The severity was assessed based on apnea hypoapneaindex(AHI) All

The severity was assessed based on apnea hypoapneaindex(AHI). All CKD patients attending the outpatient department from January 2012 to July 2013 were assessed using Cockroft and Gault formula and assigned in either of the two groups based on the GFR. Results: A total of 647 patients were screened BMS-354825 manufacturer and 302(46.67%) patients were in stage 2,3 and 4 of CKD. 87(28%) among the 302 were at high risk for berlin questionnaire). 37(42.5%) patients among the 87 patients were excluded based on the exclusion criteria. 50 patients underwent split night

sleep study, polysomnography testing. The prevalence of obstructive sleep apnea was found to be 28% after screening the population with Berlin questionnaire. The incidence of obstructive sleep apnea was found to be 25.4% in the Berlin questionnaire positive GSI-IX cell line after polysomnography. The Mann Whitney U-test statistics was applied and astatistical significance (p < 0.05) between Early and Late CKD with respect to AHI and ODI was observed. An improvement in the Late CKD is observed and the Z values for AHI and ODI were 4.273 and 2.307respectively which was statistically significant. Conclusion: This is the first study in South Indian population to assess the prevalence of obstructive sleep apnea

in non dialysis chronic kidney patients. This study indicates the necessary to screen the Non dialysis CKD population for obstructive sleep apnea. Further studies with large sample sizes are needed to re-establish the increased risk of OSA associated with decline in creatinine clearance among the study Dapagliflozin population. KOBAYASHI KANA, KUBO EIJI, ARAI SHIGEYUKI, TOMIOKA SATORU, TAMURA YOSHIFURU, KURIBAYASHI EMIKO, OHTA

TATSURU, CHANG WENXIU, UCHIDA SHUNYA Department of Internal Medicine, Teikyo University School of Medicine Introduction: With the progress of renal dysfunction, ultrasonographic findings showed morphological alterations such as the increased brightness of the kidney cortex and the kidney atrophy. However, the detailed relationships between the biochemical changes and morphological changes in CKD remain to be clarified. In the present study the association of ultrasonographic findings with the degree of kidney damages was investigated by use of morphometric analyses. Methods: 1,320 CKD patients that visited Nephrology department of our hospital from June, 2010 to March, 2012 were screened. Patients with preexisting morphological diseases such as congenital anomaly, nephrectomy and polycystic kidneys, etc. were excluded. 156 CKD patients that received both the kidney ultrasonography and biochemical examination at the same occasion were enrolled for the analysis. The kidney function was evaluated by eGFR. The morphological findings examined in the study were the length of the long and short axes of the both kidneys, cortical thickness and echogenicities of the kidney cortex.

Cryptococcus neoformans was not present within the brain parenchy

Cryptococcus neoformans was not present within the brain parenchyma. This

is the first report of a case suggesting that cryptococcal meningitis can accompany lymphocytic inflammation predominantly in cerebral deep white matter as a possible manifestation of immune reconstitution inflammatory syndrome. Cryptococcal meningitis is one of the most frequent fungal infections of the CNS and may accompany infectious granulomas (cryptococcomas) within the brain parenchyma.[1] Immune-mediated leukoencephalopathy is a rare complication of cryptococcal meningitis,[2] but the precise pathomechanism is uncertain. Here we report an autopsy case of cryptococcal meningitis accompanying lymphocytic inflammation predominantly in cerebral deep white matter, which could be considered as a unique manifestation of immune reconstitution inflammatory SCH772984 ic50 syndrome (IRIS). A 72-year-old

man presented with a slight fever and headache, followed by a subacute progression of consciousness disturbance. One year earlier, he had suffered from multiple erythemas in his lower extremities, which was diagnosed as Sweet disease by skin biopsy, and had been treated with prednisolone for 1 year; An initial dose of 50 mg/day gradually decreased to 12.5 mg/day. Twenty days after the first symptom emerged, neurological findings were unremarkable except for drowsiness. Brain MRIs were normal, and CSF findings indicated meningitis (Fig. 1, day 20). There were no findings suggestive

