2006/11/01 by Grit-Carsta Bulwin, Thomas Heinemann, Volker Bugge +13 · 23 citations
Immunology and Microbiology · Chemistry · #T-cell and B-cell Immunology #Immunotherapy and Immune Responses #Immune Response and Inflammation #CTLA-4 #Cell biology #T cell #Cell growth #Chemistry #Cytotoxic T cell #Intracellular #Biology #Cytokine #Immunology #Immune system #In vitro #Biochemistry
paper · pdf · doi:10.4049/jimmunol.177.10.6833
published in The Journal of Immunology 177(10), 6833-6841 (American Association of Immunologists)
openalex publication_date 2006/11/01 · openalex created_date 2025/10/10 · openalex updated_date 2026/07/30
Ab targeting of TIRC7 has been shown previously to inhibit T cell proliferation and Th1 lymphocyte-associated cytokine production. In this study, we demonstrate that Ab targeting of TIRC7 induces early cell surface expression of CTLA-4. The majority of stimulated CD4+ and CD8+ human T cells coexpress CTLA-4 and TIRC7. Similar to CTLA-4, TIRC7 rapidly accumulates at the site of Ag adhesion upon T cell activation. TIRC7 seems to colocalize with CTLA-4 in human T cells, and both molecules are associated with clathrin-coated vesicles, indicating they share intracellular transport systems. Moreover, Ab targeting of TIRC7 results in an early activation of CTLA-4 transcription. The inhibition of cell proliferation mediated by TIRC7 is dependent on CTLA-4 expression because the TIRC7-mediated inhibitory effects on cell proliferation and cytokine expression are abolished by Ab blockade of CTLA-4. Splenocytes obtained from CTLA-4-deficient mice are not responsive to TIRC7 Ab targeting. Thus, TIRC7 acts as an upstream regulatory molecule of CTLA-4 expression.