CEACAM1 promotes CD8+ T cell responses and improves control of a chronic viral infection

Vishal Khairnar (), Vikas Duhan, Ashwini M. Patil, Fan Zhou, Hilal Bhat, Christine Thoens, Piyush Sharma, Tom Adomati, Sarah-Kim Friendrich, Judith Bezgovsek, Janine D. Dreesen, Gunther Wennemuth, Astrid M. Westendorf, Gennadiy Zelinskyy, Ulf Dittmer, Cornelia Hardt, Jörg Timm, Joachim R. Göthert, Philipp A. Lang, Bernhard B. Singer and Karl S. Lang ()
Additional contact information
Vishal Khairnar: University Hospital Essen
Vikas Duhan: University Hospital Essen
Ashwini M. Patil: University Hospital Essen
Fan Zhou: University Hospital Essen
Hilal Bhat: University Hospital Essen
Christine Thoens: Heinrich-Heine-University
Piyush Sharma: University Hospital Essen
Tom Adomati: University Hospital Essen
Sarah-Kim Friendrich: University Hospital Essen
Judith Bezgovsek: University Hospital Essen
Janine D. Dreesen: University Hospital Essen
Gunther Wennemuth: University Hospital Essen
Astrid M. Westendorf: University Hospital Essen
Gennadiy Zelinskyy: University Hospital Essen
Ulf Dittmer: University Hospital Essen
Cornelia Hardt: University Hospital Essen
Jörg Timm: Heinrich-Heine-University
Joachim R. Göthert: University Hospital Essen
Philipp A. Lang: Heinrich-Heine-University
Bernhard B. Singer: University Hospital Essen
Karl S. Lang: University Hospital Essen

Nature Communications, 2018, vol. 9, issue 1, 1-14

Abstract: Abstract Dysfunction of CD8+ T cells can lead to the development of chronic viral infection. Identifying mechanisms responsible for such T cell dysfunction is therefore of great importance to understand how to prevent persistent viral infection. Here we show using lymphocytic choriomeningitis virus (LCMV) infection that carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1) is fundamental for recruiting lymphocyte-specific protein kinase (Lck) into the T cell receptor complex to form an efficient immunological synapse. CEACAM1 is essential for activation of CD8+ T cells, and the absence of CEACAM1 on virus-specific CD8+ T cells limits the antiviral CD8+ T cell response. Treatment with anti-CEACAM1 antibody stabilizes Lck in the immunological synapse, prevents CD8+ T cell exhaustion, and improves control of virus infection in vivo. Treatment of human virus-specific CD8+ T cells with anti-CEACAM1 antibody similarly enhances their proliferation. We conclude that CEACAM1 is an important regulator of virus-specific CD8+ T cell functions in mice and humans and represents a promising therapeutic target for modulating CD8+ T cells.

Date: 2018
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DOI: 10.1038/s41467-018-04832-2

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