ライフサイエンスコーパス: class switch

1 feration of viable B cells, but not with IgE class switch.

2 nvestigated in B cell differentiation and Ab class switch.

3 uced circulating B cells and impaired B cell class-switch.

4 a GC-like phenotype or the rate of antibody class switching.

5 ecific human CD8 T cells, and immunoglobulin class switching.

6 eir B cells could not undergo immunoglobulin class switching.

7 nd CD8 T cells, or to undergo immunoglobulin class switching.

8 t IgM-to-IgA or sequential IgM-to-IgG-to-IgA class switching.

9 ligand and secreted cytokines that guide Ig class switching.

10 full-length HA and stem alters stem-antibody class switching.

11 production of cytokines that direct antibody class switching.

12 d with progressive B-cell maturation and IgE class-switching.

13 sociated with a rapid decline in Ag-specific class-switched Ab.

14 als are characterized by decreased titers of class-switched Abs and decreased rates of somatic hyperm

15 High-affinity class-switched Abs and memory B cells are products of th

16 Twenty percent of the clones consisted of class switched and IgM(+)(IgD(+)) members, a feature tha

17 Evidence for IgG-expressing B cells, class switching and antibody maturation in normal and ma

18 IL-4 activation of B cells is essential for class switching and contributes to the induction of B ef

19 ase (AID) in engineered cells allowed for Ig class switching and generated BCR variants with improved

20 hibition, together with the rescue of B cell class switching and plasma cell survival by enforced NF-

21 a neutrophil-regulated pathway that elicited class switching and plasmablast expansion via a combinat

22 4 derived from Tfh cells is required for IgE class switching and plasmablast formation.

23 T-dependent mechanisms orchestrate Ig alpha class switching and SIgA responses against commensal and

24 gene knockout or Rab7 activity inhibition in class switching and survival, respectively, whereas prol

25 Greater apoptotic depletion of class-switched and IgM memory cells was associated with

26 vidual t1/2 of pre-established Ag-induced Ig class-switched and IgM-positive memory B cells over 402

27 e increased expression of genes related with class-switching and memory B cell development, including

28 nt infections due to impaired immunoglobulin class-switching and somatic hypermutation.

29 ally, iNKT cells drive B cell proliferation, class switch, and antibody production to induce primary

30 CD80(+) memory B-1b cells divided, class switched, and differentiated into ASC in response

31 B-cell proliferation, immunoglobulin G (IgG) class switching, and plasmablast differentiation through

32 ils and mast cells, promoting immunoglobulin class switching, and preventing excessive activation.

33 3 s.d.), four IGH locus variants influencing class switching, and ten new associations with the HLA r

34 s high-affinity antibodies, promote antibody class switching, and yield B cell memory.

35 s impaired, with fewer memory cells, reduced class-switching, and lower frequency and complexity of s

36 munity, inflammasome activation and antibody class switching; and dysregulation of CH25H may contribu

37 and hemagglutinin leads to the production of class-switched anti-MOG antibodies, dependent on the pre

38 velop systemic autoimmunity characterized by class-switched anti-nuclear Abs.

39 The production of high affinity, class switched antibodies produced by B cells hinges on

40 Expression of class-switched antibodies from Ara h 2-positive cells co

41 al center reaction and for the production of class-switched antibodies in response to thymus-independ

42 In contrast, class-switched antibodies specific to S. aureus are comm

43 Class-switched antibodies to double-stranded DNA (dsDNA)

44 ials, recruited to germinal centers, secrete class-switched antibodies, undergo somatic hypermutation

45 tial for B cell production of high-affinity, class-switched antibodies.

46 -lived and produce high-affinity, generally, class-switched antibodies.

47 essential in the induction of high-affinity, class-switched antibodies.

48 tigen-specific GC B cells, and high-affinity class-switched antibody production.

49 , supporting the induction of high-affinity, class-switched antibody responses, long-lived plasma cel

50 s, follicular CD4 T cells, and production of class-switched antibody, together with expansion of B1 B

51 hogenic infections through the generation of class-switched antibody-secreting cells (ASCs) in germin

52 tivation, antigen presentation, T cell help, class switching, antibody production and cytokine produc

53 mune responses, especially the generation of class-switched, antigen-specific antibody responses.

