ライフサイエンスコーパス: clonotype

1 ecific peptide/MHC ligation of the alphabeta clonotype.

2 at were comparable to those of the effective clonotype.

3 explaining the immunodominant usage of this clonotype.

4 age-dependent increase in a diabetogenic CD8 clonotype.

5 e observed long-term persistence of a single clonotype.

6 tributing to the selection of the public TCR clonotype.

7 tted uninhibited accumulation of low-avidity clonotypes.

8 3s that group into 30 distinct antibody V(H) clonotypes.

9 by length-matched Ag-specific CD8(+) T-cell clonotypes.

10 d proliferation (LIP) of two distinct T cell clonotypes.

11 ease disproportionally affects low-frequency clonotypes.

12 for cross-recognition compared with dominant clonotypes.

13 nes per response, of both public and private clonotypes.

14 ocess, conditioned on non-extinction of both clonotypes.

15 the numbers of T cells belonging to the two clonotypes.

16 structural role for the TCRA chain for these clonotypes.

17 t of the repertoire implies a role for these clonotypes.

18 d CD4 T cell response toward higher-affinity clonotypes.

19 itical for recognition by most of the T cell clonotypes.

20 inant as well as a nonexpanded, "supporting" clonotypes.

21 neity exists within individual CD8(+) T cell clonotypes.

22 ong behavior of CMV- and EBV-specific T cell clonotypes.

23 ents identified no additional cross-reactive clonotypes.

24 CDR3 motifs, and a high frequency of public clonotypes.

25 rare, found in only one of seven VH1-46 IgG clonotypes.

26 ogenic neoantigens and tumor-reactive T cell clonotypes.

27 r repertoires comprising exclusively private clonotypes.

28 he major part of the differences among these clonotypes.

29 These 53 clones expressed 47 unique clonotypes, 8 of which encoded proinsulin-specific T-cel

30 ximately 100 antibody clonotypes, with three clonotypes accounting for >40% of the response.

31 influenza vaccine, with boosted pre-existing clonotypes accounting for approximately 60% of the respo

32 enrichment (or diminution) of particular TCR clonotypes across all challenged animals.

33 To evaluate the dynamic nature of T cell clonotypes across time, we utilized several binary simil

34 ssential for the maintenance of low-affinity clonotypes after protein vaccination but was not suffici

35 TRAV29 clonotypes also proved cross-restricted, but conferred r

36 ertoires display highly dynamic yet distinct clonotype alterations.

37 er extended to investigate the transition of clonotypes among different biological compartments.

38 By direct and semi-nested amplification, clonotype amplicons were found to be shared by multiple

39 ll patients within 10 d of infusion, and TCR clonotype analysis showed persistence of infused cells i

40 were dispensable for the development of this clonotype and had negligible impact on the polyclonal Tr

41 ndependent and are restricted with regard to clonotype and isotype expression.

42 ies; a decrease in or loss of the pathogenic clonotype and restoration of the TCR repertoire was foun

43 ntained over time by a recruitment of non-RS-clonotypes and a shift of existing RS-clonotypes into hi

44 d similarity between multiple immunodominant clonotypes and codominant as well as a nonexpanded, "sup

45 y IgM(+) B cells were related to some IgA(+) clonotypes and switched to IgA in response to T cell-ind

46 ructural avidity between TRBV7 and non-TRBV7 clonotypes and this epitopic peptide.

47 NA sequencing procedures for identifying TCR clonotypes and transcript phenotypes in individual T cel

48 arthritis model to determine the frequency, clonotype, and specificity of T cells that infiltrate ar

49 d not cause the elimination of high-affinity clonotypes, and at a low dose, they also skewed CD4 T ce

50 rior Ag exposure, inferred from expanded TCR clonotypes, and essential phenotypic properties in their

51 er C127 expression compared with subdominant clonotypes, and TCR avidity positively correlates with P

52 sms: 1) functional improvement of persisting clonotypes; and 2) recruitment of particular clonotypes

53 t the persistence of numerous BM plasma cell clonotypes ( approximately 2%) identifiable at all point

54 Dominant clonotypes are characterized by higher PD-1 expression a

55 such expansion, ensuring that the remaining clonotypes are optimized for continued protection.

