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1 if19a into autophagosomes for degradation in airway epithelial cells.
2 plified itself and ST2 protein expression in airway epithelial cells.
3 r protein and Cas RNP delivery to refractory airway epithelial cells.
4  well as their ability to replicate in human airway epithelial cells.
5 g this innate immune response in human small airway epithelial cells.
6 sm of a discrete population of multiciliated airway epithelial cells.
7 2 strain three times in differentiated swine airway epithelial cells.
8 levels of silencing, particularly in primary airway epithelial cells.
9 fluenza virus replication in human bronchial airway epithelial cells.
10  various cell types, including primary human airway epithelial cells.
11 ocrine cells (PNECs) are the only innervated airway epithelial cells.
12 compartment or selectively lacking the GR in airway epithelial cells.
13 ncreases oxidative and nitrosative stress in airway epithelial cells.
14 odulation following a mechanical stimulus in airway epithelial cells.
15 cocorticoids in regulation of BK channels in airway epithelial cells.
16 2 in Clara cell secretory protein-expressing airway epithelial cells.
17 rus spreads rapidly and efficiently in human airway epithelial cells.
18 ced CXCL-10 via IRAK-1 depletion at least in airway epithelial cells.
19 s that are infectious in well-differentiated airway epithelial cells.
20  induced expression of both ST2 and IL-33 in airway epithelial cells.
21 ation of beta-catenin to induce EMT in human airway epithelial cells.
22 n of noggin, BAMBI, and FSTL1 in human small airway epithelial cells.
23 rity to the transcriptome for intrapulmonary airway epithelial cells.
24 Il33, and muc5ac mRNA expression in cultured airway epithelial cells.
25 E shRNA inhibited HMGB1-induced EMT in human airway epithelial cells.
26 EMT-related gene expression in human primary-airway epithelial cells.
27 excessive levels at the apical surface of CF airway epithelial cells.
28 cle DNA with plasmid DNA in transfections of airway epithelial cells.
29 P-regulated ion and fluid transport in human airway epithelial cells.
30 induced IL-33 in the induction of CXCL-10 in airway epithelial cells.
31 is study, we deleted the mouse Kif3a gene in airway epithelial cells.
32 s and dendritic cells, transfer infection to airway epithelial cells.
33  given the strict tropism of HBoV1 for human airway epithelial cells.
34 atory effects of R507 were analyzed on human airway epithelial cells.
35 y dependent on IL-33/ST2/IRAK-1 signaling in airway epithelial cells.
36 type-II interferon-gamma (IFNgamma) in human airway epithelial cells.
37 ,3-linked sialic acids on complex glycans on airway epithelial cells.
38 y observed in lung airway using primary lung airway epithelial cells.
39 es but can also inhibit influenza entry into airway epithelial cells.
40 ell-differentiated primary cultures of human airway epithelial cells.
41 d release of chemokines, including CCL20, by airway epithelial cells.
42 on TNF-regulated gene expression in cultured airway epithelial cells.
43 d its degradation in the proteasome of human airway epithelial cells.
44 racts with RV RNA and poly(I.C) in polarized airway epithelial cells.
45  a role in proinflammatory gene induction in airway epithelial cells.
46 ected differentiation of hPSCs into lung and airway epithelial cells.
47 ion are due to infection of nectin4-positive airway epithelial cells.
48 e and regulator of inflammatory signaling in airway epithelial cells.
49 ansepithelial resistance (R(T)) in polarized airway epithelial cells.
50  shedding of the ADAM17 substrate TNFR1 from airway epithelial cells.
51 CFTR by attenuating its endocytosis in human airway epithelial cells.
52 rate with IL-13 in the induction of IL-25 in airway epithelial cells.
53 g a higher proliferative capacity than large airway epithelial cells.
54 primarily on the apical surfaces of ciliated airway epithelial cells.
55  and increased TMPRSS2 expression ex vivo in airway epithelial cells.
56  screen and confirmed in primary human small airway epithelial cells.
57 P expression in edited 16HBE14o- and primary airway epithelial cells.
58  rs2076295 regulates DSP expression in human airway epithelial cells.
59 esenchymal transition in primary human small airway epithelial cells.
60 ous studies have focused on abnormalities in airway epithelial cells.
61  rhinovirus (RV)-induced IFN response in the airway epithelial cells.
