ライフサイエンスコーパス: Paneth cell

1 em cell numbers through pSTAT3 activation in Paneth cells.

2 ined by high and low proportions of abnormal Paneth cells.

3 associated with pathogenesis of CD, such as Paneth cells.

4 al Crohn's disease as a specific disorder of Paneth cells.

5 resulted in dysbiosis and the elimination of Paneth cells.

6 quired for the differentiation of goblet and Paneth cells.

7 netic risk factors of Crohn's disease affect Paneth cells.

8 g fibroblasts, bacteria, lymphoid cells, and Paneth cells.

9 ion of Wnt3 allowed growth in the absence of Paneth cells.

10 C57BL/6 background) to have deficiencies in Paneth cells.

11 nd of HD5, the other alpha-defensin of human Paneth cells.

12 r4/5 ligand R-spondin to induce formation of Paneth cells.

13 ted intact Wnt signaling despite the loss of Paneth cells.

14 ains Lgr5(+) stem cells, it does not contain Paneth cells.

15 ng and unique patterns of gene expression in Paneth cells.

16 ntibacterial function of enterocytes such as paneth cells.

17 stine, with no changes observed in goblet or Paneth cells.

18 nous population of terminally differentiated Paneth cells.

19 ypt regeneration, and differentiation toward Paneth cells.

20 seroreactivity against secretory granules of Paneth cells.

21 ed receptor 5) stem cells and Wnt3-producing Paneth cells.

22 nsins are antimicrobial peptides secreted by Paneth cells.

23 sponse against enteric defensins and loss of Paneth cells.

24 a decrease in secretory enteroendocrine and Paneth cells.

25 arrow-derived cells and epithelial secretory Paneth cells.

26 dditive effect on the proportion of abnormal Paneth cells.

27 ight affect stem cell niches directly or via paneth cells.

28 on into mature enterocytes, goblet cells and Paneth cells.

29 reduced signaling activities; maturation of Paneth cells - a Wnt-dependent cell type - is severely a

30 selectively important for the biology of the Paneth cell, a specialized epithelial cell that function

31 t of tumors containing an expanded number of Paneth cells, a hallmark of deregulated Wnt signaling, a

32 Here we find that Paneth cells, a key constituent of the mammalian intesti

33 Normal mouse colon epithelium lacks Paneth cells, a key small intestine niche cell type, and

34 It also reduced Paneth cell ablation-induced NEC and prevented dithizone

35 d localize expression of lysozyme and assess Paneth cell abundance, apoptosis, and the expression of

36 MP7(-/-) mice lack mature alpha-defensins in Paneth cells, accumulating unprocessed precursors for se

37 ceptibility loci for CD and how these affect Paneth cell activity.

38 from Atoh1 mutant mice did not grow or form Paneth cells; addition of Wnt3 allowed growth in the abs

39 f IL-17A messenger RNA (mRNA) and protein in Paneth cells after hepatic IR with laser capture dissect

40 xpression in intestinal epithelial cells and Paneth cells along the entire length of the small intest

41 hese animals exhibited diminished intestinal Paneth cell alpha-cryptdin 5 and 7 expression.

42 hout the intestinal tract, and expression of Paneth cell alpha-cryptdins and beta-defensins was deter

43 ensin Arg content, all Arg residues in mouse Paneth cell alpha-defensin cryptdin 4 (Crp4) and rhesus

44 Although Paneth cell alpha-defensin deficiency is associated with

45 rom healthy controls restored the attenuated Paneth cell alpha-defensin expression characteristic of

46 The properties of HD6, an enigmatic Paneth cell alpha-defensin, are contrasted with those of

47 In the mammalian small intestine, Paneth cell alpha-defensins are antimicrobial peptides t

48 Proteomic studies show that five abundant Paneth cell alpha-defensins in C57BL/6 mice are strain s

49 Paneth cell alpha-defensins mediate host defense and hom

50 or necrosis factor-alpha-induced shock, that Paneth cell alpha-defensins modulate the composition of

51 Thus, Paneth cell alpha-defensins secreted into the small inte

52 Mouse Paneth cells also express alpha-defensin-related Defcr-r

53 iferation and numbers of enteroendocrine and Paneth cells, an increase in numbers of goblet-like cell

54 pression of bone stromal antigen 1 (Bst1) in Paneth cells-an ectoenzyme that produces the paracrine f

