ライフサイエンスコーパス: helper

1 rast to LCMV infection, where balanced CD4 T helper 1 (Th1) and T follicular helper (Tfh) responses w

2 salivary microbiota are strong inducers of T helper 1 (TH1) cells when they colonize in the gut.

3 However, alum hardly induces T helper 1 (Th1) immune responses that are required for an

4 cal processes leading to the initiation of T helper 1 (TH1) immunity against dietary gluten and celia

5 ally distinct subsets of effector T cells (T helper 1 (TH1), TH2, and TH17) defined by expression of

6 ge of lymphocytes, regulatory T cells, and T-helper 1 and 17 cells, all major T-cell subpopulations s

7 buted predominantly to innate and adaptive T-helper 1 cell (TH1) immune responses, whereas the role o

8 dysfunction and death are promoted by the T helper 1 cytokine interferon gamma.

9 NX3, potentially involved in the increased T-helper 1 cytokine-mediated inflammatory damage in heart.

10 iTreg could also rapidly convert to CD4(+) T helper 1 or T helper 17 cells in an inflammatory environ

11 TCF1-silenced cells were T helper 1-like effectors and concentrated in the lungs.

12 ll suppression of T cell proliferation and T helper-1 (Th1) cell differentiation.

13 itic cells are of importance in generating T helper-1 biased adaptive immune responses.

14 tein level and restricts the generation of T-helper-1-like Treg cells.

15 es T-cell and monocyte activation toward a T helper-1/M1 immune response.

16 ranscription they co-regulate during mouse T helper 17 (Th17) cell differentiation.

17 ceptor 6 (CCR6) is critical for pathogenic T helper 17 (Th17) cell migration to the central nervous s

18 T helper 17 (Th17) cell plasticity contributes to both imm

19 mice, interleukin-17a (IL-17a) produced by T helper 17 (TH17) cells (CD4(+) T helper effector cells i

20 T helper 17 (TH17) cells are critically involved in host d

21 gut, we demonstrate that gingiva-resident T helper 17 (Th17) cells developed via a commensal coloniz

22 ny-stimulating factor (GM-CSF) produced by T helper 17 (Th17) cells plays an essential role in autoim

23 id, that reprograms the differentiation of T helper 17 (TH17) cells towards induced regulatory T (iTr

24 dditionally drive autoimmunity by inducing T helper 17 (TH17) cells, which can also contribute to hyp

25 SFB-dependent lung pathology requires the T helper 17 (Th17) responses.

26 TH1) immune responses, whereas the role of T-helper 17 cell (TH17) responses is less clear.

27 roduction is associated with activation of T-helper 17 cell and inhibition of regulatory T cell with

28 e, plays pivotal roles in pro-inflammatory T helper 17 cell responses linked to autoimmune and inflam

29 dependent type 3 innate lymphoid cells and T helper 17 cells and increased susceptibility to enteric

30 so rapidly convert to CD4(+) T helper 1 or T helper 17 cells in an inflammatory environment.

31 Differentiation of naive T cells into T helper 17 cells or regulatory T cells creates subtype-sp

32 We previously showed that maternal T helper 17 cells promote the development of cortical and

33 lls, CD4+CXCR5+ interleukin 21+ cells, and T-helper 17 cells, compared with before therapy.

34 concomitantly with hepatic accumulation of T helper 17 lymphocytes and myeloid dendritic cells.

35 A T helper 17 response was stimulated in freshly excised hum

36 These findings identify the dendritic cell-T helper 17-macrophage axis as a target for the developmen

37 g predominantly within highly inflammatory T-helper 17/T-cytotoxic 17 and T-follicular helper paradig

38 T-helper 2 (Th2) cell responses defend against parasites.

39 ype 2 immune responses leading to adaptive T helper 2 (Th2) immunity.