56 nd sequencing indicated that distinct T-cell clonotypes are preferentially increased in the CNS compa

57 may maintain TCR diversity and that dominant clonotypes are sensitive to antigen even after dramatic

58 Dominant clonotypes are shown to overlap among multiple recurrenc

59 te that the specificity of individual T cell clonotypes arises not only from TCR residues that create

60 ns for the number of cells belonging to each clonotype as well as a linear Fokker-Planck equation for

61 e emergence of high-avidity Melan-A-specific clonotypes as a surrogate marker of treatment efficacy.

62 )-primed mice that appears to be the "public clonotype" as it expanded in response to peptide in all

63 Here, we demonstrate that dominant clonotypes, as defined by TCR junctional sequence simila

64 Hierarchical clustering of public clonotypes associated with dietary gluten exposure ident

65 We conclude that immunodominant clonotypes associated with marrow failure may be used to

66 en by preferential expansion of high avidity clonotypes at the expense of their low avidity counterpa

67 As the two clonotypes become more similar in terms of the self-anti

68 R3, and a remarkable sharing of one dominant clonotype between individual old mice, implying operatio

69 lates, reveal that effective and ineffective clonotypes bind to the terminal portions of the peptide-

70 al susceptibility varied substantially among clonotypes but was consistent across different locations

71 nsistent with the hypothesis that the public clonotype BV8S2/BJ2S7 is a driver of disease and necessa

72 elevated levels of expression of BCR in this clonotype by making the transgenic Igh locus homozygous.

73 ing strongly focused on a few high-frequency clonotypes by adulthood.

74 I/peptide tetramers and identified different clonotypes by Vbeta chain sequence analysis.

75 ity of the AI4 TCR, as the selection of this clonotype can be influenced by multiple MHC molecules, i

76 TCR sequencing revealed that the same clonotype can develop into either help-independent or he

77 These results show that CD-associated clonotypes can be identified and that common gluten asso

78 E. coli, subspecies-level identification by clonotyping can be used to significantly improve empiric

79 action (<5%) of peripheral blood plasmablast clonotypes (CD3(-)CD14(-)CD19(+)CD27(++)CD38(++)CD20(-)T

80 and TRBV2 public motifs (>30%) and of public clonotypes characteristic of high-affinity TCRs.

81 oires, we observed that germline-encoded TCR clonotypes, characteristic of neonatal infection, persis

82 with distinct T cell antigen receptor (TCR) clonotypes, characterized by superior control of HIV-1 r

83 using graph theory, with the cross-reactive clonotypes connecting the different HLA-A2 peptides reco

84 evealed somatically mutated and expanded IgG clonotypes consistent with an Ag-targeted response.

85 To evaluate the TCR clonotype contribution to CD8(+) T-cell function, we clo

86 ction, explaining how Gag293-specific public clonotypes could be selected in individuals with diverse

87 tricate than previously described, and all 3 clonotypes (CPC, FL, t-FL) may occur simultaneously with

88 type distributions, the number of observable clonotypes decreases significantly.

89 The number of public clonotypes, defined as those that expressed identical TC

90 Dominant clonotypes demonstrated high intrinsic antigen avidity,

91 minate between pathogen-derived ligands in a clonotype-dependent manner, providing a basis for adapti

92 yet constrained by epitope specificity in a clonotype-dependent manner.

93 Clonal expansion of lower-avidity T-cell clonotypes depends on availability of MHC II-expressing

94 These clonotypes, designated BV8S2/BJ2S7 and BV16/BJ2S5, were

95 This resulted in retarded clonotype development and L chain receptor editing in vi

96 dy, we performed in-depth analysis of T cell clonotypes directed against a dominantly recognized HLA

97 We were able to clonotype directly from patient urine samples within 1 t

98 roliferation phase during which low-affinity clonotypes disappeared despite exhibiting no sign of enh

99 quency analysis shows the same two-component clonotype distribution described earlier for these reper

100 toires is insufficient to describe the older clonotype distribution.

