Loss or mismatch of MHC class I is sufficient to trigger NK cell-mediated rejection of resting lymphocytes in vivo - role of KARAP/DAP12-dependent and -independent pathways.
作者： Linda Öberg , Sofia Johansson , Jakob Michaëlsson , Elena Tomasello , Eric Vivier
关键词: Haematopoiesis 、 Biology 、 Beta-2 microglobulin 、 MHC restriction 、 Interleukin 21 、 Janus kinase 3 、 MHC class I 、 Major histocompatibility complex 、 Cell biology 、 Immunology 、 Cell killing
摘要: A prediction from the "missing self" hypothesis is that down-regulation of MHC class I on resting hematopoietic cells should be sufficient to make them susceptible NK cell killing. Using a method enabling kinetic and quantitative assessments cell-mediated rejection responses in vivo, we here show beta(2)-microglobulin-deficient (beta(2)m(-/-)) mice were rapidly rejected unmanipulated C57BL/6 (B6) mice. In situations allelic mismatches occurred but required longer time. beta(2)m(-/-) donor pre-activated with concanavalin more efficiently eliminated compared cells, as MHC(-) tumor cells. When recipient pretreated an IFN inducer activate was also enhanced. The signaling adaptor KARAP/DAP12 dispensable for (lacking MHC) critical BALB/c (mismatched B6 recipients. contrast, recipients KARAP/DAP12-independent fashion. Loss or mismatch thus convey susceptibility rejection. However, activation effector target enhanced shifted balance between different pathways involved.
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