62 ttachment to sialosides and entry into human airway epithelial cells.
63 on, normalized RV-induced IFN levels in COPD airway epithelial cells.
64 dent of rhythmic glucocorticoid signaling in airway epithelial cells.
65 -liquid interface cultures of differentiated airway epithelial cells.
66 alling pathways triggered by the allergen in airway epithelial cells.
67 e of DMSe-derived SOA as a stressor in human airway epithelial cells.
68                           In addition, human airway epithelial cells (16HBE) were challenged with HDM
69  action of extracellularly released HMGB1 in airway epithelial cells (A549 and small airway epithelia
70               Selective depletion of CSF1 in airway epithelial cells abolished the production of alle
71               Thus, HBoV1 infection of human airway epithelial cells activates antiapoptotic proteins
72 s triggered by rDer p 5 were investigated in airway epithelial cell activation assays in vitro.
73  basophil degranulation assays, and in vitro airway epithelial cell activation assays.
74            Bronchiolitis is characterized by airway epithelial cell (AEC) death; however, the mode of
75 status in early pregnancy is associated with airway epithelial cell (AEC) responses in new born infan
76                                              Airway epithelial cell (AEC) signaling might regulate HL
77                                              Airway epithelial cells (AEC) are increasingly recognize
78 that air-liquid interface cultures of murine airway epithelial cells (AECs) also actively synthesize
79 a responses in vitro in primary human infant airway epithelial cells (AECs) and in vivo using nasal a
80  is necessary for HRV-C infection of primary airway epithelial cells (AECs) and to identify molecular
81                                    Pulmonary airway epithelial cells (AECs) form a critical interface
82      Innate immune responses to allergens by airway epithelial cells (AECs) help initiate and propaga
83   DNA methylation (DNAm) profiles in central airway epithelial cells (AECs) may play a key role in pa
84                                              Airway epithelial cells (AECs) play a critical role in t
85          In this study, we looked at how the airway epithelial cells (AECs) regulate the flagellin-de
86                             Challenging lung airway epithelial cells (AECs) with LBCs decreased (by m
87 DNA methylation profiles of cultured primary airway epithelial cells (AECs) would differ between cell
88                                           In airway epithelial cells (AECs), stimulation of PAR2 by a
89 of chronic asthma and in vitro human primary airway epithelial cells (AECs).
90 ate and maintain intracellular H2S levels in airway epithelial cells (AECs).
91 rface media than in media with mock-infected airway epithelial cells (AECs).
92                                     In human airway epithelial cells, alternative splicing of the IL-
93  of P. aeruginosa grown in sputum gels using airway epithelial cells and a murine infection model.
94 sed expression of inhibitory ligands by both airway epithelial cells and APCs, further establishing a
95 lly differentiated cultures of primary human airway epithelial cells and cocultures with Pseudomonas
96 genic mice conditionally expressing Foxa3 in airway epithelial cells and developed human bronchial ep
97 ent data has highlighted the cross talk with airway epithelial cells and environmental factors (aller
98  and osmotic stress were assessed in primary airway epithelial cells and ex vivo murine lung tissue.
99              Influenza A virus (IAV) targets airway epithelial cells and exploits the host cell machi
100 erferon-stimulated gene (ISG) in vitro using airway epithelial cells and extend our findings to in vi
101  the effects of coculture of NTHI with human airway epithelial cells and heme availability on Tfp exp
102 l role for p52 in cell survival/apoptosis of airway epithelial cells and implicate noncanonical NF-ka
103 -beta2, periostin and endothelin-1, by human airway epithelial cells and in mice exposed to A fumigat
104 n expression was determined in primary human airway epithelial cells and in mice.
105  expression of pro-inflammatory mediators in airway epithelial cells and in the lung of mice by enhan
106 as attenuated in two models of primary human airway epithelial cells and in the upper and lower airwa
107 human surfactant protein A and annexin A2 on airway epithelial cells and is internalized, leading to
108 ssion in bronchial biopsies was increased in airway epithelial cells and lamina propria inflammatory
109 sociated kinase-1 (IRAK-1) depletion in both airway epithelial cells and macrophages.
110 livery to cultured human well-differentiated airway epithelial cells and mouse lungs with engineered
111 but lowers mRNA levels in O(3)-exposed human airway epithelial cells and mouse lungs.
