ライフサイエンスコーパス: somatic hypermutation

1 n the immunoglobulin variable regions during somatic hypermutation.

2 y in their use of D genes and propensity for somatic hypermutation.

3 ad epitope coverage and strong signatures of somatic hypermutation.

4 mice failed to produce IgG1 and had reduced somatic hypermutation.

5 s are clonally distinct and exhibit enhanced somatic hypermutation.

6 ass-switched antibodies and the frequency of somatic hypermutation.

7 ell responses, including class switching and somatic hypermutation.

8 s with a long CDR H3, and limited subsequent somatic hypermutation.

9 the clonally expanded Vh7 revealed signs of somatic hypermutation.

10 situ mutagenesis, as in the case of in vitro somatic hypermutation.

11 nitiate class-switch recombination (CSR) and somatic hypermutation.

12 lin (Ig) heavy chain gene class switching or somatic hypermutation.

13 of HEK293 cells, and matured using in vitro somatic hypermutation.

14 then undergo class-switch recombination and somatic hypermutation.

15 ns in immunoglobulin variable regions during somatic hypermutation.

16 n extremely broad range of affinities during somatic hypermutation.

17 Ab secretion, class switch recombination, or somatic hypermutation.

18 ecreased fine-tuning of BCR specificities by somatic hypermutation.

19 rangement initiation and to targeting during somatic hypermutation.

20 rer model for the difference between CSR and somatic hypermutation.

21 trarenal B cell clonal expansion and ongoing somatic hypermutation.

22 of class switch recombination and, possibly, somatic hypermutation.

23 unoglobulin class switching with evidence of somatic hypermutation.

24 uced deaminase (AID) and that likely undergo somatic hypermutation.

25 ases and has been proposed to play a role in somatic hypermutation.

26 aminase, an enzyme central to the process of somatic hypermutation.

27 d on junctional diversity and, subsequently, somatic hypermutation.

28 HAs underwent class-switch recombination and somatic hypermutation.

29 on in IgG1 memory B cells without additional somatic hypermutation.

30 ginal zone cells, ABCs displayed significant somatic hypermutation.

31 ching, and lower frequency and complexity of somatic hypermutation.

32 s to initiate class switch recombination and somatic hypermutation.

33 eaminase and T-bet, and exhibits evidence of somatic hypermutation.

34 to N-glycosylation sites that emerge during somatic hypermutation.

35 ssion, class-switch recombination (CSR), and somatic hypermutation.

36 hed memory B cells showed increased rates of somatic hypermutation.

37 impaired immunoglobulin class-switching and somatic hypermutation.

38 gh affinity of binding at such low levels of somatic hypermutation.

39 on of potential N-glycosylation sites during somatic hypermutation.

40 rrangements and then diversified by numerous somatic hypermutations.

41 ells, and IgG4 transcripts were analyzed for somatic hypermutations.

42 potential N-glycosylation motifs acquired by somatic hypermutation (ac-Nglycs) within Ig H chain V re

43 iberate immunization and is concomitant with somatic hypermutation activity.

44 l center and thus time for clonal expansion, somatic hypermutation, affinity maturation, and acquisit

45 In the germinal center, B cells undergo somatic hypermutation, affinity-based clonal expansion,

46 pressed activation markers and had undergone somatic hypermutation, albeit at levels lower than their

47 Within these clusters there was a range of somatic hypermutations along the IGHV germline segment-d

48 0 aa of AID are required for CSR but not for somatic hypermutation, although their role in CSR is unk

49 y and light chain variable domains shaped by somatic hypermutation and affinity maturation of B cells

50 Somatic hypermutation and affinity maturation take place

51 After undergoing Ig somatic hypermutation and Ag selection, germinal center

52 5 of 52 cases (9.6%), all of which displayed somatic hypermutation and AID-mRNA expression.

53 in sequencing promises new insights into the somatic hypermutation and antigen-driven selection proce

54 in which B cells cycle between proliferation/somatic hypermutation and antigen-driven selection.