of infection or malignancy. HIV serology was negative. The patient was diagnosed as having possible neuro-Sweet disease learn more (NSD) because HLA testing revealed HLA-Cw1, which has a strong association with NSD.[3] After we treated the patient with methylprednisolone 1 g/day for 3 days, the CSF findings rapidly improved with a remarkable decrease in the number of lymphocytes in the blood to 105/μL (Fig. 1, day Thiamet G 30). However, the patient’s consciousness still worsened after the cessation of methylprednisolone. On day 35, brain MRI showed hyperintensities in the cerebrum, cerebellum and brainstem on fluid-attenuated inversion recovery images; the cerebral deep white matter was most severely affected (Fig. 2) and the lesions were partly enhanced by gadolinium. Along with the recovery of lymphocyte numbers in blood, the CSF demonstrated Cryptococcus neoformans with a decreased level of glucose (Fig. 1, day 36). Antifungal treatment using amphotericin B did not improve the patient’s symptoms, and the patient died of respiratory failure on day 57 from the onset. Swelling of the superficial lymph nodes was not observed throughout the disease course. We considered that cryptococcal infection after treatment with methylprednisolone was fatal in our patient. A general autopsy was performed 9 h after the patient’s death. There were no malignancies in visceral organs and no abnormalities in the lymph nodes. C.

Therefore, the infants seem to consider situational constraints w

Therefore, the infants seem to consider situational constraints when attributing goals to agents’ otherwise ambiguous actions; they seem to realize that within such constraints, these actions are efficient ways for agents to achieve goals. “
“Positive shyness is a universal emotion with the specific social function of regulating our interactions by improving trust and liking, and showing politeness. The present study examined early infant production of coy smiles during social interactions

as a measure Selleckchem LY2606368 of positive shy behavior. Eighty 4-month-olds were experimentally observed during three types of interactions in front of a mirror in which (1) the infant only sees him or herself, (2) the infant only sees the other person (mother, father, or stranger), and (3) the infant sees both him or herself and the other person. Infants produced more coy smiles during the interaction with a stranger than during the interactions with their mother or their father, or when they could see only themselves in front

of a mirror. Infants also produced more coy smiles when they could see their self-reflection during the interaction than when they could not. Our results support the assumption that coy smiles indicate an early emerging emotional reaction with an important adaptive function during social situations involving novel persons and VX-765 ic50 when special attention is given to the child. “
“For several decades, many authors have claimed the existence, early in life, of a tight link between perceptual and productive systems in speech. However, the question whether this link is acquired or is already present at birth remains open. This study aimed at investigating this question by employing the

paradigm of neonatal facial imitation. We compared imitative responses of newborn infants presented either visual-only, audiovisual congruent, or audiovisual incongruent Urease models. Our results revealed that the newborns imitated significantly more quickly the movements of the model’s mouth when this model was audiovisual congruent rather than visual-only. Moreover, when observing an audiovisual incongruent model, the newborns did not produce imitative behavior. These findings, by highlighting the influence of speech perception on newborns’ imitative responses, suggest that the neural architecture for perception–production is already in place at birth. The implications of these results are discussed in terms of a link between language and neonatal imitation, which could represent a precursor of more mature forms of vocal imitation and speech development in general. “
“Language rhythm determines young infants’ language discrimination abilities. However, it is unclear whether young bilingual infants exposed to rhythmically similar languages develop sensitivities to cross-linguistic rhythm cues to discriminate their dual language input. To address this question, 3.

More than 95% of the cells were CD56+CD3- lymphocytes Enriched N

More than 95% of the cells were CD56+CD3- lymphocytes. Enriched NK cells were co-cultured with AFP (25 µg/ml, AFP-DCs) or Alb (25 µg/ml, Alb-DCs) pretreated DCs for 24 h. The cytolytic activity of NK cells co-cultured with AFP-DCs or Alb-DCs against target cells (K562, NK sensitive cells, or Huh7, human HCC cells) was assessed by 4-h 51Cr-releasing assay with or without the presence of neutralizing antibody of IL-12 (BD Pharmingen) or recombinant IL-12p70 protein (PeproTech), as described previously [14]. In some experiments,

a Transwell insert was also used to prevent direct contact of NK cells and DCs in co-culture systems, as described previously [14]. The statistical significance of differences between the two groups was determined by applying the Mann–Whitney U-test. We defined statistical significance as P < 0·05. We investigated the activity of NK cells co-cultured with Selleck BYL719 AFP-DCs or Alb-DCs. NK cells from the same healthy volunteers were co-cultured with AFP-DCs or Alb-DCs for 24 h, and we evaluated the cytolytic activity of NK cells co-cultured with DCs against K562 cells as target cells with the 51Cr-releasing assay. The cytotoxicity of NK cells Protein Tyrosine Kinase inhibitor co-cultured with AFP-DCs against K562 cells was significantly lower than those with Alb-DCs (Fig. 1a). Similarly, the cytotoxicity of NK cells co-cultured with AFP-DCs against Huh7 cells was significantly lower than