112 on quantitative trait loci of TMEM9 in nasal airway epithelial cells and MROH3P in esophagus mucosa.
113 s for presentation at the plasma membrane of airway epithelial cells and recognition by CD8(+) T cell
114 get the master IFN signal regulator STAT1 in airway epithelial cells and tested these mice for contro
115  severe asthma and primarily associated with airway epithelial cells and tissue neutrophils.
116 ease inhibitor (SLPI), which is expressed by airway epithelial cells, and IFN-gamma inversely correla
117 lveolar macrophages, monocytes, neutrophils, airway epithelial cells, and in mouse lungs.
118 ctivation was assessed in human neutrophils, airway epithelial cells, and peripheral blood monocytes
119 transcription factor NF-kappaB in conducting airway epithelial cells, and used a combination of in vi
120 ndicating that Runx3 plays a crucial role in airway epithelial cell apoptosis induced by IAV infectio
121 s study, we investigated the hypothesis that airway epithelial cells are a source of CTSS, and mechan
122                            However, although airway epithelial cells are frontline sentinels in detec
123  on gene expression changes in BEAS-2B human airway epithelial cells are reported and discussed in re
124                               Although human airway epithelial cells are the main target of respirato
125                                              Airway epithelial cells are the major target for rhinovi
126 ibroblasts and altered relative frequency of airway epithelial cells as hallmarks of lung aging.
127 iptome-wide gene expression changes in human airway epithelial cells (BEAS-2B) after exposure to DMSe
128  of isoprene SOA on gene expression in human airway epithelial cells (BEAS-2B) through an air-liquid
129 accinia virus (VACV) initially replicates in airway epithelial cells before spreading to secondary si
130 t shown to preserve the barrier integrity of airway epithelial cells better than the human AMP LL-37.
131                                           In airway epithelial cells, blocking TLR2 enhanced RV-induc
132                 Using cell lines and primary airway epithelial cells (both submerged and well-differe
133 on, and competitive fitness in primary human airway epithelial cells but maintains similar morphology
134 tic lesions in type 2 CPAM occur not only in airway epithelial cells, but also in adjacent mesenchyma
135 ic mucin MUC1 is elevated by inflammation in airway epithelial cells, but the contributions of MUC1 t
136 ductance regulator (CFTR) abundance in human airway epithelial cells by a mechanism that requires ser
137        This study indicates that HBoV1 kills airway epithelial cells by activating genes that suppres
138 roposed to be critical for host defense, and airway epithelial cell capacity for IFN signal transduct
139 inished ENaC-mediated Na(+) absorption in CF airway epithelial cells caused by internalization of a p
140                    Mechanical stimulation of airway epithelial cells causes apical release of ATP, wh
141 dexamethasone to modulate gene expression in airway epithelial cells coincided with its potency to re
142 thylation levels from DNA derived from nasal airway epithelial cells collected from 12 African Americ
143                  Under normal circumstances, airway epithelial cells connected by tight junctions sec
144 s upon pharmacological activation of AMPK in airway epithelial cells correlated with elongated cilia
145 sulatum-infected canine and feline lungs and airway epithelial cells could serve as higher animal mod
146 and its expression was associated with total airway epithelial cell count and thickness.
147 lled direct pH measurements in primary human airway epithelial cell culture models, which also sugges
148 sions: Sphingolipid metabolism is altered in airway epithelial cells cultured from people with cystic
149                       Differentiated primary airway epithelial cell cultures (F508del homozygotes) we
150  pulmonary ACE2 expression in vitro in human airway epithelial cell cultures and in vivo in mouse mod
151 inistration attenuated expression of ACE2 in airway epithelial cell cultures from patients with COPD
152 ection in this model system found that human airway epithelial cell cultures induce a strong proinfla
153                    Exposure of primary human airway epithelial cell cultures to IFN-gamma for 48 h di
154                             Human and murine airway epithelial cell cultures were also infected with
155 nfant and adult lungs, rhesus monkey primary airway epithelial cell cultures were infected with pande
156               We also examined if NETs cause airway epithelial cell damage that can be prevented by D
157 t at both temperatures, NTHI cocultured with airway epithelial cells demonstrated significantly great
158 acking MIWI2 exhibited an altered balance of airway epithelial cells, demonstrating fewer multiciliat
159 reatment-resistant asthma via neutrophil and airway epithelial cell-dependent pathways.
