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Biomedical subjects

S Hong

Publications and source records attributed to S Hong.

At least 91 records · Page 5Linked to original sources
PubMed2000

Cerebral palsy and multiple births in China.

BACKGROUND: A population-based study on prevalence of cerebral palsy in multiple births has not been carried out in China. The purpose of this paper was to determine the prevalence of cerebral palsy in multiple births and to explore the influence of multiple pregnancy on cerebral palsy after controlling for birthweight. METHODS: A cross-sectional study of cerebral palsy was carried out among 388,192 children aged <7 years in seven cities of Jiangsu province in China. Information about birthweight and plurality was obtained from routine health care records. Pediatricians at city level diagnosed all cases. All the doctors involved had taken part in a training programme held by Beijing Medical University. Stratified analysis by birthweight and its standard normal deviate was employed to compare the prevalence of cerebral palsy in multiples and singletons. RESULTS: The prevalence of cerebral palsy for children aged <7 years in multiples was 9.7 per 1000 children (95% confidence interval [CI]: 6.5-14.0), which was 6.5 times that in singletons (95% CI: 4.4-9.3). The overall neonatal mortality rate was 60.9 per 1000 liveborn multiples, being highest (944.4 per 1000) in the 500-999 g birthweight groups. Most liveborn multiples weighing <1500 g at birth probably died from diseases related to very low birthweight prior to this study. The prevalence of cerebral palsy in multiple births was likely to be higher than that reported in developed countries for children weighing 1500-2499 g even though our data were from a cross-sectional study. When stratified by birthweight, the prevalence of cerebral palsy in multiples weighing <2500 g had tended to be lower than that of singletons in the same birthweight group. In contrast, in normal birthweight categories multiple births had a higher prevalence of cerebral palsy than singletons. When stratified by birthweight normal deviate, the prevalence of cerebral palsy in multiple births was uniformly higher than that in singletons in all birthweight strata and the prevalence of cerebral palsy among multiples appeared to be augmented as birthweight increased. CONCLUSION: The prevalence of cerebral palsy in multiples, 9.7 per 1000 children, is 6.5 times that in singletons. Survival of low birthweight infants is lower in China than in developed countries and survival quality of Chinese children weighing 1500-2499 g needs to be further improved. In terms of birthweight multiples and singletons may be heterogeneous. It might be difficult to directly use actual birthweight specific prevalence to compare the prevalence of cerebral palsy in multiples and singletons. Birthweight normal deviate specific prevalence of cerebral palsy suggests that multiple pregnancy is an independent risk factor for cerebral palsy in all birthweight groups. Multiples are in adverse circumstances very early in gestation and as the foetus matures the risk of cerebral palsy increases.

Birth Weight↗
PubMed2000

Relative contribution of NK and NKT cells to the anti-metastatic activities of IL-12.

Conventional T cells, NK cells and NKT cells have been implicated in the anti-tumor activities induced by IL-12. Here we show that IL-12-induced immune responses are partially impaired in T and NKT cell-deficient RAG-2(-/-) mice, and in NKT cell-deficient CD1(-/-) mice. In response to a small dose (<1000 U) of IL-12, RAG-2(-/-) and CD1(-/-) mice demonstrated reduced cytotoxicity, serum IFN-gamma elevation and anti-metastatic activities; in contrast, in response to a high dose (>2000 U) of IL-12, the IL-12-induced immune responses of RAG-2(-/-) and CD1(-/-) mice were indistinguishable from wild-type mice. The defective responses to low-dose IL-12 of RAG-2(-/-) mice were corrected by adoptive transfer of NKT cells but not NK cells. These findings indicate that both NK and NKT cells contribute to the anti-metastatic responses induced by IL-12, and that NKT cells are mostly responsible for the low-dose activities of this cytokine.

Adoptive Transfer↗
PubMed2000

Correlation of automated visual field parameters and peripapillary nerve fiber layer thickness as measured by scanning laser polarimetry.