55 cKit marks small intestinal Paneth cells and a subset of colonic goblet cells that a

56 tg16l1(f/f) x Villin-cre mice also had fewer Paneth cells and abnormal granule morphology, leading to

57 with maintaining equipotent stem cells (SC), Paneth cells and common goblet-Paneth cell progenitors (

58 oids lacking ATG16L1 reproduced this loss in Paneth cells and displayed TNFalpha-mediated necroptosis

59 ction caused an increase in the abundance of Paneth cells and enterocytes, and broad activation of an

60 ithelium is essential for preventing loss of Paneth cells and exaggerated cell death in animal models

61 ane localization of Gpr177 in Rab8a knockout Paneth cells and fibroblasts.

62 Levels of HD-5 in Paneth cells and ileostomy fluid from control and CD pat

63 We also observed loss of Paneth cells and increases in goblet cell numbers.

64 intestine, CD166 was observed on crypt-based Paneth cells and intervening crypt-based columnar cells

65 hat both the number and relative position of Paneth cells and Lgr5+ cells are important for fission.

66 lts demonstrate that LPLUNC1 is expressed in Paneth cells and likely plays a role in modulating host

67 Caspase-8 controls necroptosis of Paneth cells and potentially the death of intestinal epi

68 poptosis, villus atrophy, loss of goblet and Paneth cells and premature death in mice.

69 rved an inverse correlation between abnormal Paneth cells and presence of granuloma.

70 uced alpha-defensin production by intestinal Paneth cells and that such impairment leads to loss of h

71 ompanied by increases in the total number of Paneth cells and the frequency of mitotic events in cryp

72 e is known about the distribution of colonic Paneth cells and the occurrence of PCM in a paediatric p

73 lium regulates crypt homeostasis through the Paneth cells and the Wnt signaling pathway.

74 Some patients with APECED lacked Paneth cells and were seropositive for defensin-specific

75 enterocytes and goblet, enteroendocrine, and Paneth cells) and are physiologically active based on re

76 robial peptide expressed in small intestinal Paneth cells, and alterations in HD-5 expression may be

77 etion and antimicrobial peptides produced by Paneth cells, and downregulation or anergy of the innate

78 including crypt base columnar stem cells and Paneth cells, and in underlying stroma.

79 or clonal expansion and differentiation into Paneth cells, and increased apoptosis.

80 f rapamycin complex 1 (mTORC1) signalling in Paneth cells, and the ISC-enhancing effects of calorie r

81 yme content, the number of lysozyme-positive Paneth cells, and the number of granules per Paneth cell

82 is mainly characterized by IgA secretion and Paneth cell antimicrobial function.

83 Compromised Paneth cell antimicrobial host defense seems to predispo

84 wn to reduce intestine luminal levels of the Paneth cell antimicrobial molecule secretory phospholipa

85 The decrease in Paneth cell antimicrobials was most pronounced in the il

86 NF-kappaB) essential modulator (NEMO) caused Paneth cell apoptosis and impaired antimicrobial factor

87 A, c-Rel, and RelB deficiency in IECs caused Paneth cell apoptosis but not colitis, suggesting that N

88 Paneth cells are a secretory epithelial lineage that rel

89 Thus, Paneth cells are dispensable for survival, proliferation

90 Because Paneth cells are easy to identify and quantify by light

91 Paneth cells are found in the proximal but not the dista

92 Paneth cells are highly specialized epithelial cells of

93 e higher stiffness and increased adhesion of Paneth cells are involved in determining the site of fis

94 lineage ablation previously had implied that Paneth cells are nonessential constituents of the stem-c

95 This recent literature identifies Paneth cells as particularly sensitive targets of endopl

96 ensors of microbial presence or cell injury, Paneth cells as the main epithelial cell type that secre

97 on average at the +4 position just above the Paneth cells, as putative stem cells.

