Reviewed by:

Georges Leclercq, Ghent University, Belgium
Alfonso Martin-Fontecha, Boehringer Ingelheim, Germany

Copyright: © 2012 Waggoner and Kumar. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in other forums, provided the original authors and source are credited and subject to any copyright notices concerning any third-party graphics etc.

*Correspondence: Stephen N. Waggoner, Department of Pathology, University of Massachusetts Medical School, 55 Lake Avenue North, Worcester, MA 01655, USA. e-mail: