ライフサイエンスコーパス: marginal zone

1 anotubes in the spleen were found within the marginal zone.

2 o the perimeter of follicles adjacent to the marginal zone.

3 +) Mphis and other cells in the red pulp and marginal zone.

4 ophils that localize in the red pulp and the marginal zone.

5 ls had reduced antigen uptake in the splenic marginal zone.

6 t and in the persistently neurogenic ciliary marginal zone.

7 ocalization of virus and pDCs to the splenic marginal zone.

8 vesicle to their destination in the ciliary marginal zone.

9 pulp of SCD mice without distinct B, T, and marginal zones.

10 Marginal zone and B-1 B cells were lost, whereas follicu

11 aly, autoantibody production, frequencies of marginal zone and B1 B cells, and renal pathology compar

12 cell development, which results in increased marginal zone and decreased follicular B cell numbers.

13 nal zone B cells migrate continually between marginal zone and follicles and establishes the marginal

14 leen, B cell movement between the blood-rich marginal zone and follicles is disrupted by GRK2 deficie

15 Marginal zone B cells shuttle between the marginal zone and follicles with at least one-fifth of t

16 differentiation of transitional B cells into marginal zone and follicular B cells.

17 k secreted and membrane-bound Ab, yet harbor marginal zone and follicular B cells.

18 p a two-photon microscopy procedure to study marginal zone and follicular B-cell movement in the live

19 lp follicles, markedly increased size of the marginal zone and germinal centers, and increased expres

20 finity self-reactive specificities in murine marginal zone and human naive B cells.

21 ells and substantially rescues maturation of marginal zone and Iglambda(+) B cells, but not Igkappa(+

22 y Nfkbid, is required for the development of marginal zone and peritoneal B-1 B cells and additionall

23 Zeb1 is also required for marginal zone and peritoneal B-1 B-cell development as w

24 ited abnormal elevated IDO expression in the marginal zone and red pulp and inhibition of IDO markedl

25 KLRG1(-) and KLRG1(+) CD8(+) T cells in the marginal zone and red pulp, which ceases prior to the fi

26 ed spleen with marked disorganization of the marginal zone and red pulp.

27 We find that iNKT cells consolidate in the marginal zone and require dendritic cells lining the spl

28 ificantly perturbed, with reduced numbers of marginal zone and transitional stage 2 B cells, expansio

29 IDO expression was confined to the splenic marginal zone and was abrogated by depletion of CD169(+)

30 ls were located in the region of the splenic marginal zone and were not detected in blood or other se

31 ecursor cell subsets that become infected in marginal zones and then migrate into GCs as fully mature

32 nguishes them from follicular, transitional, marginal zone, and B1 cells.

33 on impaired generation of mature follicular, marginal zone, and B1a B lymphocytes.

34 lusters or heterotopias were detected in the marginal zone, and disorganization of cortical cells ind

35 cell subpopulations, including transitional, marginal zone, and follicular B cells, as well as the B

36 lacked lymph nodes, Peyer's patches, splenic marginal zones, and follicular dendritic cells and faile

37 o the apical membrane, that is enriched at a marginal zone apical to tight junctions, and that drives

38 ginal zone and follicles and establishes the marginal zone as a site of S1PR1-dependent B-cell exit f

39 Marginal zone B (MZ B) cells can rapidly produce antibod

40 al zone precursors (MZPs) differentiate into marginal zone B (MZB) cells under a signaling pathway in

41 Splenic marginal zone B (MZB) cells, positioned at the interface

42 etermine whether transitional B cells become marginal zone B (MZB) or follicular B (FoB) cells in the

43 in mice, possibly by specifically enforcing marginal zone B cell accumulation, increasing X-linked i

44 A recent study showed that marginal zone B cell and B1 B cell populations are drama

45 iously known as INK1117) did not disrupt the marginal zone B cell compartment and did not block T cel

46 R7 within the B cell compartment reduces the marginal zone B cell compartment and increases B and T c

47 of B cells into the follicular mature versus marginal zone B cell compartment.