PURPOSE: To correlate Humphrey visual field mean sensitivity and peripapillary nerve fiber layer thickness as measured by scanning laser polarimetry. METHODS: The authors studied 54 eyes of 34 patients who visited a university-based glaucoma clinic and had undergone scanning laser polarimetry and Humphrey perimetry within 6 months. The study population included normal patients and those with glaucoma, ocular hypertension, and glaucoma suspect. The authors correlated visual field sensitivity with peripapillary nerve fiber thickness, and visual field mean deviation with the average deviation from the normal nerve fiber layer thickness. They also correlated the visual field mean deviation with all available GDx Nerve Fiber Analyzer parameters. RESULTS: The visual field mean sensitivity and deviation showed a bilinear correlation to peripapillary nerve fiber layer thickness. The visual field mean sensitivity changed little when the nerve fiber layer thickness was greater than 70 microm. The nerve fiber layer thickness below this level was associated with a rapid decrease in the visual field sensitivity. Similarly, the visual field mean deviation was close to 0 dB when the nerve fiber layer was within -10 microm of the normal value; below this thickness, the mean deviation became substantially more negative. There was a large individual variability around the bilinear fit. Of the scanning laser polarimetry parameters, a calculated index, referred to as the number, had the highest correlation with the Humphrey mean deviation. CONCLUSION: The bilinear correlation and its variability between the scanning laser polarimetry and visual field parameters make it difficult to predict the result of one from the other. In general, the correlation between the two is better when there is a significant visual field defect than when the visual field is close to normal.

Adult↗
PubMed2000

Treadmill exercise training blunts suppression of splenic natural killer cell cytolysis after footshock.

This study extended to treadmill exercise training our prior report (Dishman RK, Warren JM, Youngstedt SD, Yoo H, Bunnell BN, Mougey EH, Meyerhoff JL, Jaso-Friedmann L, and Evans DL. J Appl Physiol 78: 1547-1554, 1995) that activity wheel running abolished the suppression of footshock-induced natural killer (NK) cell cytolysis. Twenty-four male Fischer 344 rats were assigned to one of three groups (n = 8, all groups): 1) a home-cage control group, 2) a sedentary treatment group, or 3) a treadmill-running group (0 degrees incline, 25 m/min, 35 min/day, 6 days/wk). After 6 wk, the treadmill and sedentary groups received 2 days of footshock. Splenic NK cytotoxicity was determined by standard 4-h (51)Cr release assay. Percentages of lymphocytes were determined by flow cytometry. Plasma levels of ACTH, corticosterone, and prolactin concentration were measured by radioimmunoassay. After footshock, percentage of lysis relative to home-cage controls was 40% and 80% for sedentary and treadmill-trained animals, respectively (P < 0.05). Our results indicate that the protective effect of chronic exercise on innate cellular immunity in the Fischer 344 male rat is not restricted to activity wheel running, nor is it explained by elevations in basal NK activity, increased percentages of splenic NK and cytotoxic T cells, or increased plasma levels of ACTH, corticosterone, and prolactin.

Adrenocorticotropic Hormone↗
PubMed2000

[Retrospective analysis of 266 cases of pregnancy complicated by heart disease].

OBJECTIVE: To investigate the influence of cardiac function of pregnant women on outcome of their pregnancies. METHODS: Clinical data of 266 cases of pregnant women with heart diseases from January, 1993 to March, 1999 were analyzed retrospectively. RESULTS: (1) The highest incidence of cardiac disease with grade I to II of heart function was due to myocarditis, sequelae of myocarditis and abnormal cardiac rhythm (179 cases, 67.29%). The incidence of congenital heart disease is on the second (41 cases, 15.41%) which is higher than that of rheumatic heart disease (28 cases, 10.91%). (2) Grade III and IV cardiac function was mainly related to congenital and rheumatic heart diseases during pregnancy. The rate of grade I/II heart function in pregnant women after heart operations was 95.45%. (3) The incidence of premature delivery, low weight of newborns and perinatal mortality of mother were higher in women with grade III and IV heart function than in those with grade I and II heart function. CONCLUSIONS: The incidence of myocarditis and sequelae of myocarditis is increasing. Pregnancies complicated with congenital and rheumatic heart diseases are still major causes of perinatal morbidity and mortality of mother and baby. Heart operation can obviously improve the heart function. More effective managements should be adopted.

Adult↗
PubMed1999

Physicochemical aspects of the movement of the rieske iron sulfur protein during quinol oxidation by the bc(1) complex from mitochondria and photosynthetic bacteria.