160 tegy is verified in intestinal organoids and airway epithelial cells derived from CF patients carryin
161 m donated blood and (ii) well-differentiated airway epithelial cells derived from donor lungs.
162  of different CFTR-modulating drugs in human airway epithelial cells derived from subjects with cysti
163 initiation of TH 2 responses is regulated by airway epithelial cell-derived factors, including TRAIL
164                        In siRNA-MUC4 BEAS-2B airway epithelial cells dexamethasone produced higher an
165                 Further analysis showed that airway epithelial cells did not produce glucocorticoids
166                   Finally, HMGB1 released by airway epithelial cells due to RSV infection appears to
167 ve Rhizopus and Mucor strains and with human airway epithelial cells during fungal invasion, to revea
168  to potentiate its cytoprotective signals in airway epithelial cells during influenza infection.
169                       Knockdown of TRIM29 in airway epithelial cells enhances type I interferon produ
170 gulated after allergen challenge, notably in airway epithelial cells, eosinophils, and neutrophils.
171                 Here we report that in human airway epithelial cells Epstein-Barr virus induces TRIM2
172                                              Airway epithelial cells express FOXO3a and play an impor
173                                        Human airway epithelial cells express pannexin 1 (Panx1) chann
174 suggested that, when approximately 10-50% of airway epithelial cells expressed CFTR, they generated n
175 r work in IL-13 biology to determine whether airway epithelial cell expression of 2 key mediators cri
176                                              Airway epithelial cells form a barrier to the outside wo
177                                  In cultured airway epithelial cells, FP treatment inhibited IL-13-in
178  performed RNA sequencing on upper and lower airway epithelial cells from 63 children with or without
179 ntaining gene expression data from nasal and airway epithelial cells from children and adults with as
180 e proof of concept that miR-200b-3p protects airway epithelial cells from EMT.
181      Studies using pendrin knockout mice and airway epithelial cells from hearing-impaired subjects w
182 t in well-differentiated primary cultures of airway epithelial cells from human donors (HAE), MV infe
183 d to primary cultures of well-differentiated airway epithelial cells from human donors (HAE).
184  accumulate on the luminal membrane of upper-airway epithelial cells from mice and humans with CF.
185 ell-differentiated primary cultures of human airway epithelial cells from non-CF and CF subjects, tre
186 E2 and TMPRSS2 expression ex vivo in primary airway epithelial cells from participants with and witho
187                                              Airway epithelial cell gene expression from 155 subjects
188  Of these participants, 100 had accompanying airway epithelial cell gene expression.
189                                     Lung and airway epithelial cells generated in vitro from human pl
190 al infection and suggest a specific role for airway epithelial cells given the limitation of EV-D68 r
191 ne IL-13 on beta2AR desensitization in human airway epithelial cells (HAECs) and determine whether 15
192  Under Type 2 inflammatory conditions, human airway epithelial cells (HAECs) generate proferroptotic
193 ce of AC6, we demonstrated that AC6 knockout airway epithelial cells have longer cilia compared with
194  using primary, fully redifferentiated human airway epithelial cells homozygous for F508del and in vi
195 alveolar macrophages and primary human small airway epithelial cells (HSAEpCs) from patients with COP
196                       RSV infection of human airway epithelial cell, human lung fibroblast, and U937
197 s were shown to transform immortalized human airway epithelial cells in a sorafenib-sensitive manner.
198 -13 modulates ACE2 and TMPRSS2 expression in airway epithelial cells in asthma and atopy.
199 egulatory mechanisms of ferroptotic death in airway epithelial cells in asthma, kidney epithelial cel
200 we show that expression of SPDEF or FOXA3 in airway epithelial cells in neonatal mice caused goblet c
201            Using ex vivo modeling of primary airway epithelial cells in organotypic coculture with ma
202 was significantly increased in the nasal and airway epithelial cells in type 2 asthma and allergic rh
203 protein either incubated with cultured human airway epithelial cells in vitro, or provided as an aero
204 bits SARS-CoV-2 replication in primary human airway epithelial cells in vitro-both prophylactic and t
205 ir effects on innate interferon responses of airway epithelial cells in vitro.