55 fractional dose boosting increased antibody somatic hypermutation and avidity and sustained high pro

56 of IGHV1-69 polymorphism on V-segment usage, somatic hypermutation and B cell expansion that elucidat

57 enhanced the expression of AID and increased somatic hypermutation and chromosomal translocation freq

58 nactivation, e.g. APOBEC3G, or initiation of somatic hypermutation and class switch recombination (ac

59 also known as AICDA) enzyme is required for somatic hypermutation and class switch recombination at

60 ions and DNA breaks in Ig genes that undergo somatic hypermutation and class switch recombination dur

61 n-induced cytidine deaminase (AID) initiates somatic hypermutation and class switch recombination in

62 Germinal center somatic hypermutation and class switch recombination mac

63 cells and initiates the events that lead to somatic hypermutation and class switch recombination of

64 d antigen-dependent locus remodeling (global somatic hypermutation and class switch recombination to

65 Abs expressed by B cells are diversified by somatic hypermutation and class switch recombination.

66 tigen presentation may have implications for somatic hypermutation and class switching during affinit

67 Somatic hypermutation and class-switch recombination of

68 DNA of an IgA class-switch event, supporting somatic hypermutation and class-switch recombination wit

69 ntral processes in antibody diversification: somatic hypermutation and class-switch recombination.

70 , is the key catalyst in initiating antibody somatic hypermutation and class-switch recombination.

71 action of AID during transcription-dependent somatic hypermutation and class-switch recombination.

72 ctivation-induced deaminase (AID) to undergo somatic hypermutation and class-switch recombination.

73 against DNA damage-induced apoptosis during somatic hypermutation and class-switch recombination.

74 sity, and Joining genes, and peripherally by somatic hypermutation and class-switching of the rearran

75 Somatic hypermutation and clonal selection lead to B cel

76 plated mutations, in the related pathways of somatic hypermutation and gene conversion.

77 Finally, somatic hypermutation and gene usage in VH regions of Ig

78 ced cytidine deaminase (AID) is required for somatic hypermutation and immunoglobulin (Ig) class swit

79 D) is critical in normal B cells to initiate somatic hypermutation and immunoglobulin class switch re

80 ced cytidine deaminase (AID) is required for somatic hypermutation and immunoglobulin class switching

81 GC B cells undergo both somatic hypermutation and isotype switch, and a Darwinia

82 polyreactivity for host antigens, extensive somatic hypermutation and long, variable heavy-chain thi

83 nd achieved breadth with only 10% nucleotide somatic hypermutation and no insertions or deletions.

84 of HIV-1 strains with only approximately 11% somatic hypermutation and no insertions or deletions.

85 lications for class switch recombination and somatic hypermutation and possibly for other biological

86 ted proper cyclic selection of cells in GCs, somatic hypermutation and proliferation were maintained.

87 rates, and removing their self-reactivity by somatic hypermutation and selection in germinal centers

88 ignals to germinal center B cells undergoing somatic hypermutation and selection that results in affi

89 al view of antibody maturation has been that somatic hypermutation and subsequent clonal selection in

90 eated patients have acquired lower number of somatic hypermutation and used focused IGHV repertoire w

91 of the IgE response, where the IgE inherits somatic hypermutations and high affinity from the IgG1 p

92 scripts, however, showed high frequencies of somatic hypermutations and increased usage of downstream

93 Cognate T cell help, somatic hypermutation, and affinity maturation within ge

94 lonal expansion, class switch recombination, somatic hypermutation, and affinity maturation.

95 ture is the site of B cell clonal expansion, somatic hypermutation, and affinity-based selection, the

96 egions, variable region transcription before somatic hypermutation, and antibody heavy chain producti

97 y enhancing genetic instability and aberrant somatic hypermutation, and by negative regulation of tum

98 of criteria, including V gene usage, rate of somatic hypermutation, and CDR-H3 length and composition

99 immunoglobulin genes by V(D)J recombination, somatic hypermutation, and class switch recombination.

100 n germinal centers (GC), underwent extensive somatic hypermutation, and differentiated into memory B

101 cell responses, including isotype switching, somatic hypermutation, and limited affinity maturation,

102 sponse by facilitating isotype switching and somatic hypermutation, and promoting the generation of m

103 riants using natural diversity introduced by somatic hypermutation, and screened half-antibodies for

104 daptive immunity is driven by the expansion, somatic hypermutation, and selection of B cell clones.