40 n; (ii) functioning as regulatory T (Treg)/T helper 2 (Th2)-like cells; (iii) interfering with dendri

41 ent of tolerogenic NKT cells with a marked T helper 2 cell bias that, in turn, regulated the differen

42 nfections requires the rapid activation of T helper 2 cells (Th2 cells).

43 dritic cells to promote differentiation of T-helper 2 cells and production of their cytokines (IL4, I

44 nflammation, characterized by expansion of T-helper 2 cells in the colon and lung, and infiltration o

45 induced by naive and in vivo-primed human T helper 2 cells.

46 characterized by an mTOR/Rictor-dependent T helper 2 pathway that guides interleukin-4-dependent mac

47 In plasma, high levels of human T helper 2-type inflammatory cytokines were detectable, wh

48 st cell protease MCPT1, as well as splenic T-helper-2 cell-derived cytokine production.

49 show that autophagy selectively represses T helper 9 (TH9) cell differentiation.

50 HIV controllers showed intrinsically better helper activity than those of HIV progressors.

51 ency of IFN-gamma secreting total T cells, T-helper and CTLs against both H1N2 and H1N1 SwIV.

52 pitopes displayed by these alleles and drive helper and cytotoxic T cell responses in patients with P

53 cells (ILCs) represent innate versions of T helper and cytotoxic T cells that differentiate from com

54 imited IL-2 production, whereas T follicular helper and double negative (DN) T cells significantly ex

55 r Langerhans cells at governing T follicular helper and germinal center formation after intradermal i

56 Thus, a common Thpok-LRF node supports both helper and regulatory arms of MHC class II responses.

57 icular T cells are heterogeneous, comprising helper and regulatory subsets, has raised questions rega

58 pand and become germinal center T follicular helpers and enhances B cell IgG Ab production.

59 vironments with variable productivity, where helpers at the nest can buffer reproductive failure in h

60 nds (SaPIs), such as SaPI1, exploit specific helper bacteriophages, like 80alpha, for their high freq

61 viral infection and that this led to biased helper CD4 T cell differentiation as well as impaired an

62 significantly higher frequency of follicular helper CD4 T cells compared with the unvaccinated contro

63 Infected follicular helper CD4 T cells, TFH, present inside B-cell follicles

64 Follicular helper CD4 T cells, TFH, residing in B-cell follicles wi

65 of viral infections is heavily dependent on helper CD4(+) T cell function.

66 OK and Runx3, central regulators for the CD4-helper/CD8-cytotoxic lineage choice.

67 tion, serum IgE level, and T helper cell 2/T helper cell 17 cytokine response.

68 ew allergic inflammation from eosinophilic T helper cell 2 (TH2) to neutrophilic TH17 polarity.

69 tent regulator of immunity through its pro-T helper cell 2 activity.

70 /0) mice, which was because of an impaired T helper cell 2 polarization.

71 ophilic inflammation, serum IgE level, and T helper cell 2/T helper cell 17 cytokine response.

72 ent displayed increased TH1 and follicular T helper cell and suppressed TH17 cell responses.

73 Long noncoding RNAs play a pivotal role in T-helper cell development but little is known about their

74 mily transcription factors regulate CD4(+) T helper cell differentiation.

75 enic germinal center B-cell and T-follicular helper cell frequencies that collaborate to produce anti

76 the effect of increased STAT1 activity on T helper cell polarization and to investigate the therapeu

77 IL-1 induced IL-22 production from a mixed T helper cell population comprised of Th1, Th17, and Th22

78 ge malaria and interfere with conventional T helper cell responses and follicular T helper (TFH)-B ce

79 interferons, normalized TH1 and follicular T helper cell responses, improved TH17 differentiation, cu

80 lymph node germinal center and T follicular helper cell responses.

81 F mutations are the result of dysregulated T helper cell responses.

82 n and mucin domain 3, which down-regulates T-helper cell type 1 proinflammatory responses and is asso

83 T-helper cell type 2 (Th2) cytokines were measured in cell

84 he ability to suppress lymphadenopathy and T helper cell type 2 activation.