Crystallographic structures for the mitochondrial ubihydroquinone:cytochrome c oxidoreductase (bc(1) complex) from different sources, and with different inhibitors in cocrystals, have revealed that the extrinsic domain of the iron sulfur subunit is not fixed [Zhang, Z., Huang, L., Shulmeister, V. M., Chi, Y.-I., Kim, K. K., Hung, L.-W., Crofts, A. R., Berry, E. A., and Kim, S.-H. (1998) Nature (London), 392, 677-684], but moves between reaction domains on cytochrome c(1) and cytochrome b subunits. We have suggested that the movement is necessary for quinol oxidation at the Q(o) site of the complex. In this paper, we show that the electron-transfer reactions of the high-potential chain of the complex, including oxidation of the iron sulfur protein by cytochrome c(1) and the reactions by which oxidizing equivalents become available at the Q(o) site, are rapid compared to the rate-determining step. Activation energies of partial reactions that contribute to movement of the iron sulfur protein have been measured and shown to be lower than the high activation barrier associated with quinol oxidation. We conclude that the movement is not the source of the activation barrier. We estimate the occupancies of different positions for the iron sulfur protein from the crystallographic electron densities and discuss the parameters determining the binding of the iron sulfur protein in different configurations. The low activation barrier is consistent with a movement between these locations through a constrained diffusion. Apart from ligation in enzyme-substrate or inhibitor complexes, the binding forces in the native structure are likely to be < = RT, suggesting that the mobile head can explore the reaction interfaces through stochastic processes within the time scale indicated by kinetic measurements.

Animals↗
PubMed1999

The energy landscape for ubihydroquinone oxidation at the Q(o) site of the bc(1) complex in Rhodobacter sphaeroides.

Activation energies for partial reactions involved in oxidation of quinol by the bc(1) complex were independent of pH in the range 5. 5-8.9. Formation of enzyme-substrate complex required two substrates, ubihydroquinone binding from the lipid phase and the extrinsic domain of the iron-sulfur protein. The activation energy for ubihydroquinone oxidation was independent of the concentration of either substrate, showing that the activated step was in a reaction after formation of the enzyme-substrate complex. At all pH values, the partial reaction with the limiting rate and the highest activation energy was oxidation of bound ubihydroquinone. The pH dependence of the rate of ubihydroquinone oxidation reflected the pK on the oxidized iron-sulfur protein and requirement for the deprotonated form in formation of the enzyme-substrate complex. We discuss different mechanisms to explain the properties of the bifurcated reaction, and we preclude models in which the high activation barrier is in the second electron transfer or is caused by deprotonation of QH(2). Separation to products after the first electron transfer and movement of semiquinone formed in the Q(o) site would allow rapid electron transfer to heme b(L). This would also insulate the semiquinone from oxidation by the iron-sulfur protein, explaining the efficiency of bifurcation.

Antimycin A↗
PubMed1999

Differential expression of nitric oxide synthase in human stomach cancer.

The level of expression and cellular localization of isoenzymes of nitric oxide synthase (NOS) was detected in human stomach tumor tissues. Tumor tissues showed 70% higher activity of NOS than that of normal tissues (P < 0.01). Poorly differentiated adenocarcinoma tend to have higher activity (P < 0.05) than well differentiated and moderately differentiated tumor tissues. Aminoguanidine (AG), 2-amino-5,6-dihydro-6-methyl-4H-1,3-thiazine (AMT), NG-monomethyl-L-arginine (L-NMMA), and Nomega-nitro-L-arginine (L-NNA) inhibited NOS activity in tumor tissues by 18, 14, 11 and 13%, respectively. The TNF-alpha mRNA expression was correlated with the inducible NOS (iNOS) level, which was high in adenocarcinomas and low in normal tissues. Tumor tissues showed higher expression of iNOS in gland epithelial cells but the level of eNOS was significantly decreased with an exception of concentrated localization in the proliferating capillary endothelium. These results revealed that isoforms of NOS might contribute differentially to growth and progression of human stomach tumor.

Adult↗
PubMed1999

Hydrogen peroxide activates p70(S6k) signaling pathway.