105 nter reactions that support class switching, somatic hypermutation, and the generation of high-affini

106 blasts are oligoclonal and exhibit extensive somatic hypermutation, and their numbers decrease after

107 utational repertoire, including kataegis and somatic hypermutation, and their relative contribution c

108 nsistent with oxidative DNA damage and local somatic hypermutation appeared to contribute to this sig

109 Both class switch recombination and somatic hypermutation are initiated by activation-induce

110 Only a few somatic hypermutations are required for broad antiviral

111 required for class-switch recombination and somatic hypermutation, are prone to develop autoimmune d

112 Using somatic hypermutations as a molecular clock, we discover

113 tivation-induced cytidine deaminase-mediated somatic hypermutation, as shown by comprehensive analysi

114 Somatic hypermutation, associated with T-B interactions,

115 to a complete transcript, and the process of somatic hypermutation at individual nucleotides.

116 HIV-1 generally exhibit very high levels of somatic hypermutation, both in their CDR and framework-v

117 FOXO1-negative GC B cells displayed normal somatic hypermutation but defective affinity maturation

118 ariable (V) genes of immunoglobulins undergo somatic hypermutation by activation-induced deaminase (A

119 ial events of class switch recombination and somatic hypermutations characteristic of germinal center

120 -induced cytidine deaminase (AID), initiates somatic hypermutation, class-switch recombination, and g

121 n-induced cytidine deaminase (AID) initiates somatic hypermutation, class-switch recombination, and g

122 tivation-induced deaminase (AID) involved in somatic hypermutations/class switch recombination, in pr

123 d 9G4(+) IgG contained equivalent numbers of somatic hypermutations compared with all other VHs, a ch

124 e have hypothesized that such high levels of somatic hypermutation could pose a challenge for elicita

125 AP4 resulted in reduced GC sizes and reduced somatic hypermutation coupled with a failure to control

126 ity of the method using tumor karyotypes and somatic hypermutation data sets.

127 tance metrics that incorporate the biases of somatic hypermutation do not outperform simple Hamming d

128 Consistent with AID, comparable somatic hypermutation frequencies and class-switching in

129 ion, and by a lack of substantial changes in somatic hypermutation frequencies of IgM memory B cells.

130 subsets, B-cell subset replication history, somatic hypermutation frequencies, CSR patterns, B-cell

131 H4-34-expressing clones and showed decreased somatic hypermutation frequencies.

132 increases CSP-specific antibody avidity and somatic hypermutation frequency in CSP-specific B cells,

133 Inhibition of the AID somatic hypermutation function in BXD2 mice suppressed d

134 Suppression of the somatic hypermutation function of AID resulted in a sign

135 deaminase (AID) protein is known to initiate somatic hypermutation, gene conversion or switch recombi

136 hem to be further diversified and matured by somatic hypermutation, gene conversion, and class-switch

137 We show that these cells exhibit somatic hypermutation, gene expression characteristic of

138 mmunoglobulin class switch recombination and somatic hypermutation impact the efficacy of humoral imm

139 revealed overusage of the IGHV4-34 gene and somatic hypermutation in 71/79 (89.8%) IGHV-IGHD-IGHJ ge

140 did not change the frequency or spectrum of somatic hypermutation in Ab genes, indicating that DNA r

141 le binding to TSHR, indicating importance of somatic hypermutation in acquiring TSAb activity.

142 lalisib, but not ibrutinib, showed increased somatic hypermutation in AID off-targets.

143 ta (Pol iota) is an attractive candidate for somatic hypermutation in antibody genes because of its l

144 is also critical to determining the role of somatic hypermutation in autoimmunity and B-cell cancers

145 not H5, which supports the critical role of somatic hypermutation in broadening the bnAb response.

146 rder to find candidate genes responsible for somatic hypermutation in germinal center B cells.

147 The striking amount of somatic hypermutation in HIV bnAbs led to the hypothesis

148 ions also had significantly reduced rates of somatic hypermutation in IgG (P = .003) but not IgA or I

149 Unexpectedly, we discover high levels of somatic hypermutation in infants as young as 3 months ol

150 R failed, indicating the possible absence of somatic hypermutation in lungfish LAs.

151 y acquire breadth through moderate levels of somatic hypermutation in response to emerging viral vari

152 e of neutralization activity on the level of somatic hypermutation in the Ab framework, we applied a

153 in the light zone (LZ) and proliferation and somatic hypermutation in the dark zone (DZ).

154 diated cell death and increased frequency of somatic hypermutation in the immunoglobulin VH locus.

155 ith E3', and they exhibited modestly reduced somatic hypermutation in the Jkappa-Ckappa intronic regi

156 Somatic hypermutation in the lipogranulomas was T cell-d

157 Somatic hypermutation in the other CDRs of PGT145 were c

158 mining region (CDR) 3 grafting combined with somatic hypermutation in vitro.