that with Alb-DCs (Fig. 1b). We also evaluated the IFN-γ production from NK cells co-cultured with AFP-DCs or Alb-DCs by specific ELISA. IFN-γ production from NK cells co-cultured with AFP-DCs was significantly lower than that from NK cells co-cultured

with Alb-DCs (Fig. 1c). These results demonstrated that NK activity co-cultured with AFP-DCS was lower than that Buspirone HCl with Alb-DCs. Next, NK cells were cultured with AFP (AFP-NK cells) or Alb (Alb-NK cells) for 24 h, and we evaluated the cytolytic activity of AFP-NK and Alb-NK against K562 cells with the 51Cr-releasing assay. The cytotoxicity of AFP-NK cells was almost similar to that of Alb-NK cells, and the presence of DCs could enhance the cytotoxicity of NK cells (Fig. 2a). These results suggested that AFP does not directly impair NK cell function and that DCs play a critical role in activating NK cells. To examine whether this attenuation of NK cells was caused by the cytokine from DCs or by direct contact with DCs, NK cells were co-cultured with AFP-DCs or Alb-DCs in Transwell culture for 24 h. The cytotoxicity of NK cells co-cultured with AFP-DCs was lower than that with Alb-DCs, which was similar to the results without Transwell membrane (Fig. 2b). These results suggested that soluble factors derived from DCs played a role in activating NK cells. We next examined the function of AFP-DCs. We obtained DCs from eight healthy volunteers and cultured the DCs for 7 days in RPMI-1640 with AFP (AFP-DCs) or Alb (Alb-DCs). On day 6, we added LPS to induce DC maturation.

One startling statistic computed by Haith (1980) is that the aver

One startling statistic computed by Haith (1980) is that the average 2-month-old infant has sampled its visual environment with over 250,000 fixations (looking

times between saccades) since birth. Despite the logical advantage of the foregoing constraints—which surely must assist in dealing with Problem 2—it is nevertheless the case that laboratory demonstrations of statistical learning are highly simplified compared to what an infant is actually confronted with in the natural environment. Thus, we should be concerned that such demonstrations are little more than proof of concept that under ideal conditions a statistical-learning Selleck Proteasome inhibitor mechanism can solve certain tasks. But does this mechanism “scale up” to more natural and complex learning tasks? There are two answers to this question, at least

for studies of statistical buy Trichostatin A learning in the language domain. First, a variety of corpus analyses (Frank, Goldwater, Griffiths, & Tenenbaum, 2010; Swingley, 2005) have shown that, to a first approximation, the same types of statistical information manipulated in the laboratory are present in real language input to infants. Yet in real corpora, these statistical cues are less reliable, and thus, one worries that no one cue alone is sufficient. It is important to note, for historical purposes, that initial claims about statistical learning made precisely this point: “Although experience with speech in the real world is unlikely to be as concentrated these as it was in these studies, infants in more natural settings presumably benefit from other types of cues correlated with statistical information (p. 1928)” (Saffran et al.,

1996). Laboratory studies that eliminate all potentially useful cues except one serve the purpose of showing that the sole cue present in the input is sufficient for learning. But such studies cannot confirm that in the natural environment, where many cues are correlated, any given cue plays a necessary role in learning. The second answer to the “scale up” question is to conduct laboratory experiments in which two or more cues are presented in combination to see which one “wins” or how each cue is “weighted” in the statistical-learning process. Early work that followed this strategy suggested that statistical cues “trump” prosodic cues (Thiessen & Saffran, 2003), at least at the level of lexical prosody (i.e., whether 2-syllable words have a strong-weak or a weak-strong stress pattern). The reason that lexical prosody might take a back seat to statistics is that prosody is language-specific, whereas syllable statistics, at least in most languages, are not. Yet there are other levels of prosody that are language-general and so could reasonably serve as universal constraints on which statistics are computed.