We investigated a possible role of reactive oxygen species (ROS) in p70(S6k) activation, which plays an important role in the progression of cells from G(0)/G(1) to S phase of the cell cycle by translational up-regulation of a family of mRNA transcripts that encode for components of the protein synthetic machinery. Treatment of mouse epidermal cell JB6 with H(2)O(2) generated extracellularly by glucose/glucose oxidase led to the activation of p70(S6k) and p90(Rsk) and to phosphorylation of p42(MAPK)/p44(MAPK). The activation of p70(S6k) and p90(Rsk) was dose-dependent and transient, maximal activities being in extracts treated for 15 and 30 min, respectively. Further characterization of ROS-induced activation of p70(S6k) using specific inhibitors for p70(S6k) signaling pathway, rapamycin, and wortmannin revealed that ROS acted upstream of the rapamycin-sensitive component FRAP/RAFT and wortmannin-sensitive component phosphatidylinositol 3-kinase, because both inhibitors caused the inhibition of ROS-induced p70(S6k) activity. In addition, Ca(2+) chelation also inhibited ROS-induced activation of p70(S6k), indicating that Ca(2+) is a mediator of p70(S6k) activation by ROS. However, down-regulation of 12-O-tetradecanoylphorbol-13-acetate (TPA)-responsive protein kinase C (PKC) by chronic pretreatment with TPA or a specific PKC inhibitor Ro-31-8220 did not block the activation of p70(S6k) by ROS, indicating that the activation of TPA-responsive PKC was not required for stimulation of p70(S6k) activity by H(2)O(2) in JB6 cells. Exposure of JB6 cells to platelet-derived growth factor or epidermal growth factor led to a rapid increase in H(2)O(2), phosphorylation, and activation of p70(S6k), which were antagonized by the pretreatment of catalase. Taken together, the results suggest that ROS act as a messenger in growth factor-induced p70(S6k) signaling pathway.

Androstadienes↗
PubMed1999

Neoadjuvant chemotherapy and radiation therapy compared with radiation therapy alone in advanced nasopharyngeal carcinoma.

PURPOSE: To analyze the impact of neoadjuvant chemotherapy on the treatment of locoregionally advanced nasopharyngeal carcinoma and to assess the outcomes of patients receiving such treatment. METHODS AND MATERIALS: We analyzed 137 previously untreated and histologically confirmed advanced stage nasopharyngeal carcinoma patients treated with either radiation therapy only or combined radiation therapy and chemotherapy at the Seoul National University Hospital between 1984 and 1996. The stage distribution was as follows: AJCC Stage III-21, Stage IV-61 in the radiation therapy group (RT group); AJCC Stage III-1, Stage IV-54 in neoadjuvant chemotherapy and radiation therapy group (CT/RT group). The median follow-up for surviving patients was 48 months. RESULTS: The 5-year overall survival (OS) rates were 71% for the CT/RT group and 59% for the RT group (p = 0.04). The 5-year actuarial disease-free survival (DFS) rates were 63% for the CT/RT group and 52% for the RT group (p = 0.04). Distant metastasis (DM) incidence was significantly lower in the CT/RT group. The 5-year freedom from distant metastasis rates were 84% for the CT/RT group and 66% for the RT group (p = 0.01). The incidence of locoregional failures was also lower in the CT/RT group, although this difference did not reach statistical significance (69% vs. 56%, p = 0.09) CONCLUSION: While not providing conclusive evidence, historical evidence from this institution suggests that neoadjuvant chemotherapy significantly improves both overall and the disease-free survival of patients with advanced stage nasopharyngeal carcinoma.

Adolescent↗
PubMed1999

Multiple ink nanolithography: toward a multiple-Pen nano-plotter

The formation of intricate nanostructures will require the ability to maintain surface registry during several patterning steps. A scanning probe method, dip-pen nanolithography (DPN), can be used to pattern monolayers of different organic molecules down to a 5-nanometer separation. An "overwriting" capability of DPN allows one nanostructure to be generated and the areas surrounding that nanostructure to be filled in with a second type of "ink."

Journal Article↗
PubMed1999

Chemical mechanism of ATP synthase. Magnesium plays a pivotal role in formation of the transition state where ATP is synthesized from ADP and inorganic phosphate.