98 ped visceral hypersensitivity and defects in Paneth cells, as reported from rats, compared with mice

99 investigated whether specific phenotypes of Paneth cells associated with particular genetic suscepti

100 However, the clinical importance of Paneth cells' associations with synchronous advanced ade

101 Lower numbers of Paneth cells at diagnosis correlated with clinically mor

102 Paneth cells at the base of small intestinal crypts of L

103 Paneth cells at the base of small intestinal crypts secr

104 We found that complete loss of Paneth cells attributable to Math1 deficiency did not pe

105 appearance), and augmented intestinal crypt Paneth cell bactericidal potency via a mechanism that ma

106 Dysfunction of Paneth cell biology contributes to the pathogenesis of c

107 ptor was restricted to the basal membrane of Paneth cells both in vitro and in vivo and that the cryp

108 Calorie intake regulates mTORC1 in Paneth cells, but not ISCs, and forced activation of mTO

109 Secretory autophagy was triggered in Paneth cells by bacteria-induced endoplasmic reticulum (

110 We now show that removal of Paneth cells by Math1 mutation inhibits RZ(-/-) tumor fo

111 lps to 'build' an ISC niche by expanding the Paneth cell compartment and directly inducing Sox9, whic

112 blet cell Mucin 2, dramatic expansion of the Paneth cell compartment, abnormal Paneth cell localizati

113 ever, previous mouse models failed to remove Paneth cells completely or permanently; defining the int

114 st to the adenomas without Paneth cells, the Paneth cell-containing adenomas at distal colorectum wer

115 no statistical significance was reached for Paneth cell-containing proximal colorectal adenomas (P =

116 BACKGROUND & AIMS: Paneth cells contribute to the small intestinal niche of

117 Paneth cell counts were reproducible between centers (r(

118 vised clustering analysis of demographic and Paneth cell data divided patients into 2 principal subgr

119 Paneth cell death led to loss of antimicrobial peptides

120 production in CD4(+) T cells responsible for Paneth cell death, dysbiosis and intestinal immunopathol

121 Paneth cells, and the number of granules per Paneth cell decreased.

122 Genetic or pharmacologic depletion of Paneth cells decreased small intestinal IL-17A secretion

123 Whereas the colon lacks Paneth cells, deep crypt secretory (DCS) cells are inter

124 viously unidentified regulatory mechanism of Paneth cell defensins.

125 Paneth cell deficiency was assessed by lysozyme staining

126 Hepatic IR induced small intestinal Paneth cell degranulation and increased interleukin-17A

127 ances show that proinflammatory mediators in Paneth cell dense core secretory granules mediate tumor

128 t-7 expression could reverse hypertrophy and Paneth cell depletion caused by Lin28b.

129 Results show that Paneth cell derived Wnt signals, which have been observe

130 Intestinal Paneth cell-derived alpha-defensins constitute an integr

131 4 (Ang4) has previously been described as a Paneth cell-derived antimicrobial peptide important in e

132 Taken together, the results show that Paneth cell-derived IL-17A plays a critical role in hepa

133 contrast, cultured crypt organoids required Paneth cell-derived Wnt3.

134 1-deficient crypts counteract the absence of Paneth cell-derived Wnts and prevent CBC stem cell exhau

135 uster in future crypts early in life, before Paneth cells develop.

136 rophage homeostasis, osteoclastogenesis, and Paneth cell development.

137 a reduction of goblet cells while promoting paneth cell development.

138 1322T tumors also had more marked Paneth cell differentiation and higher frequencies of cr

139 eptor Fzd5 and of EphB2 (genes necessary for Paneth cell differentiation and localization to the cryp

140 Cdc42 deficiency resulted in defective Paneth cell differentiation and localization without aff

141 , a key small intestine niche cell type, and Paneth cell differentiation is dependent on Sox9 functio

142 ignaling can directly modulate expression of Paneth cell differentiation markers through its effects

143 abundance, apoptosis, and the expression of Paneth cell differentiation markers.

144 perproliferation and the impaired goblet and Paneth cell differentiation observed in Fbw7(DeltaIEC) m

145 suggest that, in response to ST infection, a Paneth cell differentiation program is initiated that le

146 ence of TCF7L1, including EPHB3, a marker of Paneth cell differentiation that has also been implicate

147 , a transcriptional corepressor required for Paneth cell differentiation, and repress GFI1 targets.

148 ssing intestinal tissue growth and promoting Paneth cell differentiation.

149 fates, while selecting against endocrine and Paneth cell differentiation.

150 irectly inducing Sox9, which is required for Paneth cell differentiation.

151 tream of FGFR-3 is involved in regulation of Paneth cell differentiation.

152 s APC inactivation induces redistribution of Paneth cells, direct Myc activation triggers their rapid

153 We found that Paneth cells directly sense enteric bacteria through cel

154 of Crohn's disease may emanate from primary Paneth cell disturbances.

