NKG2D is a recently described activating receptor expressed by both NK cells and CTL. In this study we investigated the role of NKG2D in the natural cytolysis mediated by NK cell clones. The role of NKG2D varied depending on the type of target cells analyzed. Lysis of various tumors appeared to be exclusively natural cytotoxicity receptors (NCR) dependent. In contrast, killing of another group of target cells, including not only the epithelial cell lines HELA and IGROV-1, but also the FO-1 melanoma, the JA3 leukemia, the Daudi Burkitt lymphoma and even normal PHA-induced lymphoblasts, involved both NCR and NKG2D. Notably, NK cell clones expressing low surface densities of NCR (NCR(dull)) could lyse these tumors in an exclusively NKG2D-dependent fashion. Remarkably, not all of these targets expressed MICA/B, thus implying the existence of additional ligands recognized by NKG2D, possibly represented by GPI-linked molecules. Finally, we show that the engagement of different HLA class I-specific inhibitory receptors by either specific antibodies or the appropriate HLA class I ligand led to inhibition of NKG2D-mediated NK cell triggering.
Purpose. The purpose of this study was to examine the acute effects of low-load blood flow restriction (LLBFR) and low-load non-BFR (LL) on neuromuscular function following a bout of standardized, fatiguing leg extension muscle actions. Methods. Fourteen men (mean age ± SD = 23±4 yrs) volunteered to participate in this investigation and randomly performed LLBFR and LL on separate days. Resistance exercise consisted of 75 isotonic, unilateral leg extension muscle actions performed at 30% of one-repetition maximum. Prior to (pretest) and after (posttest) performing each bout of exercise, strength and neural assessments were determined. Results. There was no pretest to posttest differences between LLBFR and LL for maximal voluntary isometric contraction (MVIC) torque or V-wave/M-wave responses (muscle compound action potentials assessed during a superimposed MVIC muscle action) which exhibited decreases (collapsed across condition) of 41.2% and 26.2%, respectively. There were pretest to posttest decreases in peak twitch torque (36.0%) and sEMG (29.5%) for LLBFR but not LL, and larger decreases in voluntary activation for LLBFR (11.3%) than LL (4.5%). Conclusions. These findings suggested that LLBFR elicited greater fatigue-induced decreases in several indices of neuromuscular function relative to LL. Despite this, both LLBFR and LL resulted in similar decrements in performance as assessed by maximal strength.
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