48 ise bone marrow B lymphopoiesis, but splenic marginal zone B cell development failed, and B cells und

49 cating a functional consequence of defective marginal zone B cell development in LPL(-/-) mice.

50 TCH2, a gene encoding a protein required for marginal zone B cell development, in 25 of 99 ( approxim

51 tients with chronic lymphocytic leukemia and marginal zone B cell lymphoma also underwent integrin-me

52 , 76% of p53(rev/rev) mice developed splenic marginal zone B cell lymphomas, indicating sensitivity o

53 ressed germinal center formation and reduced marginal zone B cell numbers, similar to a pan-class I i

54 ) mice, IgM and IgG3 Ab responses as well as marginal zone B cell plasma cell numbers and peritoneal

55 raf2 deletion, Traf2DN-tg mice show expanded marginal zone B cell population and have constitutive p1

56 ust increases in transitional B cell number, marginal zone B cell proliferation, and CD86, but not CD

57 n of IgA plasma cells and also the enigmatic marginal zone B cell subset that is poorly understood in

58 artments and a strong orientation toward the marginal zone B cell subset.

59 etes insulin binders from the follicular and marginal zone B cell subsets.

60 omparable to that seen in old follicular and marginal zone B cell subsets.

61 development and in peritoneal B1 and splenic marginal zone B cell-mediated Ab responses.

62 Marginal zone B cells (MZB) participate in the early imm

63 ll development, with elevated percentages of marginal zone B cells and a reduction in B-1 B cells.

64 CD22(-/-) background have restored levels of marginal zone B cells and Ab responses compared with def

65 O also leads to reduction of Ag transport by marginal zone B cells and affects the subsequent immune

66 -cell development, but led to a reduction of marginal zone B cells and an increase in splenic B1 B ce

67 B cell maturation, showed reduced numbers of marginal zone B cells and class-switched cells, and were

68 KLF2 knockout mice have increased numbers of marginal zone B cells and decreased numbers of B1 phenoy

69 is sufficient to cause a severe reduction of marginal zone B cells and inability to respond to type I

70 , allowing Notch 2-driven differentiation of marginal zone B cells and of Esam(+) dendritic cells.

71 rmore, Lbw2 congenics had greater numbers of marginal zone B cells and reduced expansion of peritonea

72 he number of spontaneous germinal center and marginal zone B cells and the level of autoantibody are

73 at phenotypes in the heart, endothelium, and marginal zone B cells are attributed to haploinsufficien

74 We show that marginal zone B cells are highly motile and exhibit long

75 ollicular B cells are decreased and those of marginal zone B cells are increased in spleens of CD28(-

76 itiation of circulation give rise to B-1 and marginal zone B cells but do not give rise to B-2 cells.

77 Marginal zone B cells expand in the knockout spleen, whe

78 wever, it increased T1 B cells and decreased marginal zone B cells in the spleen.

79 e marrow and profound loss of follicular and marginal zone B cells in the spleen.

80 mice had decreased numbers of follicular and marginal zone B cells in the spleen.

81 hereas splenic B-1 cells were unaffected and marginal zone B cells increased.

82 Finally, a well-characterized role of marginal zone B cells is the generation of a rapid humor

83 This study shows that marginal zone B cells migrate continually between margin

84 differs dramatically from the follicular and marginal zone B cells repertoires and is defined by dist

85 w that the Ab repertoire of CD21(hi)/CD23(-) marginal zone B cells shows persistent increase in level

86 Marginal zone B cells shuttle between the marginal zone

87 , a population that resembles murine splenic marginal zone B cells that mount T-independent antibody

88 ular repertoire, indicating that the loss of marginal zone B cells was not due to diversion to the fo

89 up-regulated Nod1, including follicular and marginal zone B cells with natural autoreactivity.