Mice immunized with AMH subunit vaccine generated high HspX-speci

Mice immunized with AMH subunit vaccine generated high HspX-specific IgG2a and IgG1 as well as high IFN-γ

production with the stimulation of Ag85B and HspX. The antibodies target the extracellular mycobacteria through binding to live M. tuberculosis, which can alter the specific uptake pathway used for phagocytosis [22]. High IgG2a/IgG1 reflects Th1-skewing pathway that produces IFN-γ to promote intracellular microbicidal activities by activating Erlotinib datasheet macrophages and cytotoxic T cells [17]. AMM/AMH/AMM + AMH vaccine was designed to boost BCG-primed immunity to evaluate the capability of generating protective immunity. The results showed that only AMM + AMH boosting resulted in a significant decrease in CFUs in lung tissues compared with the BCG group. Although AMM vaccine was found to be a promising candidate, it could not reduce markedly the bacterial load compared with BCG in BCG-primed and subunit vaccine-boosted strategy. Although AMH alone could

not reduce significantly CFU in lung tissues of infected mice over that of BCG, when it was combined with AMM, interestingly, fewer CFUs were found than the BCG group. AMM might induce immunity to bacteria in active multiplication condition, but inclusion of AMH Venetoclax potentially induced immune protection against dormant bacteria. Because of the comprehensive immune protection against replicating and dormant M. tuberculosis, the multi-stage vaccine, AMM + AMH, induced the most obvious protective effect among the BCG, BCG plus Ag85B or AMM or AMH groups (Fig. 4). In conclusion, AMH vaccine could generate strong antigen-specific humoral and cell-mediated immunity. Only AMM + AMH boosting led to more pronounced M. tuberculosis clearance from the lungs of mice than BCG alone. Meanwhile, the vaccine induced higher immune responses and presented small lesions. The combination of fusion protein AMM and AMH containing antigens both from replicating and dormant M. tuberculosis may be a promising multi-stage vaccine to boost BCG primed immunity for better protective efficacy. This work was funded by the National Major Science and Technology Projects of China (2008ZX-10003-01305,

2008zx1000301104) and the National High Technology Research and Development Program of China (863 Program) (2006AA02z420). for
“Efficient presentation of peptide-MHC class I (pMHC-I) complexes to immune T cells should benefit from a stable peptide-MHC-I interaction. However, it has been difficult to distinguish stability from other requirements for MHC-I binding, for example, affinity. We have recently established a high-throughput assay for pMHC-I stability. Here, we have generated a large database containing stability measurements of pMHC-I complexes, and re-examined a previously reported unbiased analysis of the relative contributions of antigen processing and presentation in defining cytotoxic T lymphocyte (CTL) immunogenicity [Assarsson et al., J. Immunol. 2007. 178: 7890–7901].

We found a complete concordance between our measurements and the

We found a complete concordance between our measurements and the pathologist’s reports: those samples that showed higher relative intensity when analysed with our method were described in the Dorsomorphin purchase report as showing traces, as opposed to complete

absence, of dystrophin (Figure 3).While there were no significant differences between the samples containing traces (samples 3, 4 and 5), the differences between them and those without traces (samples 2, 6A and 6B) were highly significant (P < 0.001). To evaluate how much variability there is in the standard samples used as controls, a set of quadriceps muscle biopsies from four individuals without a neuromuscular disease were compared. While in three cases the analysis failed to show any significant difference between the samples analysed, muscle from one control showed significantly reduced dystrophin expression (P < 0.01 or P < 0.05 between control 11, and controls 12 and 14 in Dys2 analysis) (Figure 4A). To determine if samples from different muscles of the same DMD patient contained similar levels of dystrophin, three samples from the same patient were compared

(quadriceps sample taken at the time of diagnosis, right and left EDB muscles taken 10 years later). All three samples showed very limited dystrophin intensity when analysed with both dystrophin antibodies (0.05 of control for Dys2 and 0.15 of control for P7), a similar this website decrease in the sarcolemma-associated proteins (BDG: 0.36 of control and ASG 0.65) and overexpression of UTR to an equivalent level (approximately 6.5 times the intensity of the control) (Figure 4B). There was no statistically significant difference between any of these measurements. Farnesyltransferase A range of muscular dystrophies are routinely diagnosed by immunostaining muscle biopsies, sometimes in combination with Western blot analysis. Many of these disorders, such as DMD or BMD or UCMD, are characterized by reduced expression of sarcolemmal proteins, which is sometimes subtle [13]. Secondary protein changes also often occur [1], Quantification of protein

expression from muscle biopsies is not trivial; while Western blot analysis of serial dilutions of muscle lysate can provide semiquantitative analysis, it requires an amount of tissue that is not always available [20,21]. In this study, we have compared the levels of dystrophin expression in muscle fibres of DMD, BMD, a manifesting carrier and patients with normal dystrophin expression. We first used randomly encountered regions of each image of immunostained muscle transverse sections to perform the analysis. This has the advantage of avoiding any bias from the operator, although can obviously miss discrete areas of relevance, e.g. clusters of revertant fibres in DMD [22,23] or the mosaic dystrophin expression observed in DMD manifesting carriers [17,24].