101 lthough the repertoires show broadly similar clonotype distributions, the number of observable clonot

102 This clonotype does not display conventional features of aner

103 elies on the recruitment of antigen-specific clonotypes, each defined by the expression of a distinct

104 o/8/1934 and Staphylococcus aureus USA300, a clonotype emerging as a leading contributor in postinflu

105 ant targeted reductions in the expression of clonotypes encoded by 14 specific Vkappa genes with the

106 clonotypes; and 2) recruitment of particular clonotypes endowed with superior functional capabilities

107 med in a prospective vaccine trial, in which clonotype engagement was governed by the nature of the a

108 s modulated by diverse T cell receptor (TCR) clonotypes engaging peptide-MHC class I complexes on inf

109 were significantly correlated with specific clonotypes, especially with CH40-30 (also known as H30),

110 We focus on the case where the two clonotypes exhibit negligible competition with other T c

111 Rather, a selective clonotype expansion must be included to achieve the best

112 Moreover, TCRB CDR3 clonotypes expressed by autoantigen-specific CD4(+) T ce

113 These newly recruited clonotypes expressed TCRs that engaged wild-type and mut

114 Early in development this clonotype expresses average BCR levels, but these levels

115 revealed that a dominant public CD4(+) Treg clonotype expressing Vbeta14-Jbeta1.2 with a CDR3 length

116 T cell response by recruiting lower-affinity clonotypes expressing more diverse TCR.

117 sed CD4 T cell response toward high-affinity clonotypes expressing restricted public TCR, whereas pep

118 We found that clonotypes expressing the T cell antigen receptor (TCR)

119 In the mean field approximation we show that clonotype extinction is certain and compute mean extinct

120 At low peptide concentrations, dominant clonotypes fail to survive in culture.

121 The first component includes lower frequency clonotypes for which distribution can be described by a

122 The cross-reactive clonotypes form a well-connected network that could prov

123 irs were Valpha3.2(3.5)/Vbeta14, a prominent clonotype found in the poly(F,Y,A,K)n-specific T cell li

124 P = 0.02), decreases in the number of T-cell clonotypes found within epitope-specific T cell receptor

125 in the liver than in the blood, and the peak clonotype frequency was concurrent with the peak viral l

126 The expanded clonotype from one T1D subject was detected at repeat vi

127 ects the transfer of epitope-specific T-cell clonotypes from donor to recipient; (3) less differentia

128 ctivity and identified gluten-induced T-cell clonotypes from total blood and gut TCR repertoires in a

129 d subsequent activation of the CD8(+) T-cell clonotype G9C8, which recognizes insulin B15-23 via an a

130 The most prevalent public clonotypes generated TCRs with affinities at the higher

131 Clonotype-guided antimicrobial selection significantly r

132 ssed by the dominant dextran-specific B-cell clonotype had no effect upon the magnitude of the normal

133 eptide demonstrated that Tp2(49-59)-specific clonotypes had a broad range of fine specificities for t

134 o correlated with intrinsic changes in Vbeta clonotype heterogeneity.

135 While clonotype(high) T cells induced diabetes even when IFN-g

136 Transfer of only clonotype(high)-expressing BDC T cells induced diabetes;

137 Clonotype identity was determined by fumC and fimH (CH)

138 ng the usage of a single identical VA12-JA29 clonotype in all eight older donors.

139 onses, we compared the T cell receptor (TCR) clonotype in parent and hybrid strains of respiratory sy

140 The identification of the t-FL clonotype in the previous FL sample and of the putative

141 Vbeta gene usage and greatly reduced public clonotypes in 3-d-old neonates.

142 We found that T cell clonotypes in a mouse Salmonella infection model span ea

143 strate liver-infiltrating disease-associated clonotypes in all three diseases evaluated, and evidence

144 methods for the detection of immunodominant clonotypes in blood and in historic marrow biopsies of 3

145 ed oligoclonal expansion of specific TCRbeta clonotypes in CD8(+)PD-1(+) compared with CD8(+)PD-1- TI

146 expansion, and the repertoire of responding clonotypes in chronic HIV-1 infection.

147 the role of individual T-cell receptor (TCR) clonotypes in differential antiviral CD8(+) T-cell funct

148 dance analysis, we identified gluten-induced clonotypes in each patient that were composed of a large

149 monitor the levels of putative allospecific clonotypes in posttransplant blood samples and subsequen

150 the development and maintenance of neonatal clonotypes in the brain and spleen of mice during chroni

151 urthermore, the most highly expanded TCRbeta clonotypes in the CD8(+) and the CD8(+)PD-1(+) populatio

152 The higher frequency of HCV-specific clonotypes in the liver than in peripheral blood was mai

153 The fraction of cross-reactive clonotypes in the M1(58-66) repertoire varied from 45-58

154 eas protein vaccines maintained low-affinity clonotypes in the memory compartment.