155 not ISCs, and forced activation of mTORC1 in Paneth cells during calorie restriction abolishes the IS

156 BACKGROUND & AIMS: Paneth cell dysfunction causes deficiencies in intestina

157 highest dose administered, some mice develop Paneth cell dysfunction that resembles the intestinal ph

158 or murine hypomorphic (HM) activity, causes Paneth cell dysfunction.

159 Modulation of Paneth cell dysregulation may have therapeutic implicati

160 Modulation of Paneth cell dysregulation may have therapeutic implicati

161 ssed conditional Atoh1(-/-) mice, which lack Paneth cells entirely, with Lgr5(GFP) mice to visualize

162 We conclude that Reg4(+) DCS cells serve as Paneth cell equivalents in the colon crypt niche.

163 Intestinal epithelial cells and Paneth cells express antimicrobial factors on direct or

164 In both control and CD patients, HD-5 in Paneth cell extracts was present almost exclusively in t

165 sociated with trypsin or chymotrypsinogen in Paneth cell extracts.

166 aling controls the choice between goblet and paneth cell fates by regulating Wnt/beta-catenin activit

167 that autophagy was specifically activated in Paneth cells from patients with CD, independently of muc

168 of secretory granules previously reported in Paneth cells from patients with CD.

169 ed a loss of goblet cells from the colon and Paneth cells from the small intestine upon induced delet

170 These findings provide evidence that Paneth cell function and intestinal dysbiosis are involv

171 Subtypes of CD associated with Paneth cell function have been observed even among patie

172 Because defects of Paneth cell function stemming from various etiologies ar

173 ll within the lamina propria supports normal Paneth cell function through expression of Wnt 5a, and t

174 olved in innate immune responses, goblet and Paneth cell function, ion channels, intestinal stem cell

175 rough mechanisms that include the control of Paneth cell function.

176 genetic defects, many of which likely affect Paneth cell function.

177 henotype, promoted goblet cell and inhibited paneth cell generation.

178 nal macrophages appear to transport released Paneth cell granule constituents induced by AKI, away fr

179 Germ-free Cd1d-/- mice exhibited a defect in Paneth cell granule ultrastructure and ability to degran

180 intestinal epithelia, except for a defect in Paneth cell granules.

181 nsins 5 and 6 (mainly produced by intestinal Paneth cells) had viral neutralizing activity similar to

182 4 in the large intestine, which is devoid of Paneth cells, has not been defined.

183 ealed that dysregulated IEC gene expression, Paneth cell homeostasis and intestinal barrier function

184 and that varied genetic defects that disrupt Paneth cell homeostasis are emergent as risk factors in

185 Recent evidence shows that disruption of Paneth cell homeostasis by induction of endoplasmic reti

186 he aim of this study is to determine whether Paneth cell hyperplasia or metaplasia characteristically

187 Only patients with IBD showed Paneth cell hyperplasia, assessed as more than 10 Paneth

188 Mesenchymal cells, Paneth cells, immune cells, endothelial cells and neural

189 ed HDAC3(DeltaIEC) mice demonstrated loss of Paneth cells, impaired IEC function and alterations in t

190 esults in endoplasmic reticulum (ER) stress, Paneth cell impairment and spontaneous enteritis.

191 etroviral vector promoted differentiation of Paneth cells in a cell-autonomous manner.

192 aining demonstrated expression of LPLUNC1 in Paneth cells in cholera patients and controls.

193 Recent studies have linked appearance of Paneth cells in colorectal adenomas to adenoma burden an

194 on of Gata6 caused an increase in numbers of Paneth cells in jejunum and ileum.

195 t affects homeostasis of intestinal stem and Paneth cells in mice.

196 was a statistically significant increase in Paneth cells in the caecum, ascending, transverse and de

197 Paneth cells in the ISC niche secrete cyclic ADP ribose

198 se intestinal tumorigenesis, is expressed by Paneth cells in the small intestine, while group X sPLA2

199 have a significant decrease in the number of Paneth cells in the small intestine.