Remarkably, the finding that PstS1 stimulates memory T cells spec

Remarkably, the finding that PstS1 stimulates memory T cells specific for TT, suggests the potential exploitation of PstS1 immunomodulatory properties in other infections. Although effects on other APCs cannot be excluded, our study shows that the immunomodulatory properties of PstS1 are linked to its ability to activate DCs in vitro and in vivo. In particular, PstS1 promoted

the expression of IL-6, IL-1β, and, to a minor extent, IL-23. These cytokines were recently reported to drive a fine balance of CD4+ T-cell differentiation in the effector phase of the immune response to Candida albicans and Staphylococcus aureus [44]. Of interest, other cytokines pivotal for the homeostasis of memory T cells, such as IL-7

and IL-15 for CD8+ T cells [45], or IL-12p40 for Th1 check details response [46], were EPZ-6438 not modulated by PstS1 (data not shown). The ability to stimulate DCs was peculiar to PstS1, since other immunodominant Mtb Ags such as Ag85B, Esat-6, or HBHA were unable to activate DCs (Fig. 4 and data not shown) and it was directed preferentially toward CD8α− DCs. The two major DC subsets of mouse spleen, CD8α+ and CD8α−, trigger distinct T-cell responses against pathogens. While CD8α+ DCs are thought to be specialized in antiviral response due to their unique cross-priming ability, CD8α− DCs have been involved in CD4+ T-cell immunity, particularly during bacterial infections [47]. CD8α− DCs efficiently induce CD4+ Y-27632 2HCl T-cell responses through in vivo targeting of Ag via C-type lectin receptors, such as dectin-1 and DCIR-2 [30, 48]. The preferential ability of CD8α− DCs to prime CD4+ T-cell responses has been correlated with their superior capacity to process Ags via MHC class II molecules [30]. Accordingly, we report that PstS1 endowed CD8α− DCs with a strong ability to simulate CD4+ T cells. In particular, CD8α− DCs stimulated by PstS1 were found to produce much higher amounts of IL-6, IL-1β, and IL-23 with respect

to CD8α+ DCs. Moreover, PstS1-pulsed CD8α− DCs were far superior at inducing IFN-γ, IL-17, and IL-22 release by Ag85B-specific memory T cells, compared with CD8α+ DCs. The mechanisms by which PstS1 activates DCs remain to be established. Our data on DCs deficient for TLR2, the main PRR recognized by Mtb components, suggest that this receptor is dispensable. We envisage that the TLR2-independent pathway of DC maturation induced by PstS1 strongly differs from that triggered by the Mtb Ags Rv0577, Rv1196, Rv0978c, and Rv0754, which all recognize TLR2 and induce maturation of DCs leading to either Th1 or Th2 polarization, but not to IL-17 secretion by memory CD4+ T cells [14-18].

34 The magnitude and quality of the inflammatory cytokine respons

34 The magnitude and quality of the inflammatory cytokine response depends upon the TLR agonists35 and adjuvant vehicles used.11 Chain and colleagues have shown that exposure of DCs

to interleukin (IL)-6 dramatically altered the specificity of the T-cell response to native hen egg lysozyme (HEL) and enabled the processing and presentation of HEL cryptic T-cell epitopes.36 IL-6 was shown to modulate endosomal and lysosomal pH,36 thereby affecting the activity of lysosomal enzymes (cathepsins) involved in protein Ag degradation.37 IL-6 can also impact DM levels,37 a critical cofactor in endosomal peptide loading of MHC class II molecules that favours the presentation of peptides that possess high-stability interactions with MHC class II molecules.22 In addition to IL-6, Maurer and colleagues have shown that other proinflammatory cytokines, such as tumour necrosis INCB018424 mw factor-α (TNF-α), IL-1β this website and the anti-inflammatory cytokine, IL-10, can modulate lysosomal protease activity in DCs and affect