54 the cellular interactions necessary for IgA class switching are poorly defined.

55 rogressive introduction of hypermutation and class-switching as animals age.

56 High titer, class-switched autoantibodies are a hallmark of systemic

57 m BAFF-transgenic mice spontaneously produce class-switched autoantibodies ex vivo.

58 production of IL-21, a cytokine crucial for class-switched B cell antibodies.

59 ion must be exquisitely controlled because a class-switched B cell cannot revert back to the parent i

60 5(+)), proliferation markers (Ki-67(+)), and class-switched B cells (IgG(+)); and (5) both TNFRSF17 m

61 est that Sox2 may regulate AID expression in class-switched B cells to suppress genomic instability a

62 clone assumes multiple cell fates, including class-switched B cells, antibody-secreting plasma cells,

63 otential mechanism through which appropriate class-switching can be coupled to plasmablast proliferat

64 s of somatic hypermutation (SHM) and also Ig class switching, can have a potent mutator phenotype in

65 splenic B1a cells, which differentiated into class-switched CD138(+) IgG-secreting B1a cells.

66 CD45RB(+)CD27(-) early memory population, a class-switched CD39(+) tonsil-resident population, and a

67 reduced numbers of marginal zone B cells and class-switched cells, and were associated with decreased

68 n induces terminal maturation and Ig isotype class switch (class switch recombination [CSR]).

69 Class switch-competent anti-insulin B cells fail to prod

70 These data demonstrate that class switch-competent anti-insulin B cells remain funct

71 e deficit, possibly due to an immunoglobulin class switch defect, in obesity and T2D during exacerbat

72 Notably, early IgE class switching did not require germinal center formatio

73 uman basophils enhance B cell proliferation, class switching, differentiation into PC, maturation of

74 nduced cytidine deaminase and, therefore, Ig class switch DNA recombination, as central to the matura

75 Antibody class-switch DNA recombination (CSR) is initiated by AID

76 ll intrinsic functions to moderately enhance class-switch DNA recombination (CSR), while decreasing a

77 e acceptor switch region correlates with the class switch efficiency, raising the possibility that th

78 Elevated chemokines and IgE class switching events were observed in IMT samples, con

79 These processes, including class switching, evolved with and appear inseparable fro

80 in place of Sgamma1 undergo I-SceI-dependent class switching from IgM to IgG1 at 5-10% of normal leve

81 vaccination through their effect on the IgA class-switching function of LDCs.

82 ined with a glycolipid adjuvant designed for class switch further enhanced the vaccine efficacy with

83 erns and lineage characteristics of antibody class switching have remained uncharacterized in living

84 , as well as increased levels of Ag-specific class-switched Ig production following immunization with

85 3 promoted homeostatic production of IgM and class-switched IgG antibodies to microbial capsular poly

86 We show that 'resisters' possess IgM, class-switched IgG antibody responses and non-IFN-gamma

87 In this study, we showed that the class-switched IgG autoantibody response in MRL/Fas(lpr/

88 nal to trigger secretion of autoreactive and class-switched IgG in vivo in the absence of cognate T c

89 o associated with a significant reduction in class-switched IgG, and anti-nucleosomal IgG-secreting B

90 using these particles elicited both IgM and class-switched IgG1, IgG2b, and IgG3 autoreactive Abs th

91 ly related cells exist when purified B cells class switch in vitro, suggesting that class switch reco

92 te as it is central to the initiation of IgE class switching in B cells.

93 ect activation-induced deaminase to initiate class switching in B cells.

94 f autoantigen specificities and autoantibody class switching in BXD2 and control (C57BL/6) mice and h

95 IgG responses, suggesting defective isotype class switching in CD73-deficient mice.

96 HEJ is insufficient to impact immunoglobulin class switching in DEK knockout mice.

97 hensively measured the landscape of antibody class switching in human adult twins using antibody repe

98 salivary prostaglandin E2 triggers antibody class switching in mature B cells, increasing the levels

99 We further demonstrate that AhR suppresses class switching in vivo after influenza virus infection

100 B cells undergo maturation and class-switching in response to antigen exposure and T-ce

101 globulinemia, nonspecific B cell activation, class switching, increased cell turnover, breakage of to

