ライフサイエンスコーパス: somatic hypermutation

1 n about their BCR repertoires or patterns of somatic hypermutation.

2 HAs underwent class-switch recombination and somatic hypermutation.

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

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

5 s to initiate class switch recombination and somatic hypermutation.

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

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

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

9 hed through clonal selection, expansion, and somatic hypermutation.

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

11 impaired immunoglobulin class-switching and somatic hypermutation.

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

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

14 n the immunoglobulin variable regions during somatic hypermutation.

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

16 ad epitope coverage and strong signatures of somatic hypermutation.

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

18 s are clonally distinct and exhibit enhanced somatic hypermutation.

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

20 ell responses, including class switching and somatic hypermutation.

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

22 the clonally expanded Vh7 revealed signs of somatic hypermutation.

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

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

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

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

27 then undergo class-switch recombination and somatic hypermutation.

28 ns in immunoglobulin variable regions during somatic hypermutation.

29 n extremely broad range of affinities during somatic hypermutation.

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

31 eveloped binding to group 1 subtypes through somatic hypermutation.

32 of class-switched Abs and decreased rates of somatic hypermutation.

33 for low-fidelity DNA polymerases to generate somatic hypermutation.

34 of CSR events occurred prior to the onset of somatic hypermutation.

35 e than predicted by the mutation profiles of somatic hypermutation.

36 fic genes in B cells are off-target sites of somatic hypermutation.

37 ginal zone cells, ABCs displayed significant somatic hypermutation.

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

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

40 rrangements and then diversified by numerous somatic hypermutations.

41 G1, IgG3 and IgA1 transcripts showed reduced somatic hypermutations.

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

43 are not explained by the Neuberger model of somatic hypermutation: 1) across multiple data sets ther

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

45 n ~24 months of emergence of the lineage and somatic hypermutations accumulated at key contact residu

46 iberate immunization and is concomitant with somatic hypermutation activity.

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

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

49 Somatic hypermutation after immunization indicates that

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

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

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

53 Somatic hypermutation and affinity maturation take place

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

55 5 of 52 cases (9.6%), all of which displayed somatic hypermutation and AID-mRNA expression.

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

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

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

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

60 tigen-driven BCR affinity maturation through somatic hypermutation and cellular selection in germinal

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

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

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

64 Germinal center somatic hypermutation and class switch recombination mac

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

66 n-induced cytidine deaminase (AID) initiates somatic hypermutation and class switch recombination of

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

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

69 Somatic hypermutation and class-switch recombination of

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

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

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

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

74 Somatic hypermutation and clonal selection lead to B cel

75 utralizing antibodies display high levels of somatic hypermutation and cross-react with circulating H

76 shared B cell clones had high frequencies of somatic hypermutation and encoded broadly cross-reactive

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

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

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

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

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

82 All three lineages had modest levels of somatic hypermutation and normal antibody-loop lengths a

83 gical range, AID and Blimp1 expression, CSR, somatic hypermutation and plasma cell differentiation.

84 exhibited significantly lower frequencies of somatic hypermutation and predominantly encoded strain-s

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

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

87 lecular programs must balance proliferation, somatic hypermutation and selection to both provide effe

88 These antibodies had low levels of somatic hypermutation and showed a strong enrichment in

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

90 tagenesis" process is a major contributor to somatic hypermutation and therefore Ig diversification i

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

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

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

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

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 ll signaling, increased rounds of productive somatic hypermutation, and B-cell selection strength are

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 , secrete class-switched antibodies, undergo somatic hypermutation, and differentiate into memory B c

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

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 elatively stable as per heavy chain isotype, somatic hypermutations, and clonal composition.

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

110 wever, breaks in V regions that arise during somatic hypermutation are poorly understood.

111 Only a few somatic hypermutations are required for broad antiviral

112 Using somatic hypermutations as a molecular clock, we discover

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

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

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

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

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

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

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

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

121 antibodies, which exhibited a high degree of somatic hypermutation, consistent with chronic antigen e

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

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

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

125 We identified high rates of somatic hypermutations, especially targeting RGYW/WRCY h

126 odies, the diversity of which is expanded by somatic hypermutation following antigen exposure(1).