The chemical mechanism by which ATP synthases catalyze the synthesis of ATP remains unknown despite the recent elucidation of the three-dimensional structures of two forms of the F(1) catalytic sector (subunit stoichiometry, alpha(3)beta(3)gammadeltaepsilon). Lacking is critical information about the chemical events taking place at the catalytic site of each beta-subunit in the transition state. In an earlier report (Ko, Y. H., Bianchet, M. A., Amzel, L.M., and Pedersen, P. L. (1997) J. Biol. Chem. 272, 18875-18881), we provided evidence for transition state formation in the presence of Mg(2+), ADP, and orthovanadate (V(i)), a photoreactive phosphate analog with a trigonal bipyramidal geometry resembling that of the gamma-P of ATP in the transition state of enzymes like myosin. In the presence of ultraviolet light and O(2,) the MgADP.V(i)-F(1) complex was cleaved within the P-loop (GGAGVGKT) of a single beta-subunit at alanine 158, implicating this residue as within contact distance of the gamma-P of ATP in the transition state. Here, we report that ADP, although facilitating transition state formation, is not essential. In the presence of Mg(2+) and V(i) alone the catalytic activity of the resultant MgV(i)-F(1) complex is inhibited to nearly the same extent as that observed for the MgADP. V(i)-F(1) complex. Inhibition is not observed with ADP, Mg(2+), or V(i) alone. Significantly, in the presence of ultraviolet light and O(2,) the MgV(i)-F(1) complex is cleaved also within the P-loop of a single beta-subunit at alanine 158 as confirmed by Western blot analyses with two different antibodies, by N-terminal sequence analyses, and by quantification of the amount of unreacted beta-subunits. These novel findings indicate that Mg(2+) plays a pivotal role in transition state formation during ATP synthesis catalyzed by ATP synthases, a role that involves both its preferential coordination with P(i) and the repositioning of the P-loop to bring the nonpolar alanine 158 into the catalytic pocket. A reaction scheme for ATP synthases depicting a role for Mg(2+) in transition state formation is proposed here for the first time.

ATP Synthetase Complexes↗
PubMed1999

Analysis of methyl tert.-butyl ether and its degradation products by direct aqueous injection onto gas chromatography with mass spectrometry or flame ionization detection systems.

A method was developed to analyze methyl tert.-butyl ether (MTBE) and its degradation products by gas chromatography with mass spectrometry (GC-MS) or flame ionization detection (FID) with direct aqueous injection. The column had dimensions of 30 m x 0.25 mm with film thickness 0.25 microm and a stationary phase of FFAP (nitroterephthalic acid-modified polyethylene glycol). The optimized GC conditions for non-acid components were as follows: carrier gas flow-rate,l mL/min; oven temperature, 35 degrees C for 5.5 min, ramped to 90 degrees C at 25 degrees C/min, then ramped to 200 degrees C at 40 degrees C/min and held at 200 degrees C for 8 min. The conditions for the acid components were: carrier gas flow-rate, 1 mL/min; oven temperature, 110 degrees C for 2 min, ramped to 150 degrees C at 10 degrees C/min, then ramped to 200 degrees C at 40 degrees C/min. The injection port contained a silanized-glass reverse-cup liner filled with Carbofrit. The minimum concentrations for the linear range for the selective ion monitoring mode were 30 to 100 microg/L, depending on the analytes. The minimum detection limit was 1 mg/L for MTBE and tert.-butanol when using FID. More components could be analyzed with the FFAP-type column than with the cyanopropylphenyl-dimethyl polysiloxane-type column.

Chromatography, Gas↗
PubMed1999

Cutting edge: activation of NK T cells by CD1d and alpha-galactosylceramide directs conventional T cells to the acquisition of a Th2 phenotype.

NK T cells recognize glycolipid Ags such as alpha-galactosylceramide (alpha-GalCer) presented by the MHC class I-like molecule CD1d. In this paper we have studied the in vivo effects of alpha-GalCer on the generation of adaptive immune responses. Treatment of mice with alpha-GalCer resulted in rapid activation of NK T cells and production of the cytokines IL-4 and IFN-gamma. However, after this initial stimulation, NK T cells became polarized for the production of IL-4. Further, as soon as 6 days after alpha-GalCer injection, a marked increase in serum IgE levels was observed. Administration of alpha-GalCer at the time of priming of mice with protein Ag resulted in the generation of Ag-specific Th2 cells and a profound increase in the production of IgE. Collectively, these findings indicate that alpha-GalCer may be useful for modulating immune responses toward a Th2 phenotype during prophylaxis and therapy.

Adjuvants, Immunologic↗
PubMed1999

Pathways for proton release during ubihydroquinone oxidation by the bc(1) complex.