90 follicular regulatory cells, an expansion of marginal zone B cells, and early increases in regulatory

91 subsets of B cells, in mature follicular and marginal zone B cells, and in activated B cells, includi

92 yed defects in multiple cell types including marginal zone B cells, B1 B cells, IL-10-producing B cel

93 l(-/-) mice, finding a relative expansion of marginal zone B cells, B1 cells, and plasma cells associ

94 IgM when the cells mature into follicular or marginal zone B cells, but the transacting factors respo

95 d Zfp318 exon 10 abolished IgD expression on marginal zone B cells, decreased IgD on follicular B cel

96 As with mouse marginal zone B cells, human IgM(+)CD27(+) B cells activ

97 e latency mice, i.e., increased frequency of marginal zone B cells, hyperplasia, and hyperglobulinemi

98 served more mature naive B cells, especially marginal zone B cells, in BLyS-treated mice.

99 We found that in addition to marginal zone B cells, mature follicular B cells signifi

100 immune response at various levels, including marginal zone B cells, plasmacytoid dendritic cells and

101 m follicles to the marginal zone, but unlike marginal zone B cells, they fail to undergo integrin-med

102 9-activated peripheral B cells, and splenic marginal zone B cells.

103 B cells mature into follicular and then into marginal zone B cells.

104 n use the 44.1-idiotype and are dependent on marginal zone B cells.

105 1b peritoneal cells, but not in B1a cells or marginal zone B cells.

106 and suggest that the 44.1-Id is derived from marginal zone B cells.

107 cked B1 B cells and exhibited a reduction in marginal zone B cells.

108 eas heterozygous deficiency caused a loss of marginal zone B cells.

109 ost dramatically affected the maintenance of marginal zone B cells.

110 the physiological differentiation of spleen marginal zone B cells.

111 racellular ATP and loss of CD21 and CD62L on marginal zone B cells.

112 he spleen and enabled efficient shuttling of marginal zone B cells.

113 llular, albeit with a relative deficiency of marginal zone B cells.

114 is, including increased development of B-1a, marginal zone B, gamma/delta (gammadelta) T cells, and n

115 fibrosis identified a common upregulation of marginal zone B- and B1-cell-specific protein (MZB1), th

116 s lacking Ig translocations, such as splenic marginal zone B-cell lymphoma or Waldenstrom macroglobul

117 patient, who had liver granuloma, extranodal marginal zone B-cell lymphoma, and autoimmune neutropeni

118 , diffuse large B-cell lymphoma, and splenic marginal zone B-cell lymphoma.

119 orbidities associated with primary cutaneous marginal zone B-cell lymphomas (PCMZLs).

120 GCs, showing a modest increase in naive and marginal-zone B cells and a significant decrease in GC B

121 haperone that is preferentially expressed in marginal-zone B cells and is highly upregulated during p

122 iptional hub that determined the identity of marginal-zone B cells by promoting their proper localiza

123 Nkx2-3-deficient mice exhibit the absence of marginal-zone B cells, transgenic mice with expression o

124 or studying the biology and therapy of human marginal-zone B-cell lymphomas.

125 y and the remaining cells fail to situate in marginal zone bridging channels.

126 r B cells also transit from follicles to the marginal zone, but unlike marginal zone B cells, they fa

127 beta, and included genes expressed by normal marginal zone cells and memory B cells.

128 B cell development validate the identity of marginal zone cells and the maturation status of human C

129 However, in contrast to the follicular and marginal zone cells, ABCs displayed significant somatic

130 ressed by progenitors in the circumferential marginal zone (CMZ) and is upregulated by Muller glia in

131 Retinal progenitors in the circumferential marginal zone (CMZ) and Muller glia-derived progenitors

132 erentiation, and stem cells from the ciliary marginal zone (CMZ) being responsible for late neurogene

133 our and retinal morphology including ciliary marginal zone (CMZ) cell death and decreased photorecept

134 cts stem and progenitor cells in the ciliary marginal zone (CMZ) of the amphibian retina, a well-char

135 eural stem cells that form a circumferential marginal zone (CMZ) that lines the periphery of the reti

136 at the rim of the retina, called the ciliary marginal zone (CMZ).

