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Earlier studies found that B7H3 (also known as B7H3) promotes the activation of T cells. Chapoval et al. confirmed that in the presence of anti-CD3 antibodies, B7H3 can promote the proliferation of CD4 and CD8+ T cells and selectively promote the secretion of IFN-γ. And B7H3 transfection into tumor cells can enhance the killing ability of CTL. Further research found that only TLT-2 transgenic cells could bind to mouse B7H3 with high affinity, and TLT-2 was determined to be the receptor molecule of B7H3. Moreover, Hashiguchi et al. confirmed that the B7H3-TLT-2 pathway enhanced T cell activation. However, Leitner et al. did not find the specific binding of B7H3 to TLT-2 by flow cytometry, therefore, the exact receptor molecule of B7H3 is still unclear.
On the other hand, studies have found that B7H3 can also suppress T-cell immune responses. Some studies have shown that B7H3 can inhibit human and mouse T cells by activating or inhibiting NFTA (nuclear factor for activated T cells), NF-KB (nuclear factor kB) and AP-1 (activator protein-1) pathways. activation. In addition, results have demonstrated that B7H3 may inhibit T cell immune responses by inhibiting the activity of Thl. The study of Leiner et al. also found that B7H3 can down-regulate the secretion of IL-2 in T cells to inhibit the activity of T cells.