102 , nonspecific B cell activation, nonspecific class switching, increased cell turnover, breakage of to

103 arable somatic hypermutation frequencies and class-switching indicated affinity-matured antibodies in

104 Antibody class switching is a feature of the adaptive immune syst

105 ability of A2 mice to undergo immunoglobulin class switching is due to deficient CD4 helper T cell fu

106 Even though class switching is essential for mounting a protective r

107 atible with the idea that division-linked Ig class switching is in part due to CDK2-regulated AID nuc

108 ngraftment, but also significantly increased class switched memory B cells and serum immunoglobulin G

109 arkers on peripheral blood DN, IgD(-)CD27(+) class-switched memory (CSM) and IgD(+)CD27(-) naive B ce

110 Frequencies of AF DENV(+) class-switched memory B cells (IgD(-)CD27(+) CD19(+) cel

111 Numbers of total memory (CD27(+)) and class-switched memory B cells (IgM(-)) were significantl

112 cted to those patients with severely reduced class-switched memory B cells and an elevated level of C

113 B-cell lymphopenia, decreased frequencies of class-switched memory B cells and hypogammaglobulinemia

114 reased (healthy donors) MHC-II expression as class-switched memory B cells and intermediate costimula

115 e number of iNKT cells and the percentage of class-switched memory B cells and propensity to lymphopr

116 Class-switched memory B cells showed: accumulation of FA

117 Deep sequencing of the BCR from E2-specific class-switched memory B cells sorted from two independen

118 HCV-specific class-switched memory B cells were detected in 3 out of

119 ealthy controls revealed that frequencies of class-switched memory B cells were increased in the pati

120 latory molecule expression between naive and class-switched memory B cells, indicating their potentia

121 n thymic failure and the severe reduction in class-switched memory B cells, while gathering longitudi

122 ny large B-cell clones, especially among non-class-switched memory B cells.

123 ly diverse compartment of IgM(+)(IgD(+)) and class-switched memory B cells.

124 of naive, mature CD5(+), IgM(+) memory, and class-switched memory B cells.

125 cell induced plasma cells (PCs) that secrete class-switched neutralizing antibody are paramount to ef

126 rlichial infection is to promote appropriate class switching, not lineage specification.

127 Class switching occurs by a deletional recombination bet

128 creased proliferation, survival, and thereby class switching of ex vivo-activated B cells.

129 C T cell frequency, GC B cell frequency, and class switching of GC B cells to IgG1.

130 ar differentiation, GC B cell frequency, and class switching of GC B cells to IgG1.

131 protein (CD40-muIg) binding, and rescued IgG class switching of naive B cells in vitro.

132 found significant expansion, retention, and class-switching of autoreactive B cells in GCs under con

133 e lupus-associated, somatically mutated, and class-switched pathogenic autoantibodies are generated i

134 ted and delineates a two-tiered hierarchy of class switch pathways.

135 -cell subsets to generate IgE(+) PCs and the class switching pathways involved.

136 cells to promote B cell differentiation into class-switched plasmablasts and led to downregulation of

137 ycle time of approximately 11 h, and that Ig class switching preferentially occurred in the late G1 o

138 s and supports a controllable immunoglobulin class-switching reaction.

139 ve mice without memory T cells recapitulated class-switched recall alloantibody responses.

140 ls, including DSBs generated during antibody class switch recombination (CSR) and DSBs generated by i

141 mphocytes use two DNA alteration mechanisms, class switch recombination (CSR) and somatic hypermutati

142 o immunoglobulin (Ig) loci promotes antibody class switch recombination (CSR) and somatic hypermutati

143 re B cells diversify their antibody genes by class switch recombination (CSR) and somatic hypermutati

144 uced cytidine deaminase (AID) initiates both class switch recombination (CSR) and somatic hypermutati

145 ing (V(D)J) recombination and immunoglobulin class switch recombination (CSR) are key processes in ad

146 d the mechanisms underlying abnormalities in class switch recombination (CSR) associated with the hum

147 n this study, we show that Ab production and class switch recombination (CSR) depend on autocrine C3a

148 Class switch recombination (CSR) diversifies antibodies

149 In mature B cells, class switch recombination (CSR) generates different ant

150 Class switch recombination (CSR) generates isotype-switc

151 recombination in developing lymphocytes and class switch recombination (CSR) in antigen-stimulated B

152 ernative-end-joining (Alt-EJ) pathway during class switch recombination (CSR) in B cells, and HMCES d

153 Antibody class switch recombination (CSR) in B lymphocytes replac

154 e fidelity functions of 53BP1 coevolved with class switch recombination (CSR) in the immune system.

