![]() Moreover, mut-CALR elicits antigen-specific responses from both CD4 + and CD8 + T cells, confirming its broad applicability as an immunogen. Significantly, blockade of PD-1 and CLTA4 ex vivo by mAbs and of PD-1 in vivo by pembrolizumab administration restores mut-CALR–specific T-cell immunity in some patients with CALR + MPN. Here, we demonstrate that although a subset of patients with CALR + MPN develop specific T-cell responses against the mut-CALR C-terminus, PD-1 or CTLA4 expression abrogates the full complement of responses. All patients carrying these mutations ( CALR + MPN) share an identical sequence in the C-terminus of the mutated CALR protein (mut-CALR), with the potential for utility as a shared neoantigen. Somatic frameshift mutations in the calreticulin ( CALR) gene are key drivers of cellular transformation in myeloproliferative neoplasms (MPN). ![]()
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