85 ubtypes associated with high expression of T-helper cell type 2 cytokines and lack of corticosteroid

86 ignificantly increased induction of airway T-helper cell type 2 responses.

87 the most from specific agents that target T-helper cell type 2-mediated inflammation and/or corticos

88 Germinal center T follicular helper cells (GCTfh) in lymphatic tissue are critical fo

89 the function of CD4(+)CXCR5(+) follicular T helper cells (Tfh).

90 regulatory cells (Treg cells) and effector T helper cells (Th cells), and recently identified innate

91 ay be related to development of T follicular helper cells and antiviral inflammatory sequelae derived

92 We enumerated subsets of CD4(+) T helper cells and assessed cytokine production and transc

93 lisation assays and circulating follicular T-helper cells and plasmablast cells were measured in seru

94 6 is critical for initiation of T follicular helper cells and production of high-affinity IgG.

95 e upregulation of type 2 anti-inflammatory T helper cells and the suppression of type 1 T helper cell

96 ween the frequency of tonsillar T follicular helper cells and tonsillar Ag-specific Ab-secreting cell

97 es further understanding of how T follicular helper cells are regulated in health and disease.

98 Activation of T helper cells by MHC-II on Schwann cells thus promotes po

99 T follicular helper cells contribute to the development of long-lasti

100 As such, T follicular helper cells impact immunodeficiencies, autoimmunity, an

101 induce the expansion of Th17 cells (CD4(+) T helper cells producing IL-17).

102 The activation of T helper cells requires antigens to be exposed on the surf

103 that Env engagement of the CD4 receptor on T-helper cells results in anergic effects on T-cell recrui

104 Signals delivered by T follicular helper cells were not required to initiate differentiati

105 Thus, T helper cells with specificity for an antigen in cardiomy

106 GS did abrogate germinal center T follicular helper cells, and blunted PE-specific germinal center B

107 ver time exclusively on cytotoxic T cells, T-helper cells, and regulatory T cells.

108 he IL-23R(-/-)MRL.lpr had fewer T follicular helper cells, B cells, and plasma cells, leading to decr

109 fferences between TPH cells and T follicular helper cells, including altered expression of BCL6 and B

110 te acquisition of the virus because CD4(+) T helper cells, required for an effective immune response,

111 Like PD-1(hi)CXCR5(+) T follicular helper cells, TPH cells induce plasma cell differentiati

112 helper cells and the suppression of type 1 T helper cells.

113 interaction between B cells and T follicular helper cells.

114 irs the development of Th17 and T follicular helper cells.

115 targeting the viral RNA silencing suppressor helper-component proteinase (HCpro), presumably in assoc

116 es alone and in synergy with the signature T helper cytokines of either disease, IL-13 and IL-17.

117 erstanding of the mechanism underlying HBoV1 helper-dependent AAV2 replication may also provide insig

118 s of an oncolytic adenovirus (Onc.Ad) with a helper-dependent Ad (HDAd) that expresses a PD-L1 blocki

119 r hand, adeno-associated virus 2 (AAV2) is a helper-dependent dependoparvovirus, and productive AAV2

120 is results in severe defects in T follicular helper development and TH2 polarization, as seen in a ho

121 critical in regulating and assisting early T helper dichotomy toward Th2 responses, which are detrime

122 tential target for developing antimicrobial "helper" drugs that restore the efficacy of existing anti

123 oduced by T helper 17 (TH17) cells (CD4(+) T helper effector cells involved in multiple inflammatory

124 actor (TF) that directs the acquisition of T-helper effector programs during the development of multi

125 with its homolog LRF, supports CD4(+) T cell helper effector responses.

126 examined, Ag-specific interleukin-4 (IL-4) T-helper enzyme-linked immunosorbent spot (ELISpot) assays

127 may limit competition for cellular and viral helper factors and, hence, creates a biological niche fo

128 ration-dependent activity of Irf4 "writes" T helper fate choice.