155 In B lymphocytes, Ig class switch recombination (CSR) is induced by activatio

156 In B cells, Ig class switch recombination (CSR) is initiated by activat

157 Immunoglobulin (Ig) class switch recombination (CSR) is initiated by the tra

158 IgH class switch recombination (CSR) occurs through the deli

159 to initiate somatic hypermutation (SHM) and class switch recombination (CSR) of antibody genes.

160 ine, and the somatic hypermutation (SHM) and class switch recombination (CSR) pipeline.

161 Class switch recombination (CSR) plays an important role

162 Immunoglobulin heavy chain class switch recombination (CSR) requires targeted forma

163 Naive B cells undergo class switch recombination (CSR) to generate antibodies

164 gE(+) cells in vivo and the low frequency of class switch recombination (CSR) to IgE ex vivo.

165 Immunoglobulin class switch recombination (CSR) to IgE is a tightly reg

166 uch as those occurring during immunoglobulin class switch recombination (CSR), are repaired by non-ho

167 globulin switch (S) regions is essential for class switch recombination (CSR), but no molecular funct

168 eaminase (AID) initiates immunoglobulin (Ig) class switch recombination (CSR), somatic hypermutation

169 atory intermediates for Ig heavy chain (Igh) class switch recombination (CSR).

170 lls undergo Immunoglobulin Heavy Chain (IgH) class switch recombination (CSR).

171 serves as a novel DNA repair regulator of Ig class switch recombination (CSR).

172 ions has been implicated in regulation of Ig class switch recombination (CSR).

173 on, indicating a reduced capacity to undergo class switch recombination (CSR).

174 rmutation or DNA double-strand breaks during class switch recombination (CSR).

175 d plays a central function in the process of class switch recombination (CSR).

176 ate antibody somatic hypermutation (SHM) and class switch recombination (CSR).

177 hat needs isotype-switched Abs generated via class switch recombination (CSR); however, stimulating t

178 inal maturation and Ig isotype class switch (class switch recombination [CSR]).

179 l center (GC) reaction where B cells undergo class switch recombination and clonal selection to gener

180 GC reaction in primary B cells by impairing class switch recombination and memory B and plasma cell

181 Our rigorous analysis included ex vivo class switch recombination and plasmablast differentiati

182 ) is a genome-mutating enzyme that initiates class switch recombination and somatic hypermutation of

183 tidine deaminase (AID) is a key regulator of class switch recombination and somatic hypermutation of

184 lack the ability to undergo normal levels of class switch recombination and somatic hypermutation, tw

185 hat targets immunoglobulin genes to initiate class switch recombination and somatic hypermutation.

186 uced cytidine deaminase (AID), the enzyme of class switch recombination and somatic hypermutation; th

187 of B cells involves the sequential events of class switch recombination and somatic hypermutations ch

188 dergone the affinity-maturation processes of class switch recombination and, possibly, somatic hyperm

189 ing transcription, alternative splicing, and class switch recombination are required to facilitate de

190 ich accumulates in the nucleus and increases class switch recombination as well as chromosomal transl

191 nzymatic function of host UNG in an in vitro class switch recombination assay.

192 ells and revealed that the inhibition of IgE class switch recombination by IL-21 was attenuated by CD

193 region and Aicda locus, E-proteins regulated class switch recombination by inducing both Igh germline

194 tant role in repairing DSBs generated during class switch recombination by promoting the classical NH

195 region super-enhancer and leads to decreased class switch recombination efficiency.

196 e functionality of AID by evaluating in vivo class switch recombination in 52 MCL cases; and sought f

197 d break repair protein that is essential for class switch recombination in B lymphocytes and for sens

198 protein ATM has long been known to influence class switch recombination in ex vivo-cultured B cells.

199 ated in NP, and there was evidence for local class switch recombination in NP.