159 for natural antibodies that are subjected to somatic hypermutation in vivo.

160 lished studies, suggest an expanded role for somatic hypermutation in which both binding affinity and

161 ifferentiate from the frequent occurrence of somatic hypermutations in Ig sequences.

162 tially, it was the finding that the level of somatic hypermutations in rearranged IG heavy-chain gene

163 nal activity revealed a precise targeting of somatic hypermutation indicative of an active, ongoing i

164 gene required for class switch recombination/somatic hypermutation induction inhibits T1D development

165 although whether the sequence has undergone somatic hypermutation is dependent on the maturation sta

166 to favor a glycan site at N332 on gp120, and somatic hypermutation is required to accommodate the nei

167 ional process that generates these lineages, somatic hypermutation, is biased by hotspot motifs which

168 is dispensable for normal GC cellularity and somatic hypermutation, it is required for the efficient

169 ntibody clonal lineage analysis reveals that somatic hypermutation levels are increased in both infan

170 or" B cells showed reduced proliferation and somatic hypermutation levels, whereas these were normal

171 igand trap for Ang2 by harnessing the B cell somatic hypermutation machinery and coupling this to sel

172 evelop CRISPR-X, a strategy to repurpose the somatic hypermutation machinery for protein engineering

173 nce, in which impaired apoptosis and ongoing somatic hypermutation may lead to an increased risk of l

174 ting of Hashimoto's thyroiditis and aberrant somatic hypermutation may play a role.

175 mbling those generated by the IgV-associated somatic hypermutation mechanism, but were not detected a

176 with BCL2/IgH rearrangements as a result of somatic hypermutation normally occurring at the IgH locu

177 Somatic hypermutation normally occurs as a consequence o

178 or both class-switch recombination (CSR) and somatic hypermutation of Ab genes.

179 Diversity arises from somatic hypermutation of an ultralong DH with a severe c

180 oire diversification in infants and toddlers.Somatic hypermutation of antibodies can occur in infants

181 hat initiates class switch recombination and somatic hypermutation of antibodies in jawed vertebrates

182 However, somatic hypermutation of Ig genes and heavy-chain CDR3 s

183 so contribute to mutagenesis observed during somatic hypermutation of Ig genes.

184 The somatic hypermutation of Ig variable regions requires th

185 g to myoferlin was preserved despite ongoing somatic hypermutation of Ig variable regions.

186 hat initiates class switch recombination and somatic hypermutation of immunoglobulin genes (Ig) in B

187 so is involved in mutagenic processes during somatic hypermutation of immunoglobulin genes.

188 regulator of class switch recombination and somatic hypermutation of immunoglobulin in B cells, yet

189 Studies on somatic hypermutation of the antigen binding region, rec

190 syndrome (including those unable to generate somatic hypermutations of immunoglobulin genes) displaye

191 on-induced deaminase (AID) are essential for somatic hypermutations of this gene during antibody matu

192 tion-induced (cytosine) deaminase to promote somatic hypermutation on both DNA strands to generate do

193 egions, promoting antibody diversity through somatic hypermutation or class switching.

194 lead to either point mutations in V exons in somatic hypermutation or deletion of intervening DNA seq

195 ll lymphomas, is an off-target of the normal somatic hypermutation process taking place in GC B cells

196 b repertoire diversity is based in part on a somatic hypermutation process that introduces adjacent n

197 We show that VH gene repertoires and somatic hypermutation rates of atypical and classical MB

198 Somatic hypermutation rates point to a CSF antigen-drive

199 Ig class switch recombination (CSR) and somatic hypermutation require activation-induced cytidin

200 during class switch recombination (CSR) and somatic hypermutation requires RNA polymerase II (polII)

201 Somatic hypermutation (SH) generates point mutations wit

202 rsification occurs when Ig V regions undergo somatic hypermutation (SHM) and affinity-based selection

203 immunoglobulins (Igs) during the process of somatic hypermutation (SHM) and also Ig class switching,

204 ool, the immune repertoire pipeline, and the somatic hypermutation (SHM) and class switch recombinati

205 n-induced cytidine deaminase (AID) initiates somatic hypermutation (SHM) and class switch recombinati

206 munoglobulin (Ig) genes to initiate antibody somatic hypermutation (SHM) and class switch recombinati