200 in of function specific to ATG16L1-deficient Paneth cells including increased expression of genes inv

201 expression of genes characteristic of mature Paneth cells, including human alpha-defensins 5 and 6 (H

202 n or bilateral nephrectomy, small intestinal Paneth cells increased the synthesis and release of IL-1

203 uantities were accompanied by alterations of paneth cells, indicating that Shp2/MAPK signaling might

204 Mice with defects in Paneth cells (induced by maternal separation or genetica

205 Paneth cells integrate complex genetic, immune, and envi

206 We conclude that the enumeration of duodenal Paneth cells is a readily available index of disease sev

207 In ileitis-prone SAMP1/YitFc mice, Paneth cell levels of CRS4C mRNAs and peptides are induc

208 In the sustained absence of Paneth cells, Lgr5(+) CBCs occupied the full crypt base,

209 xpression and amplification; and (v) CRIS-E: Paneth cell-like phenotype, TP53 mutations.

210 Intestinal Paneth cells limit bacterial invasion by secreting antim

211 ion of the Paneth cell compartment, abnormal Paneth cell localization, elevated endoplasmic reticulum

212 s displayed RIPK3-dependent IEC necroptosis, Paneth cell loss and focal erosive inflammatory lesions

213 ath1-deficient crypt cells tolerated in vivo Paneth cell loss and maintained active beta-catenin sign

214 ighlighting the potential clinical impact of Paneth cell loss in gastrointestinal (GI) acute graft-ve

215 -induced NEC and prevented dithizone-induced Paneth cell loss in mice.

216 ) and RIPK3 prevented epithelial cell death, Paneth cell loss, and colitis development in mice with e

217 d mice are injected with dithizone to induce Paneth cell loss, followed by Klebsiella pneumoniae infe

218 intestinal hypertrophy, crypt expansion, and Paneth cell loss.

219 an alpha-defensins 5 and 6 (HD5 and HD6) and Paneth cell lysozyme, whereas enterocytic differentiatio

220 llus cells encompassed ectopic expression of Paneth cell markers (a lineage normally confined to the

221 (-/-) ileal epithelial enteroids had reduced Paneth cell markers and were highly sensitive to inflamm

222 FGFR-3 is also required for the induction of Paneth cell markers in addition to and independent of th

223 Loss of Paneth cell markers was associated with reduced nuclear

224 th the transgene expression included loss of Paneth cell markers, increases in goblet cells, and migr

225 in pathway was required for the induction of Paneth cell markers.

226 livery in producing cells and is crucial for Paneth cell maturation.

227 vironmentally controlled UPR function within Paneth cells may therefore set the threshold for the dev

228 Paneth cells mediate immunity and maintain the small int

229 Defective Paneth cell-mediated innate immunity due to inadequate W

230 this shift was associated with a decrease in Paneth-cell-mediated antimicrobial host defence that com

231 Paneth cell metaplasia (PCM) is well described in adults

232 d in T-cell infiltration of the gut, loss of Paneth cells, microbial dysbiosis, and the induction of

233 We have assumed that mature Paneth cells migrating upwards undergo anoikis.

234 Depletion of Paneth cell numbers by pharmacological (with dithizone)

235 D) groups there was a gradient of decreasing Paneth cell numbers from caecum to rectum.

236 Finally, depletion of Paneth cell numbers significantly decreased small intest

237 Secretory autophagy was disrupted in Paneth cells of mice harboring a mutation in autophagy g

238 a key antimicrobial peptide produced by the Paneth cells of the allograft, fall as the graft becomes

239 n-4 (Crp4) is an alpha-defensin expressed in Paneth cells of the mouse small intestine and the most b

240 nsin (HD) 6 is highly expressed by secretory Paneth cells of the small intestine.

241 e hypothesis that enteric alpha-defensins of Paneth cell origin persist in a functional state in the

242 icrobial peptides produced as a component of Paneth cell (PC) secretory granules in the small intesti

243 Paneth cells (PCs) are terminally differentiated, highly

244 h cell hyperplasia, assessed as more than 10 Paneth cells per 10 well-oriented crypts at any site.

245 ed with IgG-treated mice, with the number of Paneth cells per crypt also significantly reduced.