155 LA-A2 adult subjects, we identified the BV19 clonotypes in the recall response to the influenza epito

156 bit negligible competition with other T cell clonotypes in the repertoire, since this case provides a

157 ssue was used to quantitate and track T-cell clonotypes in these treated subjects with prostate cance

158 ral homology was observed for immunodominant clonotypes in three individuals.

159 ortion of the homologous CD8(+) EBV-specific clonotypes, in the "fluctuant" group was substantial hig

160 imumab triggered increases in the numbers of clonotypes, including newly detected clones and a declin

161 anisms that blocked the local propagation of clonotypes independently of antigen dose and not as a co

162 und that the predominant conventional T cell clonotypes infiltrating target lesions express antigen r

163 ation of MHC promiscuous autoreactive CD4(+) clonotypes into antidiabetogenic autoregulatory T cells.

164 non-RS-clonotypes and a shift of existing RS-clonotypes into higher frequencies.

165 results in the diversion of Treg cell-biased clonotypes into pathogenic conventional T cells.

166 The recruitment of new clonotypes into the low-frequency component of the reper

167 We prove that the ultimate fate of both clonotypes is extinction and provide a bound on mean ext

168 al number of peptides recognized by a single clonotype, is as high as six.

169 I, making the full genealogy of the type III clonotype known.

170 ed initially rare high-avidity CD4(+) T cell clonotypes, known to mediate protection.

171 ne the antibody repertoire at the individual clonotype level in the sera of young adults before and a

172 Further analysis at the clonotype level is important for understanding the struc

173 Clonotype(low) BDC T cells were required for LTP.

174 ) T-LGL leukemia and suggest that many T-LGL clonotypes may be private to the disease and may not be

175 Amplification or transfer of such clonotypes may contribute to immunotherapeutic approache

176 and suggest that cross-reactive, subdominant clonotypes may retain greater capacity to suppress repli

177 be cross-recognized by identical CD8 T cell clonotypes mobilized in vivo, yet even subtle difference

178 ments to sequencing reads and assembling the clonotypes, most of them are not designed to track and e

179 of innate B-1 cells and secretion of T15/EO6 clonotype natural IgM antibodies, which bind the PC of O

180 including singletons, i.e., the fraction of clonotypes observed only once, and repertoire diversity.

181 Tracking clonotypes of anti-insulin B cells in H chain-only VH125

182 ment of T-cell receptor (TCR) alpha and beta clonotypes of the initial HIV-1-specific CD8(+) T cells

183 (CDR3), can serve as a molecular signature (clonotype) of a T-cell clone.

184 ion that can serve as a molecular marker, or clonotype, of the disease-specific T cells.

185 cines may expand distinct Ag-specific T cell clonotypes or induce disparate degrees of protection are

186 tween HIV-1 and virus-specific CD8(+) T-cell clonotypes orchestrated at the TCR-antigen interface.

187 An average clonotype overlap of 0.85% was detected among PSC sample

188 diabetogenic TCRs, BDC2.5 and 4.1, generate clonotype-positive T cells and develop diabetes.

189 the thymus, before any exposure to antigen, clonotype-positive T reg and T conv cells express a seco

190 Escherichia coli species into clonal groups (clonotypes) predicts antimicrobial susceptibility or cli

191 Ag immunization expanded immunodominant PBL clonotypes present in the islets and PLN.

192 s representing variant epitopes, subdominant clonotypes produce higher relative levels of cytokines a

193 ation of MHC-promiscuous autoreactive T-cell clonotypes, promoting their deviation into autoregulator

194 ble family genes encoded the same amino acid clonotypes, providing additional support for antigen-dri

195 rms of the self-antigens they recognise, one clonotype quickly becomes extinct in a process resemblin

196 se TCR repertoire comprising several private clonotypes rarely observed in control mice or in the pre

197 Yet, all T cell clonotypes recognize tumor antigen with similar function

198 We find that clonotypes recognizing HLA class II-restricted epitopes

199 Thus, the pattern of antigen-specific clonotype recruitment within a protective CD8(+) T cell

200 verall hierarchy of dominant T cell receptor clonotypes remained stable compared to that pre-ART.