137 enance of cells in the murine follicular and marginal zone compartments is thought to involve differi

138 tion stages and allows the classification of marginal zone-derived (JAM-C-positive) and germinal cent

139 Interestingly the dorso-lateral marginal zone (DLMZ) is only able to promote the express

140 ce with expression of NKX2-3 in B cells show marginal-zone expansion that leads to the development of

141 er, Listeria organisms remain trapped in the marginal zone, failed to traffic into the PALS, and were

142 d require dendritic cells lining the splenic marginal zone for activation following administration of

143 -borne antigens, lymphocyte migration in the marginal zone has not been intravitally visualized due t

144 The splenic marginal zone is a unique microenvironment where residen

145 Follicular B-cell egress via the marginal zone is sphingosine-1-phosphate receptor-1 (S1P

146 al numbers but with abnormal distribution of marginal zone-like and memory B cells.

147 s of hypermutated, rheumatoid factor-bearing marginal zone-like IgM(+)CD27(+) peripheral B cells usin

148 xposed women had more atypical MBC and fewer marginal zone-like MBC, and their levels correlated with

149 argin) and the retreated ice sheet (with the marginal zone located far inland).

150 sion, as were mantle cell lymphoma (0 of 5), marginal zone lymphoma (0 of 6), follicular lymphoma (0

151 or rarely expressed in samples from splenic marginal zone lymphoma (2/20; 10%), CLL (1/26; 4%), mult

152 The most frequent subtype was extranodal marginal zone lymphoma (EMZL) (68.4% [180 of 263]), foll

153 The histologic subtype was extranodal marginal zone lymphoma (EMZL) in 51 patients (81.0%).

154 re most consistent with pulmonary extranodal marginal zone lymphoma (ENMZL; Fig 2 ).

155 Marginal zone lymphoma (MZL) is a heterogeneous B-cell m

156 Marginal zone lymphoma (MZL) is the third most common su

157 s macroglobulinemia (n = 2, 11%), extranodal marginal zone lymphoma (n = 2, 11%), plasmablastic lymph

158 , Waldenstrom macroglobulinemia (n = 4), and marginal zone lymphoma (n = 3).

159 10 patients with follicular lymphoma (n=50), marginal zone lymphoma (n=30), and small lymphocytic lym

160 Nodal marginal zone lymphoma (NMZL) is a rare form of indolent

161 Nodal marginal zone lymphoma (NMZL) is a rare, indolent B-cell

162 Nodal marginal zone lymphoma (NMZL) is a small B-cell neoplasm

163 lamydophila psittaci (Cp) and ocular adnexal marginal zone lymphoma (OAMZL) and the efficacy of doxyc

164 5% confidence interval (CI): 2.25, 4.30) and marginal zone lymphoma (OR = 5.80, 95% CI: 3.82, 8.80);

165 across major B-cell NHL subtypes, including marginal zone lymphoma (P-interaction = 0.02) and follic

166 ell tumor that is distinguished from splenic marginal zone lymphoma (SMZL) by the different pattern o

167 Splenic marginal zone lymphoma (SMZL) is a B cell malignancy of

168 Splenic marginal zone lymphoma (SMZL) is a mature B-cell neoplas

169 Splenic marginal zone lymphoma (SMZL) is a rare B-cell malignanc

170 ned significance (IgM-MGUS), 84 with splenic marginal zone lymphoma (SMZL), and 52 with B-cell chroni

171 Splenic marginal zone lymphoma (SMZL), the most common primary l

172 tiate from HCL-like disorders (e.g., splenic marginal zone lymphoma and HCL variant).

173 ortunity to better understand the biology of marginal zone lymphoma and optimize therapy by using dem

174 ocytic leukemia (ALL), mantle cell lymphoma, marginal zone lymphoma and Sezary syndrome.

175 Exposure of splenic marginal zone lymphoma cell lines to a demethylating age

176 lymphoma and follicular lymphoma, as well as marginal zone lymphoma for dichloromethane.

