Summary NKG2D is a potent activating receptor on NK cells which acts as a molecular sensor for stressed cells expressing NKG2D ligands such as infected or tumor transformed cells. Although NKG2D is expressed on NK cell precursors, its role in NK cell development is still not known. We have generated NKG2D-deficient mice by targeting the Klrk1 locus. Here we provide evidence for an important regulatory role of NKG2D in the development of NK cells. The absence of NKG2D causes faster division of NK cells, perturbation in size of some NK cell subpopulations and their augmented sensitivity to apoptosis. As expected, NKG2D−/− NK cells are less responsive to tumor targets expressing NKG2D ligands. NKG2D−/− mice, however, show an enhanced NK cell-mediated resistance to MCMV infection as a consequence of NK cell dysregulation. Altogether, these findings provide evidence for yet unknown regulatory function of NKG2D in NK cell physiology.

There were no significant gender-related differences regarding nonconventional MRI measures. GM and central atrophy are more advanced in male patients, whereas WM atrophy is more advanced in female patients. These gender-related MRI differences may be explained by the effect of sex hormones on brain damage and repair mechanisms.

The NKG2D receptor is one of the most potent activating natural killer cell receptors involved in antiviral responses. The mouse NKG2D ligands MULT-1, RAE-1, and H60 are regulated by murine cytomegalovirus (MCMV) proteins m145, m152, and m155, respectively. In addition, the m138 protein interferes with the expression of both MULT-1 and H60. We show here that one of five RAE-1 isoforms, RAE-1␦, is resistant to downregulation by MCMV and that this escape has functional importance in vivo. Although m152 retained newly synthesized RAE-1␦ and RAE-1␥ in the endoplasmic reticulum, no viral regulator was able to affect the mature RAE-1␦ form which remains expressed on the surfaces of infected cells. This differential susceptibility to downregulation by MCMV is not a consequence of faster maturation of RAE-1␦ compared to RAE-1␥ but rather an intrinsic property of the mature surface-resident protein. This difference can be attributed to the absence of a PLWY motif from RAE-1␦. Altogether, these findings provide evidence for a novel mechanism of host escape from viral immunoevasion of NKG2D-dependent control.Cytomegaloviruses (CMVs) are ubiquitous pathogens causing morbidity in immune suppressed and immunodeficient hosts (34). Since CMVs are strictly species-specific viruses, the infection of mice with murine CMV (MCMV) represents a widely used model for studying CMV infection and disease (22,40).Natural killer (NK) cells play a crucial role in the control of many viruses and are among the first cells to sense proinflammatory cytokines, as well as the perturbations in the expression of major histocompatibility complex (MHC) class I molecules and other surface molecules induced by viral infection (13). Both human CMV (HCMV) and MCMV have evolved strategies to compromise innate immunity-mediated by NK cells (20,49).Although proinflammatory cytokines released during the early stage of MCMV infection induce NK cell activation, this is usually not sufficient for virus control (11). Namely, most mouse strains fail to mount an effector phase of NK cell response against infected cells (42), in spite of the fact that MCMV infection causes the downmodulation of MHC I molecules (17), which should activate NK cells via a "missing-self" mechanism (28). The lack of NK cell activation by MCMV is even more puzzling considering that NK cells possess activating receptors that recognize cellular ligands induced by infection. Among these is the activating receptor NKG2D, a C-type lectinlike receptor encoded by a single gene in humans and rodents (39). Engagement of NKG2D transduces a strong activating signal to promote NK cell stimulation. NKG2D also serves as a costimulatory receptor on CD8 ϩ T cells (2). Several NKG2D ligands have been described in mice: MULT-1, H60a, H60b, H60c, and RAE-1␣, -1␤, -1␥, -1␦, and -1ε isoforms (4-6, 10, 14, 32, 35, 44). What prevents the activation of NK cells via the NKG2D receptor during MCMV infection? We and others have characterized four MCMV proteins involved in the downmodulation of NKG2D ligands (15,23...

We aimed to investigate whether mild cognitive impairment (MCI) in Parkinson's disease (PD) is characterized by region-specific gray matter (GM) atrophy and to explore correlations between GM and cognition in PD. Magnetic resonance images of 42 newly diagnosed PD patients (of which 11 had MCI) and 37 normal controls were analyzed using voxel-based morphometry. Analyses comparing groups showed no regional atrophy, and in patients there were no significant correlations between cognitive domain test performance and GM loss. In conclusion, GM atrophy does not seem to be a major feature of cognitive dysfunction in incident PD.

To our knowledge this is the first reported case of extraosseous Ewing's sarcoma in the rectovaginal septum.

In fungal abscesses, the dual-rim sign is not present but a prominent peripheral rim or central susceptibility effects on SWI will be seen. The appearance of pyogenic abscesses on SWMRS depends on the used sequence, with the dual-rim sign a specific feature of pyogenic brain abscesses on SWI.

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The aim of this study is to report the first case of simultaneous appearance of cerebral venous thrombosis (CVT) and bilateral subdural hematomas (SDHs) following epidural analgesia for labor and delivery and to point out the difficulty of establishing such a diagnosis in the presence of postpartum headache. A 26-year old primigravida with a history of epilepsy received epidural analgesia for delivery. Three days after the uneventful spontaneous vaginal delivery she complained about the headache. Patient responded very well to the pain medication and oral hydration, and the headache was relieved. Ten days after the delivery, the headache reoccurred, and an epidural blood patch was performed that successfully relieved her symptom. Stronger progressive headache with nausea reappeared two days later and the parturient was readmitted to hospital. Urgent neuroimaging examinations detected CVT of right the transverse sinus, ipsilateral cortical veins, and partially occluded superior sagittal sinus, as well as bilateral subacute/chronic SDHs. The treatment of the patient with low molecular weight heparin and antiaggregation therapy was effective. In this case, the diagnosis was delayed because of atypical clinical presentation and potentially confounding events (epidural analgesia and assumption that it was a case of PDPH). It is important to carefully observe patients in such conditions and promptly conduct suitable diagnostic tests. Otherwise, unrecognized intracranial complications and delay of appropriate therapy could be life-threatening.