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

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

129 y B cells that displayed significantly lower somatic hypermutation frequencies than their counterpart

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

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

135 Somatic hypermutation generates a myriad of Ab mutants i

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

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

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

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

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

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

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

143 udy can play an important role in generating somatic hypermutation in cancers as well as in noncancer

144 G repertoire diversity, clonal expansion and somatic hypermutation in cells from mice immunized with

145 a striking genome-wide increase in aberrant somatic hypermutation in EBV-positive tumors, supporting

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 ching to IgG and IgA subclasses with limited somatic hypermutation in the initial weeks of infection.

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

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 one marrow, blood B and plasma cell subsets, somatic hypermutations in Ig genes, and in vitro prolife

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

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

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

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

166 Similarly, somatic hypermutation is almost negligible at the JH4 in

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

168 y detectable binding to AQP4, revealing that somatic hypermutation is required for the generation of

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

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

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

172 h distributions, class switch recombination, somatic hypermutation levels and in features of V(D)J re

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

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

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

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

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

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

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

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

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

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

188 DN B cells are Ag experienced, as shown by somatic hypermutation of their Ig genes in adaptive immu

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

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

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

192 converted into untemplated mutations during somatic hypermutation or DNA double-strand breaks during

193 nal NR1 autoantibodies showed low numbers of somatic hypermutations or were unmutated.

194 suggested that J9 and J8 followed divergent somatic hypermutation pathways, and that a limited numbe

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

196 y that analyses both V(D)J segment usage and somatic hypermutation profiles, we elucidate physiologic

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 These persistent antibodies displayed higher somatic hypermutation relative to transient serum antibo

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

201 antigen had several 'unusual residues' (rare somatic hypermutations, rSHM, with positional frequency

202 Somatic hypermutation (SH) generates point mutations wit

203 However, somatic hypermutation (SHM) and affinity maturation can

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

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

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

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

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

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

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

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

212 Somatic hypermutation (SHM) and class-switch recombinati

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

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

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

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

217 d from these plasmablasts had high levels of somatic hypermutation (SHM) and recognized the HA stem r

218 effective antibodies, B cells undergo rapid somatic hypermutation (SHM) and selection for binding af

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

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

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

222 Somatic hypermutation (SHM) diversifies the V region of

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

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

225 on-induced cytidine deaminase (AID)-mediated somatic hypermutation (SHM) following neurotropic corona

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

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

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

229 Somatic hypermutation (SHM) generates much of the Ab div

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

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

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

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

234 uced deoxycytidine deaminase (AID) initiates somatic hypermutation (SHM) in immunoglobulin variable (

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

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

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

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

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

240 During somatic hypermutation (SHM) of Ig genes in germinal cent

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

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

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

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

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

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

247 ealed broad dissemination and high levels of somatic hypermutation (SHM) of most lineages, including

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

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

250 llicular lymphoma B cells undergo continuous somatic hypermutation (SHM) of their immunoglobulin vari

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

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

253 ct, it regulates both the antigen-stimulated somatic hypermutation (SHM) process and plays a central

254 70% of cases (107/154) bearing an imprint of somatic hypermutation (SHM) ranging from minimal to pron

255 e of this difference may be linked to B cell somatic hypermutation (SHM) targeting, including error-p

256 n and, notably, the frequency of VH with low somatic hypermutation (SHM) was strikingly higher, espec

257 ze the importance of affinity maturation via somatic hypermutation (SHM) within the Ig variable H (VH

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

259 bulin (Ig) class switch recombination (CSR), somatic hypermutation (SHM), and gene conversion by conv

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 During somatic hypermutation (SHM), deamination of cytidine by

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

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

266 ntibody class switch recombination (CSR) and somatic hypermutation (SHM), whereas AID targeting of no

267 enes by class switch recombination (CSR) and somatic hypermutation (SHM), which are both dependent on

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

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

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

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

272 n infected livers proliferated and underwent somatic hypermutation (SHM).

273 cells with severely decreased frequencies of somatic hypermutations (SHMs), but their underlying mole

274 quence may differ due to the accumulation of somatic hypermutations (SHMs).

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

276 ndings, vaccines driving immunoglobulin gene somatic hypermutation should be a priority to protect el

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 3abs, and immunoglobulin heavy variable gene somatic hypermutation status, we propose a novel hierarc

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

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

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

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

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

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

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

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

288 enic autoantibodies after the acquisition of somatic hypermutations that improve affinity for self-an

289 We identified somatic hypermutations that were recurrently selected in

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

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

292 -glycans and minor contributions of antibody somatic hypermutations to epitope contacts.

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

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

295 However, somatic hypermutation was increased specifically on the

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

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

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-