177 Splenic marginal zone lymphoma is a rare lymphoma.

178 ercent of the cases reported were extranodal marginal zone lymphoma of mucosa-associated lymphoid tis

179 y accepted prognostic indices for extranodal marginal zone lymphoma of mucosa-associated lymphoid tis

180 stemic treatment of patients with extranodal marginal zone lymphoma of mucosa-associated lymphoid tis

181 bserved across strata of sex for CLL/SLL and marginal zone lymphoma subtypes as well as age for the f

182 Extranodal marginal zone lymphoma was the predominant (76.2%) histo

183 ution, patients with follicular lymphoma and marginal zone lymphoma were given lenalidomide, orally,

184 n profiling identifies 2 subtypes of splenic marginal zone lymphoma with different clinical and genet

185 ALL, B-chronic lymphocytic leukemia, splenic marginal zone lymphoma) is well characterized, there is

186 atified by histology (follicular lymphoma vs marginal zone lymphoma), treatment intent (palliative or

187 w-grade non-Hodgkin lymphoma, 27% extranodal marginal zone lymphoma).

188 rent treatments (eg, HCL-variant and splenic marginal zone lymphoma).

189 leukemias/lymphomas (HCL-variant and splenic marginal zone lymphoma).

190 Of 27 evaluable patients with marginal zone lymphoma, 18 (67%) had a complete response

191 ith HCL, 1 with HCL variant, 91 with splenic marginal zone lymphoma, 29 with Waldenstrom macroglobuli

192 7 with non-mucosa-associated lymphoid tissue marginal zone lymphoma, and 38 with lymphoplasmacytic ly

193 e local control, with follicular lymphoma or marginal zone lymphoma, who had received no previous tre

194 atients with IgM-MGUS progressed to WM or to marginal zone lymphoma.

195 le cell, or other indolent lymphomas such as marginal zone lymphoma.

196 patients), small lymphocytic lymphoma (28), marginal-zone lymphoma (15), and lymphoplasmacytic lymph

197 The most common subtypes were extranodal marginal-zone lymphoma (EMZL) (37% [n = 32]), follicular

198 samples from patients with multiple myeloma, marginal-zone lymphoma, or IgM monoclonal gammopathy of

199 Extranodal marginal zone lymphomas (EMZL) are the most common lymph

200 The histological distribution was 37 marginal zone lymphomas (MZLs), 2 lymphoplasmacytic lymp

201 lobulin (Ig)G4-related disease (IgG4-RD) and marginal zone lymphomas (MZLs).

202 d IGH translocations, have been described in marginal zone lymphomas (MZLs); however, these known gen

203 B) signaling, have been described in splenic marginal zone lymphomas and multiple myeloma.

204 of p53 deficiency in development of splenic marginal zone lymphomas and provides a model for study o

205 16 follicular lymphomas (FLs), 9 extranodal marginal zone lymphomas, and 8 reactive lymph nodes and

206 tumour cells from a subset of patients with marginal-zone lymphomas, but not with other B-cell malig

207 al clinical and biological features of human marginal-zone lymphomas.

208 Marginal zone macrophages (MZM) are strategically locate

209 Marginal zone macrophages (MZMs) act as a barrier to ent

210 s in the spleens of BXD2 lupus mice disrupts marginal zone macrophages (MZMs), which normally clear A

211 Accordingly, marginal zone macrophages and pDC precursors were elimin

212 ) BMDC-dependent protection required CD169(+)marginal zone macrophages and the macrophage-derived che

213 cial effects require microparticle uptake by marginal zone macrophages expressing the scavenger recep

214 1 expression and IL-10 production by splenic marginal zone macrophages leading to Ag-specific T cell

215 ystem, namely Kupffer cells of the liver and marginal zone macrophages of the spleen.

216 Marginal zone macrophages, some DCs, and myeloid cells i

217 irrors aged Bim(-/-) mice, including loss of marginal zone macrophages, splenomegaly, lymphadenopathy

218 it the clearance of apoptotic cells (ACs) by marginal zone macrophages.