206 f tools to analyze IFN signaling specific to airway epithelial cells in vivo.
207 3(Delta2-3/Delta2-3)/CC10 mice as well as in airway epithelial cells in which ORMDL3 was inhibited wi
208        Knocking out these genes in mammalian airway epithelial cells increased levels of infection.
209 RNA isolated from primary normal human small airway epithelial cells indicated that IL-17A (100 ng/ml
210 g results showed that RSV infection of human airway epithelial cells induced a significant release of
211    In addition, conditioned media from human airway epithelial cells infected with Pseudomonas aerugi
212 he transcriptional response of primary mouse airway epithelial cells infected with rhinovirus at 33 d
213 hagy as has been the reported scenario in CF airway epithelial cells, infectious diseases, and lysoso
214 ase 6 (AC6), a highly abundant AC isoform in airway epithelial cells, inhibits degradation of Kif19a
215  IL-1beta secretion from monocytes and cause airway epithelial cell injury, but the role of eDNA, NET
216          The delivery of biologic cargoes to airway epithelial cells is challenging due to the formid
217 hat stimulation of EGFR activation by ATP in airway epithelial cells is closely associated with dynam
218 ivity of Vero cell-derived virus for primary airway epithelial cells is increased 5-fold if the virus
219   However, the role of HMGB1 in EMT of human airway epithelial cells is still unclear.
220 he potential dysregulation of methylation in airway epithelial cells is unknown.
221 Ns, and this pathway is dysregulated in COPD airway epithelial cells, leading to exaggerated IFN prod
222  observations, deletion of IGF-1 receptor in airway epithelial cells led to exacerbated lung inflamma
223 oreover, using both clonal cells and a human airway epithelial cell line endogenously expressing beta
224    siRNA-based knock down of these TFs in an airway epithelial cell line model demonstrated significa
225 -/-) mice and a stable FOXO3a knockout human airway epithelial cell line.
226 s on airway branching and differentiation of airway epithelial cell lineages.
227 uated wound closure and mucous expression in airway epithelial cell lines.
228               IL-13 levels were increased in airway epithelial cells, macrophages, type 2 innate lymp
229           When applied directly to polarized airway epithelial cells, mature aCif triggers a reductio
230 ed interferon response to viral infection by airway epithelial cells may be a mechanism leading to lu
231 d, ozone (O3) interacts with cholesterols of airway epithelial cell membranes or the lung-lining flui
232 es DSP expression and the function of DSP in airway epithelial cells.Methods: Using CRISPR (clustered
233 ects on asthma pathophysiology, including on airway epithelial cells, mucus hypersecretion, and airwa
234                                     Thus, in airway epithelial cells, MV spread requires the nectin-4
235  A549 cells and were all cytotoxic for small airway epithelial cells, NCI-H441, and normal human lung
236                                  Using human airway epithelial cells obtained from young children, we
237 so used to reconstitute ORMDL3 expression in airway epithelial cells of Ormdl3 knockout mice.
238 bout the interactions of M. haemolytica with airway epithelial cells of the respiratory mucosa which
239  and repair in large (LAEC) and small (SAEC) airway epithelial cells of transplant patients.
240                     Cultured human or murine airway epithelial cells or mice were subjected to acute
241  to supernatants from IL-1beta-stimulated CF airway epithelial cells (P < .01).
242               (2020) describe a novel distal airway epithelial cell population with high regenerative
243      Active H(+) and HCO(3) (-) secretion by airway epithelial cells produce an ASL that is acidic co
244  Together, these results suggest beta2ARs on airway epithelial cells promote the asthma phenotype and
245                        The results show that airway epithelial cells regulate local immune responses,
246                                   Therefore, airway epithelial cells release less ATP in response to
247                 Many cells, including murine airway epithelial cells, respond to a variety of inflamm
248 hat hRV infection of polarized primary human airway epithelial cells resulted in increased adherence
249  channel (VDCC)-intervened calcium influx in airway epithelial cells, resulting in a rapid IGF2 secre
250 nt stem cells (iPSC) from normal human small airway epithelial cells (SAEC) to investigate epigenetic
251 e CS on the differentiation of primary small airway epithelial cells (SAEC) were investigated, using
252 e physiologically relevant cell lines--small airway epithelial cells (SAECs), macrophages (THP-1 cell
253 nce in both human lung fibroblasts and small airway epithelial cells (SAECs).