201 c virus type 1; (ii) T cell antigen receptor clonotype repertoires; and (iii) microbial data from inf

202 Despite this shift in clonotype representation indicative of differential sele

203 an be complex, composed of a large number of clonotypes represented at low copy numbers, while mainta

204 equences were extremely diverse, without any clonotype representing more than 2% of the overall TCR p

205 ing within an individual reveals private AST clonotypes resident in the memory population, as would b

206 nsion of already prevalent autoimmune T cell clonotypes residing in the endogenous islets.

207 minant alloreactive clones; 10 corresponding clonotypes restricted to activated T cells were identifi

208 High-definition analysis of individual clonotypes revealed that the Ag loss-induced gain of fun

209 ective alleles' is modulated by specific TCR clonotypes selected during natural infection, which prov

210 e NY-ESO-1-specific and TRAG-3-specific Treg clonotypes share a common TCR CDR3 Vbeta usage with Foxp

211 Other AST clonotypes share CDR3beta amino acid sequences through c

212 Notably, we found no clonotype sharing between subjects, indicating a predomi

213 We found extensive TCR clonotype sharing in Ag-activated cells, especially from

214 tained the initial advantage of high-avidity clonotypes, slower completion permitted uninhibited accu

215 gate TCR-pMHC interactions from multiple CTL clonotypes specific for a well-defined HIV-1 epitope.

216 We also observed clonotype-specific differences in antiviral efficacy for

217 ction, followed by liquid hybridization with clonotype-specific probes.

218 c Taqman polymerase chain reaction (PCR) and clonotype-specific sequencing.

219 igen-specific T regs maintain high levels of clonotype-specific T cell receptor expression and exert

220 f the individual, as evidenced by discordant clonotype-specific transitions directed against differen

221 repeat visits spanning >15 mo, demonstrating clonotype stability.

222 However, the RS-clonotype subset showed a significant decline in the fra

223 proportion of polyreactive and self-reactive clonotypes, suggesting that activation checkpoints exist

224 recognized the autologous tumor and included clonotypes targeting mutated antigens.

225 ance hinder the contribution of high-avidity clonotypes targeting residues 206-214 of islet-specific

226 red resistance toward dominant CD8(+) T-cell clonotypes targeting stage III tumor cells.

227 toire is polyclonal with a large fraction of clonotype that are only observed once.

228 cribed an Ig-transgenic, autoreactive B cell clonotype that undergoes a novel tolerance pathway.

229 competition process between a pair of T cell clonotypes that are similar in terms of the self-antigen

230 ymic development producing individual T cell clonotypes that express TCRs with unique patterns of Ag

231 es that were longer than telomeres of T cell clonotypes that failed to persist (6.2 vs 4.5 kb, respec

232 e skewing and the presence of high-frequency clonotypes that had undergone significant in vivo expans

233 hierarchy of recurrence rates for individual clonotypes that is determined by relative production fre

234 ure of the memory repertoire and whether the clonotypes that make up the repertoire decay at random.

235 Furthermore, individual TIL-derived T cell clonotypes that persisted in vivo following adoptive cel

236 that were composed of four different T-cell clonotypes that specifically targeted KRAS G12D.

237 accination by electroporation primed for TCR clonotypes that were associated with HIV control, highli

238 ified patient-specific putative pathogenetic clonotypes that were not detectable in controls.

239 Albeit infrequent, clonotypes that were prevalent in the islets but not fou

240 erum repertoire comprised between 40 and 147 clonotypes that were specific to each of the three monov

241 xposure identified subsets of highly similar clonotypes, the most proliferative of which showing sign

242 olerance, we followed the behavior of BDC2.5 clonotype thymocytes in fetal thymic organ cultures (FTO

243 , hence, avidity for autoantigen allows this clonotype to bypass conventional tolerance mechanisms.

244 phenotype, trafficking of the same expanded clonotype to different regions of the kidney and to the

245 acy is inherently dynamic, allowing each TCR clonotype to have a wide range of agonists while avoidin

246 The contribution of TCR clonotype to inhibitory potency was investigated by deli

247 ion profiles of dominant and subdominant TCR clonotypes to evaluate the relationship between the comp

248 Clonotype tracking within an individual reveals private

249 Interestingly, antigen-specific Th cell clonotypes unevenly assort into these peripheral compart

250 e profound expansion and shrinkage of T cell clonotypes upon antigenic triggering and, more important

251 ther than the context of exposure and public clonotype usage was associated with enhanced recognition

252 patient, but notably all six cross-reactive clonotypes used VH1-46.