246 microscopy, we evaluated the mean number of Paneth cells per high-powered field (hpf) in 116 duodena

247 A threshold of 4 Paneth cells per hpf stratified patients according to no

248 Histologic analysis of Paneth cell phenotypes can be used to divide patients wi

249 The disordered and diffuse abnormal Paneth cell phenotypes were associated with an altered t

250 Paneth cell phenotypes were classified as normal or abno

251 To uncover the molecular basis of the Paneth cell phenotypes, we developed methods to determin

252 initiated that leads to an expansion of the Paneth cell population and that the transit amplifying c

253 Infection-induced expansion of the Paneth cell population may represent an acute intestinal

254 d the gut epithelium by promoting goblet and Paneth cells population and reinstating the E-cadherin a

255 ecretory or absorptive progenitors, and from Paneth cell precursors, revealing a high degree of plast

256 One reports that quiescent crypt cells are Paneth cell precursors.

257 Paneth cell presence in the adenomas of distal colorectu

258 GSI increased Paneth cell production in wild-type mice but failed to d

259 m cells (SC), Paneth cells and common goblet-Paneth cell progenitors (CGPCPs) intermingling at the cr

260 on of CBC, and it was recently proposed that Paneth cells provide a crucial niche by secreting Wingle

261 y transgenic expression of alpha-defensin in Paneth cells rescued the Th1 inflammatory phenotype.

262 Paneth cells reside in the small intestine and produce a

263 Paneth cells residing at the base of the small intestina

264 cluster of Lgr5+ cells between at least two Paneth-cell-rich domains establishes the site for the up

265 l niche requires clarity with respect to the Paneth cell role.

266 Perhaps more intriguing, Paneth cells secrete factors that help sustain and modul

267 ulations and experimental validations reveal Paneth cell-secreted WNT as the key intercellular coupli

268 tdins (Crps) in mice, are highly abundant in Paneth cell secretions and inherently resistant to prote

269 We suggest that Paneth cell signaling overrides any direct nutrient sens

270 esponse to infection with ST, the intestinal Paneth cell-specific lysozyme content, the number of lys

271 nduction and spontaneous ileitis emerge from Paneth-cell-specific deletion of Xbp1.

272 for the role of Ephrin mediated motility of Paneth cells, specifically that it is required to constr

273 When dysfunctional in the Paneth cell, spontaneous inflammation can emerge that ma

274 SIRT1 (SIRT1 iKO) had abnormal activation of Paneth cells starting at the age of 5-8 months, with inc

275 We prospectively reviewed and recorded Paneth cell status in the colorectal adenomas consecutiv

276 ver, synchronous CRC was not associated with Paneth cell status, or a history of AA or CRC.

277 engagement, which is especially prominent in Paneth cells such that, in the absence of both, severe s

278 Small intestinal Paneth cells supply Wnt3, EGF, and Notch signals to neig

279 Paneth cells support stem cells by secreting Wnt, but li

280 hin the intestinal epithelium and especially Paneth cells that are of considerable importance to the

281 side deep in the crypt, mingled among mature Paneth cells that are well positioned for short-range si

282 , expressed and released by small intestinal Paneth cells, that exhibits antibacterial activity again

283 ed that, in contrast to the adenomas without Paneth cells, the Paneth cell-containing adenomas at dis

284 KI induces IL-17A synthesis and secretion by Paneth cells to initiate intestinal and hepatic injury b

285 tine reveals that caloric restriction causes Paneth cells to repress mTORC1 signaling; this in turn s

286 ural relaxation explains the localisation of Paneth cells to the crypt bottom in the absence of activ

287 ll intestine, resulting in mispositioning of Paneth cells to the upper crypt region.

288 al cell lineages (enterocytes, goblet cells, Paneth cells, tuft cells and enteroendocrine cells), pre

289 strated by the loss of goblet, endocrine and Paneth cell types in null mice.

290 The proportion of abnormal Paneth cells was associated with the number of CD-associ

291 In addition, high proportions of abnormal Paneth cells were associated with shorter time to diseas

292 Paneth cells were counted at 6 anatomical sites in the c

293 Paneth cells were not seen in the distal colon in the co

294 CRS4C-1 peptides are found exclusively in Paneth cells where they occur only in dense core granule

295 lial growth factor, and interleukin-1beta in Paneth cells, whereas NF-kappaB and COX-2 were more stro

296 erimental models have shown that the loss of Paneth cells, which are located in the small intestine a

297 show autophagosome formation in hypomorphic Paneth cells, which is linked to ER stress via protein k

298 ll4, and epidermal growth factor, similar to Paneth cells, which were also marked by cKit.

299 high Wnt signalling will differentiate into Paneth cells while those migrating out from the crypt bo

300 y secretory tissues such as plasma cells and Paneth cells, yet its function in granulocyte maturation