129 well as their cytolytic potential and their helper function for Ab production.

130 beta2GPI-specific T cells display helper function for monocyte matrix metalloproteinase-9

131 acute retrovirus infection seems to be their helper function for other immune cells.

132 We also examined the helper function of beta2GPI-specific T cells for monocyt

133 The helper function of HBoV1 for AAV2 is not limited to HAE

134 Importantly, the helper function of HBoV1 for AAV2 relies on neither HBoV

135 Here we asked whether BCL6 controlled helper function through down-regulation of specific micr

136 s the expression of molecules that control T-helper function, such as CD40L and SAP.

137 ctive and attenuated viruses via HR with the helper gene provided in trans.

138 assisted algorithms redistribute codons in a helper gene, thereby eliminating regions of homology, wh

139 ed during complementation with an unmodified helper gene.

140 bias and CpG content to effectively titrate helper-gene protein levels.

141 ggested roles of substrate templating and Na helper ions in driving brookite formation.

142 Accordingly, MR1T cells exhibited distinct T helper-like capacities upon MR1-dependent recognition of

143 in DLNs acquired an alternative, follicular helper-like fate.

144 We hypothesized that polarized T helper lymphocyte responses orchestrate progression of i

145 roliferation and enhanced the frequency of T-helper/memory and cytotoxic T cells (CTLs) in peripheral

146 and rescues, at least in part, T follicular helper numbers and the abnormal Ab production previously

147 T-helper 17/T-cytotoxic 17 and T-follicular helper paradigms with consequent thymic damage and impai

148 r had no effect on the number of nonbreeding helpers per group.

149 ged into phage-like transducing particles by helper phages like 80alpha or phiNM1.

150 of nodal T-cell lymphomas with follicular T helper phenotype.

151 As in other transposome systems, no helper plasmids are required since transposases are not

152 2/8/9 by co-transfecting AAV2, AAV8 and AAV9 helper plasmids at a ratio of 1:1:1.

153 this study, we co-transfected AAV2 and AAV8 helper plasmids at different ratios (3:1, 1:1 and 1:3) t

154 by the synergistic co-assembly of mRNA with helper proteins.

155 l subsets, including peripheral T follicular helper (pTfh) cells, which provide help to B cells for d

156 Enhanced helper responses are dependent on IL-6 production by the

157 g an innate checkpoint to control adaptive T helper responses, which has important implications for t

158 SaPI1 redirects the helper's assembly pathway to form small capsids that can

159 ment (WRE), at times potentiated by a nearby Helper site.

160 ein, we exhibit that CD26 identifies three T helper subsets with distinct immunological properties in

161 reased frequencies of circulating follicular helper T (cTFH) cells.

162 ion and effector function of IL-17-producing helper T (T(H)17) cells during autoimmune responses, inc

163 found that LBNSE-CXCL13 recruited follicular helper T (Tfh) and germinal center (GC) B cells, promote

164 tional analyses included in vitro follicular helper T (TFH) cell differentiation and cTFH/naive B-cel

165 regulated genes characteristic of follicular helper T (TFH) cell lineage, including Bcl6, Tcf7 and Cx

166 s were previously included in the follicular helper T (TFH) cell subset, which consists of cells that

167 Recent work identified PD-1(+) follicular helper T (Tfh) cells as an important cellular compartmen

168 Abnormal development of follicular helper T (TFH) cells can induce the GC response to self-

169 hin secondary lymphoid follicles, follicular helper T (TFH) cells have previously been shown to be hi

170 upon the repertoire of different follicular helper T (Tfh) cells in germinal centers.

171 cally mutated B-cell receptors by follicular helper T (TFH) cells in germinal centres.