219 Furthermore, the splenic marginal zone microarchitecture was substantially distur

220 organisms, initially located in the splenic marginal zone, migrated to the periarteriolar lymphoid s

221 Marginal zone (MZ) and B1 B cells have the capacity to r

222 -3 in B cells resulted in significantly more marginal zone (MZ) and fewer follicular (FO) B cells.

223 ion of apoptotic cell (AC) debris within the marginal zone (MZ) and increased loading of AC Ags on MZ

224 the time of leading process contact with the marginal zone (MZ) and occurs primarily by neurite exten

225 Innate-like splenic marginal zone (MZ) and peritoneal cavity B1 B lymphocyte

226 the majority of NKT cells patrol around the marginal zone (MZ) and red pulp (RP) of the spleen.

227 es from splenic stromal cells located in the marginal zone (MZ) and requires B cells that express lym

228 on of irf4-deleted follicular B cells in the marginal zone (MZ) area.

229 Marginal zone (MZ) B and B1 cells were not rescued, indi

230 elopment, and LFNG and MFNG are required for marginal zone (MZ) B cell development.

231 Kruppel-like factor 3 (KLF3, BKLF) increases marginal zone (MZ) B cell numbers, a phenotype shared wi

232 nificant reduction in the absolute number of marginal zone (MZ) B cells and their immediate precursor

233 Marginal zone (MZ) B cells are an innate-like population

234 Although splenic marginal zone (MZ) B cells are considered to be importan

235 Splenic marginal zone (MZ) B cells are innate-like lymphocytes t

236 portant roles in promoting the generation of marginal zone (MZ) B cells at the expense of follicular

237 Expansion of autoimmune-prone marginal zone (MZ) B cells has been implicated in type 1

238 Therefore, the contribution of marginal zone (MZ) B cells in experimental atheroscleros

239 chanism in which follicular translocation of marginal zone (MZ) B cells in the spleens of BXD2 lupus

240 Marginal zone (MZ) B cells reside in the splenic MZ and

241 ase in splenic macrophages, neutrophils, and marginal zone (MZ) B cells that was inhibited by IL-10 s

242 y, type I IFNs increase the translocation of marginal zone (MZ) B cells to the follicular region of t

243 ordinates immunometabolic reconfiguration of marginal zone (MZ) B cells, a pre-activated lymphocyte s

244 s study, we found binding of PTX3 to splenic marginal zone (MZ) B cells, an innate-like subset of ant

245 After 2 h, OVA-TNP was detected on marginal zone (MZ) B cells, and a substantial amount of

246 -independent (TI) antibody production by the marginal zone (MZ) B cells, leaving the contribution of

247 decrease in memory B cells, particularly of marginal zone (MZ) B cells.

248 ection, with significant colocalization with marginal zone (MZ) B cells.

249 ell-specific Notch2-deficient mice that lack marginal zone (MZ) B cells.

250 e production, and substantial restoration of marginal zone (MZ) B cells.

251 of the B-cell subsets [B-1a, B-1b, B-2, and marginal zone (MZ) B cells] in the mouse has been discus

252 of anti-gp120 B cells in follicular (FO) and marginal zone (MZ) B-cell compartments of naive WT mice

253 gered by increased plasma cell frequency and marginal zone (MZ) B-cell hyperplasia.

254 Extranodal marginal zone (MZ) B-cell lymphomas of the mucosa-associ

255 splenic B-cell numbers, mostly of the B1 and marginal zone (MZ) B-cell subtypes; 2) enlarged germinal

256 Specialized B cells residing in the splenic marginal zone (MZ) continuously survey the blood for ant

257 egg chamber development, being lost from the marginal zone (MZ) in stage 9 before abruptly returning

258 The splenic marginal zone (MZ) is comprised of specialized populatio

259 us-4 (MuHV-4) enters the spleen by infecting marginal zone (MZ) macrophages, which provided a conduit

260 ere we identified RORgammat(+) ILCs near the marginal zone (MZ), a splenic compartment that contains

261 llular matrix (ECM) niche in the spleen, the marginal zone (MZ), characterized by the basement membra

262 haracteristic perifollicular rim marking the marginal zone (MZ), which is the interface between the n

263 to DC-inhibitory receptor 2 (DCIR2) found on marginal zone (MZ)-associated CD8alpha(-) DCs in mice le

264 Mutations in NOTCH2, a gene required for marginal-zone (MZ) B cell development, represent the mos

265 d low blood memory B-cells counts (including marginal zone [MZ] B-cell counts).