pMHCII presentation.38 Altogether, these studies suggest that the inflammatory cytokine environment determined by the adjuvant can influence pMHCII presentation and change the TCR repertoire of the responding CD4 T cells (Fig. 2b). In addition to their capacity to alter pMHCII presentation by DCs, adjuvants can also modulate the expression level of costimulatory molecules on the surface of DCs.6 These changes in costimulatory molecule expression can either positively why or negatively impact TCR–pMHCII interactions and thus regulate CD4 T-cell clonal selection. Allison and colleagues have suggested that engagement of cytotoxic T lymphocyte antigen-4 (CTLA-4), a receptor for costimulatory molecules CD80 and CD86 on the surface of activated CD4 T cells, regulates the breadth of the CD4 T-cell response39

by selectively inhibiting the expansion of high-affinity clonotypes.40 For CD8 T cells, there is also evidence that the balance of costimulatory signals on the surface of APCs can regulate the expansion of high-avidity CD8 T cells.41–43 Hence, by modulating the costimulatory context in which pMHCII presentation occurs, adjuvants can alter the clonotypic diversity of the CD4 T-cell compartment (Fig. 2c). Our experiments indicate that adjuvants with the capacity to create Ag depot at the site of injection broadens the CD4 T-cell repertoire by propagating lower-affinity clonotypes.25 It is possible that the propagation of low-affinity clonotypes during an immune response requires pMHCII presentation by specific APCs that are targeted by depot-forming adjuvants. Several APCs, including tissue-derived DCs (Langerhans’ cells, dermal DCs), LN-resident DCs, monocyte-derived inflammatory DCs and B cells have been shown to be involved in CD4 T-cell responses to protein Ag44–48 but little is known about the impact of adjuvants on their capacity to present pMHCII.

GFAP-Cre FasLfl/fl mice were unable to resolve EAE and suffered f

GFAP-Cre FasLfl/fl mice were unable to resolve EAE and suffered from persisting demyelination and paralysis, while FasLfl/fl control mice recovered. In contrast to FasLfl/fl mice, GFAP-Cre FasLfl/fl mice failed to induce Dinaciclib molecular weight apoptosis of Fas+ activated CD4+ T cells and to increase numbers of Foxp3+ Treg cells beyond day 15 post immunization, the time

point of maximal clinical disease in control mice. The persistence of activated and GM-CSF-producing CD4+ T cells in GFAP-Cre FasLfl/fl mice also resulted in an increased IL-17, IFN-γ, TNF, and GM-CSF mRNA expression in the CNS. In vitro, FasL+ but not FasL− astrocytes induced caspase-3 expression and apoptosis of activated T cells. In conclusion, FasL expression of astrocytes plays an important role in the control and elimination of autoimmune T cells from the CNS, thereby determining recovery from EAE. EAE is a widely used animal model to study MS, an inflammatory demyelinating Ferroptosis inhibitor disease mediated by accumulation of T lymphocytes and macrophages in the CNS [1, 2]. EAE can be induced by either active immunization with myelin Ags including myelin oligodendrocyte glycoprotein (MOG) peptide or passive transfer of myelin-reactive CD4+ T cells, which are both initiators and effectors of EAE. Among CD4+

T lymphocytes, GM-CSF-producing CD4+ T cells, IFN-γ-secreting Th1 cells, and IL-17-secreting Th17 cells have been identified as the most important mediators in the immunopathogenesis of EAE [3-6] and all of them can

induce EAE independently, although recent studies point to an essential role of GM-CSF-producing CD4+ T cells, which can induce EAE independent of IFN-γ and IL-17 [7]. Infiltrating T lymphocytes trigger an inflammatory response in the CNS culminating in demyelination and axonal damage clinically resulting in paralysis [8]. Correspondingly, recovery from EAE requires termination of inflammation and the induction of T-cell Endonuclease apoptosis in the CNS [9]. Fas ligand (FasL; CD95L), a cytotoxic cytokine belonging to the TNF superfamily, acts through Fas, a death receptor of the TNFR superfamily, to induce programed cell death via caspase signaling [10]. Local expression of FasL in immunoprivileged organs including eyes, testis, and placenta is essential for deletion of infiltrating inflammatory cells [11-13]. Fas/FasL interaction is of particular importance for homeostasis of the immune system and its dysregulation has been implicated in various autoimmune diseases. Mice carrying autosomal recessive mutations in the Fas (lpr) and FasL (gld) genes develop a spontaneous autoimmune syndrome similar to human systemic lupus erythematosus [14, 15].