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TIGIT-CD155 Interactions in Melanoma: A Novel Co-Inhibitory Pathway with Potential for Clinical Intervention Karsten Mahnke, Alexander H. Enk Journal of Investigative Dermatology Volume 136, Issue 1, Pages 9-11 (January 2016) DOI: /j.jid Copyright © 2015 The Authors Terms and Conditions
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Figure 1 Direct and indirect mechanisms of TIGIT-CD155–induced suppression. Inozume et al. (2016) report that melanomas express high levels of CD155. The engagement of TIGIT on CTLs leads to the recruitment of SHP1 to the ITT domain and abrogation of MAPK signaling. Also activation via CD226 dimerization is blocked. Thus, CTL effector functions are downregulated. In addition, TIGIT+ Treg are enriched in tumor tissues and engagement of TIGIT leads to gene expression and enhanced suppressive function of Treg. CTL, cytotoxic T cells; ITT, immunoreceptor tail tyrosine; MAPK, mitogen-activated protein kinase; TIGIT, T-cell Ig and ITIM domain. Journal of Investigative Dermatology , 9-11DOI: ( /j.jid ) Copyright © 2015 The Authors Terms and Conditions
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