266 by IgD and CD27 expression: IgD(+)CD27(+) ("marginal zone [MZ]"), IgD(-)CD27(+) ("memory," including

267 Marginal zones (MZs) are architecturally organized for c

268 ding to the 'modern-scale' ice sheet (with a marginal zone near the present ice-sheet margin) and the

269 rtant signaling centers including the dorsal marginal zone, notochord and floorplate.

270 IM, localized largely to the splenic marginal zone of naive CD11b-diphtheria toxin (DT) recep

271 -55 degrees C for 10 minutes, simulating the marginal zone of RFA treatment.

272 On OCT, in the marginal zone of the lesions, a disappearance of the int

273 me-capturing macrophages were present in the marginal zone of the spleen and in the subcapsular sinus

274 ghout the spleen at rest, consolidate in the marginal zone of the spleen early after activation, and

275 ells of lymphoid tissues and in cells in the marginal zone of the spleen, while administration of an

276 ternating currents applied to the middle and marginal zones of isolated TM segments evoke motions at

277 mesoderm-inducing signals to the vegetal and marginal zones of the pre-gastrula Xenopus laevis embryo

278 n ICECAP aerogeophysical data, demarcate the marginal zones of two distinct quasi-stable EAIS configu

279 +) and SIGN-R1(+) macrophages of the splenic marginal zone or draining lymph node, respectively, foll

280 primarily in GCs and not in the T cell zone, marginal zone, or red pulp areas of the spleen.

281 xpressed B surface markers compatible with a marginal zone origin.

282 osis with an immunophenotype consistent with marginal-zone origin (CBL-MZ) is poorly understood.

283 Costimulatory blockade increased IL-10 in marginal zone precursor (MZP) B cells, but not other sub

284 ly elevated CD69 and CD86 observed in RBP(+) marginal zone precursor B cells in the spleens of BXD2 m

285 n-D1 was not required for B cell maturation, marginal zone precursor development, dark and light zone

286 requency and greater numbers of RBP-reactive marginal zone precursor, transitional T3, and PDL-2(+)CD

287 Mouse splenic marginal zone precursors (MZPs) differentiate into margi

288 entry points for peripheral Ags: the splenic marginal zone, red pulp, and lymph node sinuses.

289 persistence maps anatomically to the splenic marginal zone/red pulp and is defined by prolonged motil

290 ce, with exosomes freely accessing the outer marginal zone rim of SIGN-R1(+) macrophages and F4/80(+)

291 architecture and the function of the splenic marginal zone significantly influence the pathogenesis o

292 0 was significantly increased on FO, but not marginal zone, splenic B cells after SAT development.

293 uximab, depletes the follicular (FO) but not marginal zone subset of B cells, efficiently inhibited d

294 transitional 2 (T2), follicular mature, and marginal zone subsets identified in mice.

295 ssed in multiple cell types in the preplate, marginal zone, subventricular zone (SVZ), and ventricula

296 Males had a smaller marginal zone than females with a repertoire that was di

297 dent on CD4(+) T cell help but appear to use marginal zone versus follicular B cells, respectively.

298 at apoptotic Ag-SP accumulate in the splenic marginal zone, where their uptake by F4/80(+) macrophage

299 plate cells extend a primary dendrite to the marginal zone, whereas all dendrites of P7 subplate cell

300 cortical neurons overmigrate and invade the marginal zone, which are characteristics similar to a ph