207 ondary diversification of antibodies through somatic hypermutation (SHM) and class switch recombinati

208 Antibody diversification through somatic hypermutation (SHM) and class switch recombinati

209 ion repair (BER) or mutagenically to produce somatic hypermutation (SHM) and class switch recombinati

210 ines at immunoglobulin (Ig) loci, initiating somatic hypermutation (SHM) and class switch recombinati

211 tosine deaminase (AID) is essential for both somatic hypermutation (SHM) and class switch recombinati

212 D) converts cytosine into uracil to initiate somatic hypermutation (SHM) and class switch recombinati

213 nd Ab responses to Ag stimulation require Ig somatic hypermutation (SHM) and class-switch recombinati

214 Somatic hypermutation (SHM) and class-switch recombinati

215 ions and deletions in antibody genes through somatic hypermutation (SHM) and class-switch recombinati

216 antibody diversity in B cells by initiating somatic hypermutation (SHM) and class-switch recombinati

217 Somatic hypermutation (SHM) and immunoglobulin (Ig) clas

218 To analyze its suggested role in somatic hypermutation (SHM) and possible contribution to

219 Ig) class switch DNA recombination (CSR) and somatic hypermutation (SHM) are critical for the maturat

220 IgH) class switch recombination (CSR) and Ig somatic hypermutation (SHM) by deaminating cytidines wit

221 itiates class switch recombination (CSR) and somatic hypermutation (SHM) by deaminating cytosine resi

222 ar lymphoma (FL) is apparent from studies of somatic hypermutation (SHM) caused by activation-induced

223 Somatic hypermutation (SHM) diversifies the V region of

224 f infected adults and exhibit high levels of somatic hypermutation (SHM) due to years of affinity mat

225 el hybrid nucleotide motif: the signature of somatic hypermutation (SHM) enzyme, Activation Induced D

226 ells with respect to their B-cell receptors, somatic hypermutation (SHM) features in HCL were examine

227 es, AID initiates antibody variable (V) exon somatic hypermutation (SHM) for affinity maturation in g

228 uced cytidine deaminase (AID) initiates both somatic hypermutation (SHM) for antibody affinity matura

229 e to unusual traits of bnAbs, including high somatic hypermutation (SHM) frequencies and in-frame ins

230 Effects on somatic hypermutation (SHM) have been varied depending o

231 occurred as evidenced by elevated levels of somatic hypermutation (SHM) in Ab sequences isolated at

232 es both class switch recombination (CSR) and somatic hypermutation (SHM) in antibody diversification.

233 ediates class-switch recombination (CSR) and somatic hypermutation (SHM) in B cells, but the mechanis

234 h recombination (CSR) and Ig variable region somatic hypermutation (SHM) in B lymphocytes by deaminat

235 talyses class switch recombination (CSR) and somatic hypermutation (SHM) in B lymphocytes to enhance

236 B cell repertoire diversification occurs by somatic hypermutation (SHM) in germinal centers followin

237 nvestigated the clonal overlap and extent of somatic hypermutation (SHM) in the ASC (effector) and AB

238 lls into germinal centers where they undergo somatic hypermutation (SHM) in V(D)J exons for the gener

239 Somatic hypermutation (SHM) is an integral process in th

240 he ANA originate from V(D)J recombination or somatic hypermutation (SHM) is not known.

241 ed neutralization associated with increasing somatic hypermutation (SHM) levels over time.

242 We showed, using laser microdissection, that somatic hypermutation (SHM) occurred efficiently at extr

243 Somatic hypermutation (SHM) of Ig genes in B cells is cr

244 Somatic hypermutation (SHM) of Ig genes is initiated by

245 ial for class-switch recombination (CSR) and somatic hypermutation (SHM) of Ig genes.

246 ivation-induced deaminase (AID) mediates the somatic hypermutation (SHM) of Ig variable (V) regions t

247 Somatic hypermutation (SHM) of immunoglobulin (Ig) genes

248 The process of somatic hypermutation (SHM) of immunoglobulin (Ig) genes

249 diating class-switch recombination (CSR) and somatic hypermutation (SHM) of immunoglobulin genes, is

250 During somatic hypermutation (SHM) of immunoglobulin genes, ura

251 ecause they are not accompanied by extensive somatic hypermutation (SHM) of targeted regions and beca

252 Ig-CSR may also be associated with impaired somatic hypermutation (SHM) of the Ig V regions.

253 mulated germinal center (GC) B cells undergo somatic hypermutation (SHM) of V(D)J exons followed by s

254 ransformed (t-FL) lymphomas, we analyzed the somatic hypermutation (SHM) pattern of the variable regi

255 Analyses of somatic hypermutation (SHM) patterns in B cell Ig sequen

256 70% of cases (107/154) bearing an imprint of somatic hypermutation (SHM) ranging from minimal to pron

257 Both class switch recombination (CSR) and somatic hypermutation (SHM) require transcription and th

258 adaptive immune system by coupling in vitro somatic hypermutation (SHM) with mammalian cell display.