Quinol oxidation by the bc(1) complex of Rhodobacter sphaeroides occurs from an enzyme-substrate complex formed between quinol bound at the Q(o) site and the iron-sulfur protein (ISP) docked at an interface on cytochrome b. From the structure of the stigmatellin-containing mitochondrial complex, we suggest that hydrogen bonds to the two quinol hydroxyl groups, from Glu-272 of cytochrome b and His-161 of the ISP, help to stabilize the enzyme-substrate complex and aid proton release. Reduction of the oxidized ISP involves H transfer from quinol. Release of the proton occurs when the acceptor chain reoxidizes the reduced ISP, after domain movement to an interface on cytochrome c(1). Effects of mutations to the ISP that change the redox potential and/or the pK on the oxidized form support this mechanism. Structures for the complex in the presence of inhibitors show two different orientations of Glu-272. In stigmatellin-containing crystals, the side chain points into the site, to hydrogen bond with a ring hydroxyl, while His-161 hydrogen bonds to the carbonyl group. In the native structure, or crystals containing myxothiazol or beta-methoxyacrylate-type inhibitors, the Glu-272 side chain is rotated to point out of the site, to the surface of an external aqueous channel. Effects of mutation at this residue suggest that this group is involved in ligation of stigmatellin and quinol, but not quinone, and that the carboxylate function is essential for rapid turnover. H(+) transfer from semiquinone to the carboxylate side chain and rotation to the position found in the myxothiazol structure provide a pathway for release of the second proton.

Amino Acid Sequence↗
PubMed1999

IL-7 up-regulates IL-4 production by splenic NK1.1+ and NK1.1- MHC class I-like/CD1-dependent CD4+ T cells.

NK T cells are an unusual subset of T lymphocytes. They express NK1. 1 Ag, are CD1 restricted, and highly skewed toward Vbeta8 for their TCR usage. They express the unique potential to produce large amounts of IL-4 and IFN-gamma immediately upon TCR cross-linking. We previously showed in the thymus that the NK T subset requires IL-7 for its functional maturation. In this study, we analyzed whether IL-7 was capable of regulating the production of IL-4 and IFN-gamma by the discrete NK T subset of CD4+ cells in the periphery. Two hours after injection of IL-7 into mice, or after a 4-h exposure to IL-7 in vitro, IL-4 production by CD4+ cells in response to anti-TCR-alphabeta is markedly increased. In contrast, IFN-gamma production remains essentially unchanged. In beta2-microglobulin- and CD1-deficient mice, which lack NK T cells, IL-7 treatment does not reestablish normal levels of IL-4 by CD4+ T cells. Moreover, we observe that in wild-type mice, the memory phenotype (CD62L-CD44+) CD4+ T cells responsible for IL-4 production are not only NK1.1+ cells, but also NK1.1- cells. This NK1.1-IL-4-producing subset shares three important characteristics with NK T cells: 1) Vbeta8 skewing; 2) CD1 restriction as demonstrated by their absence in CD1-deficient mice and relative overexpression in MHC II null mice; 3) sensitivity to IL-7 in terms of IL-4 production. In conclusion, the present study provides evidence that CD4+MHC class I-like-dependent T cell populations include not only NK1.1+ cells, but also NK1.1- cells, and that these two subsets are biased toward IL-4 production by IL-7.

Animals↗
PubMed1999

Natural killer cells determine development of allergen-induced eosinophilic airway inflammation in mice.

The earliest contact between antigen and the innate immune system is thought to direct the subsequent antigen-specific T cell response. We hypothesized that cells of the innate immune system, such as natural killer (NK) cells, NK1.1(+) T cells (NKT cells), and gamma/delta T cells, may regulate the development of allergic airway disease. We demonstrate here that depletion of NK1.1(+) cells (NK cells and NKT cells) before immunization inhibits pulmonary eosinophil and CD3(+) T cell infiltration as well as increased levels of interleukin (IL)-4, IL-5, and IL-12 in bronchoalveolar lavage fluid in a murine model of allergic asthma. Moreover, systemic allergen-specific immunoglobulin (Ig)E and IgG2a levels and the number of IL-4 and interferon gamma-producing splenic cells were diminished in mice depleted of NK1.1(+) cells before the priming regime. Depletion of NK1.1(+) cells during the challenge period only did not influence pulmonary eosinophilic inflammation. CD1d1 mutant mice, deficient in NKT cells but with normal NK cells, developed lung tissue eosinophilia and allergen-specific IgE levels not different from those observed in wild-type mice. Mice deficient in gamma/delta T cells showed a mild attenuation of lung tissue eosinophilia in this model. Taken together, these findings suggest a critical role of NK cells, but not of NKT cells, for the development of allergen-induced airway inflammation, and that this effect of NK cells is exerted during the immunization. If translatable to humans, these data suggest that NK cells may be critically important for deciding whether allergic eosinophilic airway disease will develop. These observations are also compatible with a pathogenic role for the increased NK cell activity observed in human asthma.

Allergens↗