172 interactions between B cells and follicular helper T (Tfh) cells occurring in lymphoid germinal cent

173 Follicular helper T (Tfh) cells promote germinal center (GC) B cell

174 Follicular helper T (TFH) cells support terminal B-cell differentia

175 A large number of follicular helper T (Tfh) cells were also detected in draining lymp

176 A new T-cell subset, follicular helper T (TFH) cells, is specialized in supporting B-cel

177 ocess is known to be regulated by follicular helper T (TfH) cells, the mechanism by which B cells ini

178 bstantially impaired formation of follicular helper T (Tfh) cells, which are essential for humoral im

179 st density of cognate peptides to follicular helper T (Tfh) cells, which provide survival signals to

180 defense requires the specification of CD4(+) helper T (Th) cells into distinct fates, including Th1 c

181 iewed as a type 2-regulated disease, type 17 helper T (Th17) cells are known to be influential in ast

182 Multiple exposure to type 2 helper T cell (Th2)-inducing stimuli further enhances bo

183 wn-regulated pathogenic pro-inflammatory and helper T cell 1 (Th1) responses and up-regulated benefic

184 rmine whether blockade of the interleukin 23-helper T cell 17 (IL-23-TH17) pathway with ustekinumab r

185 A4, identifying neuropilin-1 (NRP1); and the helper T cell marker, CD4.

186 itory circuit that stabilizes the follicular helper T cell program at least in part through the contr

187 s in an impaired ability to stimulate CD4(+) helper T cell responses.

188 In multimarker analysis, the helper T cell type 1 (TH1)-related markers interferon-ga

189 L-5 circumsporozoite protein (CSP) ratios, a helper T cell type 2 cytokine, correlated with higher od

190 ell (Treg) subset that suppresses follicular helper T cell-mediated B cell responses in the germinal

191 Follicular helper T cells (Tfh ) are located within germinal center

192 Aberrant population expansion of follicular helper T cells (TFH cells) occurs in patients with lupus

193 Follicular helper T cells (TFHs) are a key component of adaptive im

194 p 2 innate lymphoid cells (ILC2s) and type 2 helper T cells (Th2 cells) are the primary source of int

195 interleukin-33 (IL-33), which induces type-2 helper T cells (Th2 cells) at the site of infection to p

196 CD4+ helper T cells and cytotoxic CD8+ T cells are key player

197 ed genes, increased the number of follicular helper T cells and plasmablasts in the spleen, and led t

198 g cells) and the inflammatory TH17 subset of helper T cells leads to the development of autoimmune an

199 ry T cells and lymph node-derived follicular helper T cells of patients with CVID compared with those

200 nt for differentiation of the TH17 subset of helper T cells remain unclear.

201 the expression of genes in the TH2 subset of helper T cells to enhancer occupancy by the BATF-IRF4 tr

202 he generation of antigen-specific follicular helper T cells, antigen-specific GC B cells, and high-af

203 ulates differentiation of the TH17 subset of helper T cells, thymic T cell development and lymph-node

204 thogen containment to the differentiation of helper T cells, yet the cues that position cells in this

205 tigen-presenting cells (APC) with sensitized helper T lymphocytes (TC) producing Th2 cytokines may de

206 ting immune activation was assessed based on helper T-cell and regulatory T-cell activation in mice.

207 ondary complications and a skewed follicular helper T-cell differentiation in defined monogenic immun

208 We analyzed CD4(+) helper T-cell subsets from peripheral blood or cerebrosp

209 t mRNA level ratio, consistent with a type 2 helper T-cell-type inflammatory response, and subacute f

210 a population of PD-1(hi)CXCR5(-) 'peripheral helper' T (TPH) cells that express factors enabling B-ce

211 specially effective at inducing T follicular helper (Tfh) and LLPC responses to Pfs25 when coupled to

212 T follicular helper (Tfh) and Th17 cells are known to promote inflamm

213 g) cell responses, but inhibits T follicular helper (TFH) cell development.