259 During somatic hypermutation (SHM), activation-induced deaminas

260 Molecular analysis of replication histories, somatic hypermutation (SHM), and immunoglobulin class-sw

261 They play major roles in regulating somatic hypermutation (SHM), class switch DNA recombinat

262 orrelate and assess their ability to perform somatic hypermutation (SHM), class-switch recombination

263 Somatic hypermutation (SHM), coupled with Ag selection,

264 During somatic hypermutation (SHM), deamination of cytidine by

265 red for class switch recombination (CSR) and somatic hypermutation (SHM), processes that ensure antib

266 ody class switch DNA recombination (CSR) and somatic hypermutation (SHM), through direct activation o

267 anisms, class switch recombination (CSR) and somatic hypermutation (SHM), to re-engineer their antibo

268 Class-switch DNA recombination (CSR) and somatic hypermutation (SHM), which require activation-in

269 sma cells (PCs) from CD lesions have limited somatic hypermutation (SHM).

270 anisms: class switch recombination (CSR) and somatic hypermutation (SHM).

271 lobulin class-switch recombination (CSR) and somatic hypermutation (SHM).

272 through class-switch recombination (CSR) and somatic hypermutation (SHM).

273 nal expansions and had significant levels of somatic hypermutation (SHM).

274 ations within the antigen-binding V regions (somatic hypermutation, SHM) and double-strand DNA breaks

275 esponsive B cells were characterized by more somatic hypermutation, shorter CDR3 segments, and less n

276 dominant-negative (DN) form of Aicda at the somatic hypermutation site (BXD2-Aicda-DN-transgenic mic

277 CSR efficiency and only modestly affects the somatic hypermutation spectrum in vitro.

278 ell subset composition, replication history, somatic hypermutation status, and class-switch recombina

279 LC- and HC-MBL had similar somatic hypermutation status, yet different IGHV gene re

280 mbination with clonal expansion and signs of somatic hypermutation suggest a CD4(+) T lymphocyte-depe

281 develop breadth, and extraordinary level of somatic hypermutation suggested commonalities in maturat

282 of the tract and have higher frequencies of somatic hypermutation, suggesting extensive and serial r

283 nfluenza strain and exhibited high levels of somatic hypermutation, suggesting they were derived from

284 of unconventional GC B cells that underwent somatic hypermutation, survived despite losing antigen r

285 pulations, creating lineage trees, inferring somatic hypermutation targeting models, measuring repert

286 ntensive analysis of a published database of somatic hypermutations that arose in the IGHV3-23*01 hum

287 the enzyme of class switch recombination and somatic hypermutation; the transcription factor E47, cru

288 anded by Y. enterocolitica porins to undergo somatic hypermutation to acquire a cross-reactive pathog

289 mal levels of class switch recombination and somatic hypermutation, two mutagenic DNA processes used

290 ously experienced malaria continue to induce somatic hypermutations upon malaria rechallenge.

291 However, somatic hypermutation was increased specifically on the

292 Somatic hypermutation was very low in fetal IPP and the

293 ddition, class switch recombination, but not somatic hypermutation, was impaired in Pms2EK/EK B cells

294 Sequencing revealed 82% with somatic hypermutation, whereas 18% had >98% germ-line id

295 to antibody variable (V) regions results in somatic hypermutation, whereas its recruitment to switch

296 from self-reactive B cells having undergone somatic hypermutation with affinity selection and class

297 High-affinity antibodies are generated by somatic hypermutation with nucleotide substitutions intr

298 Dengue plasmablasts had high degrees of somatic hypermutation, with a clear preference for repla

299 ficantly associated (P < 0.001) with lack of somatic hypermutation within the clonotypic immunoglobul

300 VDJ rearrangement and somatic hypermutation work together to produce antibody-