253 is of responses to B51-TI8 revealed a public clonotype using TRAV17/TRBV7-3 TCR genes in six out of s

254 and PLN, although the frequency of specific clonotypes varied.

255 us sequence variant, another circulating TCR clonotype was able to preferentially recognize the varia

256 A single TCR clonotype was also identified that was largely restricte

257 The lack of dominant clonotypes was not affected by the stage of maturation o

258 nother viral challenge, the rebound of these clonotypes was seen prior to an appreciable reconstituti

259 Based on the sequence of immunodominant CDR3 clonotypes, we designed quantitative assays for monitori

260 the methods used to identify immunodominant clonotypes, we were able to follow the behavior of poten

261 es characteristic of the highly autoreactive clonotype were not reversed by an intrinsic FcgammaRIIB

262 r TV9 and the characteristics of constituent clonotypes were assessed by ex vivo priming of circulati

263 In contrast, subdominant clonotypes were characterized by lower intrinsic aviditi

264 In PSC and PBC, disease-associated clonotypes were detected among patients with human leuko

265 In contrast, BV16/BJ2S5 and numerous private clonotypes were either Th1 or Th2 and persisted followin

266 en primary Ab-forming cell responses of both clonotypes were equivalently increased by such a deficie

267 Tumour clonotypes were identified in pretreatment specimens fro

268 In total, 81 immunodominant signature clonotypes were identified.

269 We found that cross-reactive CD8+ T cell clonotypes were mobilized to counter the rapid emergence

270 esolved infection, identical T cell receptor clonotypes were present in liver and peripheral blood.

271 Only 2/839 TCRB clonotypes were shared between patients and none associa

272 o thymic involution, a substantial number of clonotypes were stable, e.g., detected at two times.

273 cy and the number of Gag CM9-specific public clonotypes were strongly correlated with VIA mediated by

274 From eight to 42 clonotypes were uniquely detected in each of the three d

275 Culture- and biopsy-derived clonotypes were used to design sequence-specific quantit

276 son, antibodies with 18 different CDRH3s (12 clonotypes) were represented in the antigen-specific IgG

277 mory CD4 TCR repertoire toward high-affinity clonotypes whereas protein vaccines maintained low-affin

278 ifferential testing enabled the detection of clonotypes which were significantly changed across time.

279 e early mobilization of public CD8(+) T-cell clonotypes, which can exert profound biological effects

280 unity at the level of individual constituent clonotypes, which were identified according to the expre

281 etramers to selectively eradicate pathogenic clonotypes while leaving overall T-cell immunity intact.

282 ertoire structure might provide a panoply of clonotypes whose differential avidity for the epitope wo

283 0 of the most representative public TCR beta clonotypes, whose abundance among the top 100,000 clones

284 Tandem HTS-based clonotyping will facilitate studying AST dynamics, epito

285 The associations of clonotype with antimicrobial susceptibility and clinical

286 types, with 93% of the isolates belonging to clonotypes with >/= 2 isolates.

287 less, certain public and conserved CDR3alpha clonotypes with distinct molecular signatures were ident

288 ntigens for the selection of superior T-cell clonotypes with enhanced antigen recognition properties.

289 Presence of dominant clonotypes with limited TCR gene usage for both TCR alph

290 In addition, clonotypes with low frequencies were found in significan

291 Together, these findings indicate that TCR clonotypes with superior functions are associated with H

292 CH typing divided the isolates into >200 CH clonotypes, with 93% of the isolates belonging to clonot

293 ertoire comprises approximately 100 antibody clonotypes, with three clonotypes accounting for >40% of

294 30 (also known as H30), a recently described clonotype within sequence type 131 (ST131).

295 1 was expressed at higher levels on dominant clonotypes within epitope-specific responses before and

296 ion of PD-1 on T cell populations and T cell clonotypes within epitope-specific responses from these

297 These data indicate that dominant clonotypes within HIV-specific T cell responses display

298 o decryption by interrogation of constituent clonotypes within the antigen-experienced T cell pools.

299 agnitude, the efficacy of constituent T-cell clonotypes within the primed population can be poor.

300 ) T cells, we hypothesized that neonatal TCR clonotypes would be locked in the brain and persist into