214 nity.Excessive expansion of the T follicular helper (TFH) cell pool is associated with autoimmune dis

215 ired for the differentiation of T follicular helper (TFH) cell populations.

216 , and CD4+CXCR5+interleukin 21+ follicular T-helper (Tfh) cells (P < .01).

217 Cognate interactions between T follicular helper (Tfh) cells and B cells are essential for promoti

218 SE-IL-7 induced higher rates of T follicular helper (Tfh) cells and germinal center (GC) B cells from

219 nAbs led to the hypothesis that T follicular helper (Tfh) cells and germinal centers (GC) play a crit

220 T follicular helper (TFH) cells and infiltrating stromal cells have b

221 egulatory T cells that suppress T follicular helper (Tfh) cells and the generation of high affinity a

222 Recent evidence suggests that T follicular helper (Tfh) cells are the primary producer of IL-4 in t

223 d ICOS(hi) PD-1(hi) circulating T follicular helper (Tfh) cells decreased after rituximab treatment.

224 T follicular helper (TFH) cells have been shown to be critically requ

225 egulation of humoral responses: T follicular helper (Tfh) cells support germinal center formation and

226 long-lasting interactions with T follicular helper (Tfh) cells, a process that depends on antigen up

227 required for differentiation of T follicular helper (TFH) cells, but not TH1 effectors, elicited by v

228 d on CD4(+) T cells, especially T follicular helper (Tfh) cells, in HIV-infected lymph nodes.

229 ential transcription factor for T follicular helper (TFH) cells, is critical as aberrant TFH cell exp

230 erentiation and accumulation of T follicular helper (TFH) cells.

231 ervoirs in germinal center (GC) T follicular helper (Tfh) cells.

232 on and increased recruitment of T follicular helper (TFH) cells.

233 lanced CD4 T helper 1 (Th1) and T follicular helper (Tfh) responses were induced, Ad5 immunization re

234 zation of human Th1, Th2, Th17, T follicular helper (Tfh), Treg, and Tr1 cells has helped to define u

235 nal T helper cell responses and follicular T helper (TFH)-B cell interactions in germinal centers.

236 at plant sterols and stanols can shift the T helper (Th) 1/Th2 balance toward a Th1-type immune respo

237 Levels of interleukin 23 (IL23) and T-helper (Th) 17 cell pathway molecules are increased in i

238 T-helper (Th) 17 cells are important in the control of Str

239 T cells and lower frequency of pathogenic T helper (Th) 17 cells.

240 Interleukin-4 (IL-4)-induced T helper (Th) 2 cells promote susceptibility to the protoz

241 owever, the precise mechanisms involved in T helper (Th) 2 polarization by dendritic cells (DCs) are

242 nary sarcoidosis is classically defined by T-helper (Th) cell type 1 inflammation (e.g., IFN-gamma pr

243 T cells; however, the potential of CD4(+) T helper (Th) cells for ACT is gaining interest.

244 lterations contribute to the expression of T helper (TH) lineage-defining factors is unknown.

245 Upon T cell receptor stimulation, CD4(+) T helper (Th) lymphocytes release extracellular vesicles (

246 ting CD3(+)CD8(+) cytotoxic and CD3(+)CD4(+) helper (Th) T lymphocytes, together with increased Th1,

247 ssociated with persistent pro-inflammatory T-helper (TH)2 and TH17 responses.

248 ndent and overlapping lineages, defined as T helper (Th)22 and IL-22(+) Th17 cells.