200 cells class switch in vitro, suggesting that class switch recombination is directed toward specific i

201 l not fully understood where in the body IgE class switch recombination of food allergen-specific B c

202 se (AID) initiates somatic hypermutation and class switch recombination of the immunoglobulin genes.

203 n genes encoded proteins contributing to IgE class switch recombination or B-cell receptor signaling.

204 in the normal G+C-rich context of mammalian class switch recombination regions, R-loops are obligato

205 In B cells, STAT6 is required for class switch recombination to IgE and for germinal cente

206 remodeling (global somatic hypermutation and class switch recombination to major isotypes) in activat

207 Class switch recombination to several isotypes was also

208 genes associated with B cell activation and class switch recombination was measured by qRT-PCR.

209 Class switch recombination was partly lost due to a fail

210 s attenuated by CD40 signaling, whereas IgG1 class switch recombination was potentiated by IL-21 in t

211 in switch (S) regions during immunoglobulin class switch recombination, a physiological, deletion/re

212 rmal primary humoral responses, encompassing class switch recombination, affinity maturation, and ger

213 ir functionality, somatic mutational status, class switch recombination, and oncogenic Ig translocati

214 o B cells to facilitate affinity maturation, class switch recombination, and plasma cell differentiat

215 pair, V(D)J recombination and immunoglobulin class switch recombination, as well as innate immune and

216 joining recombination in vivo but not during class switch recombination, for which PAXX appeared to b

217 and joining recombination and immunoglobulin class switch recombination, here, using Cre/lox-specific

218 ase (AID) involved in somatic hypermutations/class switch recombination, in primary human B cells.

219 underwent efficient V(D)J recombination and class switch recombination, indicating that phosphorylat

220 xpression, germ-line transcription preceding class switch recombination, interactions between targete

221 sured the expression of two miRs crucial for class switch recombination, miR-155 and miR-16, in human

222 ne segment usage, CDR3 length distributions, class switch recombination, somatic hypermutation levels

223 erate double-strand DNA breaks for efficient class switch recombination.

224 , Id3-depleted B cells displayed a defect in class switch recombination.

225 ting Ab production, affinity maturation, and class switch recombination.

226 G1 Abs, demonstrating a functional effect on class switch recombination.

227 deletion of intervening DNA sequences during class switch recombination.

228 ution and impedes B cell differentiation and class switch recombination.

229 tation but defective affinity maturation and class switch recombination.

230 homologous end-joining during immunoglobulin class switch recombination.

231 s endonuclease activity is essential for IgA-class switch recombination.

232 induced cytidine deaminase gene required for class switch recombination/somatic hypermutation inducti

233 Class-switch recombination (CSR) alters the Ig isotype t

234 eviously unappreciated role for Flt3 in IgG1 class-switch recombination (CSR) and production.

235 AID mediates class-switch recombination (CSR) and somatic hypermutati

236 tidine deaminase (AID), the enzyme-mediating class-switch recombination (CSR) and somatic hypermutati

237 CD103(+) and CD24(+)CD11b(+) DCs induced IgA class-switch recombination (CSR) by activating B cells t

238 y initiating somatic hypermutation (SHM) and class-switch recombination (CSR) during transcription of

239 e same, BXD2-p19(-/-) mice exhibited a lower class-switch recombination (CSR) in the GC B cells, lead

240 Somatic hypermutation (SHM) and class-switch recombination (CSR) increase the affinity a

241 Class-switch recombination (CSR) is a DNA recombination

242 M(+) mouse B cells and hybridomas, we induce class-switch recombination (CSR) of the IgH chain to the

243 enes through somatic hypermutation (SHM) and class-switch recombination (CSR) processes.

244 atory functions that control IgH expression, class-switch recombination (CSR), and somatic hypermutat

245 Following class-switch recombination (CSR), antigen-activated B ce

246 lity to perform somatic hypermutation (SHM), class-switch recombination (CSR), or both.

247 IgH switch (S) region DNA breaks (DSBs) for class-switch recombination (CSR).

248 insights into the process of immunoglobulin class-switch recombination (CSR).