254 ucing factor in the RSV-infected human small airway epithelial cell secretome and was differentially
255 pregnancy and aspects of stimulated neonatal airway epithelial cell secretory function that may in tu
256                                   FOXO3a K/O airway epithelial cells show attenuated IFN responses to
257                                         COPD airway epithelial cells showed attenuated IL-8 responses
258              Genome-wide effect of pulmonary airway epithelial cell-specific Bmal1 deletion.
259 regulating antiviral responses, we generated airway epithelial cell-specific Foxo3a knockout (Scga1b1
260             In cultured normal human primary airway epithelial cells, ST2 overexpression (OE) increas
261                 We report location-dependent airway epithelial cell states and a novel subset of tiss
262 ally, experiments using human cord blood and airway epithelial cells suggested that DEP might induce
263 nt-resistant membrane fraction prepared from airway epithelial cells, suggesting that it may partitio
264 gamycin and quercetin is lower in CF-derived airway epithelial cells than in non-CF cells.
265 monary neuroendocrine cells (PNECs) are rare airway epithelial cells that also uniquely harbor neuron
266 ntrinsic developmental differences in infant airway epithelial cells that may contribute to the incre
267 n vitro studies, NETs caused cytotoxicity in airway epithelial cells that was prevented by disruption
268 ed G protein are less infectious for primary airway epithelial cells, the natural RSV target.
269  also demonstrated that compared with normal airway epithelial cells, those from patients with chroni
270 MiR-570-3p is induced by oxidative stress in airway epithelial cells through p38 MAP kinase-c-Jun sig
271 nd following short-term in vitro exposure of airway epithelial cells to cigarette smoke (FDR < 0.05).
272 l type 2 (Th2) cytokine, transforms cultured airway epithelial cells to goblet cells, and this is not
273                         TNF signaled through airway epithelial cells to reprogram them and promote Th
274 adapt the protocol to expose living ciliated airway epithelial cells to smoke generated by electronic
275 and regulating the innate immune response of airway epithelial cells to viral infection.
276 moke and other environmental stimuli acts on airways epithelial cells to induce neutrophil chemotaxin
277 1 in airway epithelial cells (A549 and small airway epithelial cells) to establish its role in RSV in
278  the susceptibility of cells, especially the airway epithelial cells, to hRSV infection.
279 bunit of NF-kappaB, and RNA polymerase II in airway epithelial cells treated with dexamethasone, TNF,
280                                              Airway epithelial cells treated with IL-4 followed by AD
281 was the only PYHIN protein expressed in both airway epithelial cell types.
282 protein connexin43 (Cx43) in polarized human airway epithelial cells upon infection by PAO1.
283 ibition of elevated miR-570-3p in COPD small airway epithelial cells, using an antagomir, restores si
284  steroid-resistant inflammatory signature in airway epithelial cells via constitutively expressed LTb
285  to date suggest that these viruses kill the airway epithelial cells via the apoptotic or necrotic pa
286 x-dependent regulation of EGFR activation in airway epithelial cells was found to strongly depend on
287 sis of Clara cell secretory protein-positive airway epithelial cells was observed in transgenic mice
288          While replication kinetics in human airway epithelial cells was on par with that of seasonal
289  proteins unique to RSV-infected human small airway epithelial cells was regulated by the transcripti
290  global run-on sequencing (GRO-seq) in human airway epithelial cells, we show that glucocorticoid sig
291                          Numbers of necrotic airway epithelial cells were elevated and correlated wit
292 on IFN-gamma treatment, fully differentiated airway epithelial cells were exposed to ammonium chlorid
293                                              Airway epithelial cells were obtained from bronchial and
294                                              Airway epithelial cells, which are the first line of def
295 obustly localizes within the motile cilia of airway epithelial cells, which likely represents the ini
296         Here we show that infection of human airway epithelial cells with Streptococcus pneumoniae le
297 he cells express markers of various lung and airway epithelial cells, with a predominance of cells id
298 infection down-regulated FOXA2 expression in airway epithelial cells, with concomitant overexpression
299 y(I:C) to selectively upregulate IFN-beta in airway epithelial cells without a concomitant inflammato
300 s feasible to augment IFN-beta production in airway epithelial cells without excessive costimulation

 
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