249 Class-switch recombination and antibody affinity maturat

250 ous end-joining (NHEJ) during immunoglobulin class-switch recombination and consequently impairs immu

251 Because BAFF promotes B cell class-switch recombination and humoral autoimmunity, we

252 bility, confirming that these AHAs underwent class-switch recombination and somatic hypermutation.

253 Immunoglobulin class-switch recombination defects (CSR-D) are rare prim

254 We find that AhR negatively regulates class-switch recombination ex vivo by altering activatio

255 receptor participates in the control of IgE class-switch recombination in B cells.

256 e authors show that IgE can be generated via class-switch recombination in IgG1 memory B cells withou

257 ic gene expression, antigen presentation and class-switch recombination in plasmablasts.

258 Somatic hypermutation and class-switch recombination of the immunoglobulin (Ig) ge

259 in various physiological processes, such as class-switch recombination or crossing-over during meios

260 ty of the double-strand break repairs in the class-switch recombination process in vivo.

261 immunoglobulin M (IgM) BCR despite an active class-switch recombination process, and by the introduct

262 4 as a regulator of PARP1-dependent NHEJ and class-switch recombination, providing a molecular basis

263 in various basic nuclear processes, such as class-switch recombination, transcription termination an

264 over extended regions during immunoglobulin class-switch recombination.

265 s recruitment to switch (S) regions leads to class-switch recombination.

266 y diversification: somatic hypermutation and class-switch recombination.

267 delayed-type hypersensitivity responses, and class-switch recombination.

268 and Toll receptor stimuli and undergo normal class-switch recombination.

269 ver, TET2-deficient B cells showed defective class-switch recombination.

270 d DNA lesions in cells attempting to undergo class-switch recombination.

271 to become Ab-producing cells and to undergo class-switch recombination.

272 ugh upregulating differentiation-related and class switching-related genes, indicating a potential ro

273 Ig class switching requires cell proliferation and is divis

274 PP IgA class switching requires innate lymphoid cells, which pr

275 prevented the age-dependent accumulation of class-switched resting memory B cells.

276 lp in germinal center reactions that support class switching, somatic hypermutation, and the generati

277 ) unswitched (unsw)MBCs and IgG(+) or IgA(+) class-switched (sw)MBCs from humans of different age, se

278 induce B cell maturation and immunoglobulin class switching than cells from HIV progressors.IMPORTAN

279 ls, end-joining activity, and immunoglobulin class switching that rely on 53BP1.

280 production is thought to involve sequential class-switching that requires input from T cells.

281 e they act to limit TfH responses and B cell class switching through antigen presentation.

282 TNFSF13, a cytokine involved in plasma cell class switching to IgA.

283 n in response to interleukin 4 (IL-4), hence class switching to IgE and IgG1, is not fully understood

284 th cytokines synergistically promoted B-cell class switching to IgE and plasma cell differentiation.

285 B cells determines their capacity to undergo class switching to IgE ex vivo, with the GC-derived B ce

286 0 signaling, cell proliferation, and de novo class switching to IgE were analyzed by RT-PCR and FACS.

287 s with broader IGHV gene usage and extensive class switching to IgG and IgA subclasses with limited s

288 patches and provide indirect help for B-cell class switching to IgG1 in both transnuclear and wild-ty

289 ve macrophage activation, and immunoglobulin class switching to IgG1, were enhanced in Batf3(-/-) mic

290 gM(+)IgD(+)CD27(+) B cells into PCs, induced class switching to IgG2, and was reproducible in cocultu

291 increased B cell death, low impairs antibody class switching to the pro-inflammatory IgG2c antibody i

292 Secondary analyses of GBCA class, switching to an alternative GBCA, and allergy ski

293 o bNAb lineages, M4008_N1 and M1214_N1, that class-switched to immunoglobulin G (IgG) and IgA.

294 We found that class-switching to IgG1 biased the fate choice made by B

295 class switch was analyzed by quantitation of class switch transcripts.

296 activity of IgG1 and IgG2a anti-erythrocyte class-switch variants of 34-3C monoclonal autoantibody.

297 IgE class switch was analyzed by quantitation of class switc

298 Ig class switching was completely reconstituted by expressi

299 numbers with Stat3-deficient TFH cells, IgG1 class switching was greatly increased.

300 atic hypermutation (SHM), and immunoglobulin class-switching was performed.