249 blood iNKT, as well as their switch from a T helper (Th-2; ie IL-4, IL-13) to Th-1 (ie IFN-gamma) cyt

250 Here we show that type 1 T helper (TH1) cells play a crucial role in vessel normali

251 T cell receptor activation in naive T cells, helper Th17 T cells and regulatory T cells, and Ca(2+) s

252 f naive T cells towards a pro-inflammatory T helper (TH17) cell state and away from a regulatory T ce

253 suppressing interleukin (IL)-17-producing T helper (Th17) cells are widely reported, the effect of t

254 nnate lymphoid cells (ILC2s) resemble type 2 helper (Th2) cells in cytokine production and contribute

255 crete and permanent functional categories of helpers that resemble the caste systems found in eusocia

256 Both in steady and in T helper type 1 (Th1) cell-driven inflammatory states, the

257 Immunization with low doses of gp96 primes T helper type 1 (Th1) immune responses, whereas high-dose

258 Type 1 reaction (T1R) is an acute T-helper type 1 (Th1) inflammatory episode in patients wit

259 onders or through conversion of Tregs into T helper type 1 (Th1) or type 17 (Th17) effector lymphocyt

260 riers was stimulated with viable S. aureus T-helper type 1 (Th1), Th2, and Th17 cytokine expression w

261 ll responses, we examined the frequency of T-helper type 1 (Th1)/Tc1, Th2/Tc2, Th9/Tc9, Th17/Tc17, Th

262 In this study, we show that the T helper type 1 cell (Th1 cell) transcriptional regulators

263 onse to infection and in the generation of T-helper type 1 cells, favoring cell-mediated immunity.

264 , inflammatory morphea is characterized by T helper type 1 cytokine imbalance in serum, particularly

265 morphea serum (P < 0.0001), as were other T helper type 1 cytokines.

266 are responsible for the activation of the T helper type 1 immune response in humans, therefore const

267 lyclonal (ie, they expressed CD4 and CD8), T-helper type 1 polarized, and polyfunctional (ie, they pr

268 Multiplex cytokine analysis confirmed the T helper type 1-polarized response induced by these protei

269 ver, the immune phenotype and functions of T helper type 17 (Th17) cells induced by healthy (PH) vers

270 f immunoinflammatory mediator performance (T-helper Type 17 [Th17]/Th2 and Th1/Th2 cell levels) were

271 ised psoriasiform phenotypes and defective T helper type 17 response.

272 ly inhibited IL-17A production from murine T helper type 17-differentiated T lymphocytes.

273 ts in defective maintenance of AD-specific T helper type 2 (Th2) and psoriasis-specific Th17 cells in

274 nterleukin (IL)-4 and IL-13, released from T-helper type 2 (Th2) cells, drive macrophage polarization

275 ertoire of resting and activated ILC2s and T helper type 2 (TH2) cells.

276 g cells (iTreg cells) by repression of the T helper type 2 (TH2) transcriptional program.

277 nnate antiviral activity) contributes to a T helper type 2 biased response and predisposes to feature

278 ion of CD4(+) T cells into tumor-promoting T helper type 2 cell (Th2 cell), Th17 cell, and regulatory

279 IL-5, prostaglandin D2, and eosinophil and T-helper type 2 cell chemokines compared with healthy subj

280 It is caused by a T-helper type 2 cell response to food antigens in contact

281 T3(mut) patient lymphocytes with increased T helper type 2 cytokine expression and elevated IgE.

282 Interleukin (IL)-13 is a pleiotropic T helper type 2 cytokine frequently associated with asthma

283 f eosinophils and mast cells, elevation of T helper type 2 cytokines/chemokines expression, and reduc

284 1 and TLR6 may cause polarization toward a T helper type 2 immune response via the release of IL-25 a

285 thermore, bleomycin-dependent induction of T helper type 2-skewed immune polarization, M2 macrophage

286 h the inhibition of fibroblast activation, T helper type 2-skewed immune polarization, M2 macrophage

287 ced IL-1beta and IL-18 production, lowered T-helper type-1 immune responses, and reduced atherosclero

288 ave elucidated functional roles for CD4(+) T-helper type-2 lymphocytes (TH 2 cells), their associated

289 AAV2 replication requires coinfection with a helper virus (e.g., adenovirus or herpesvirus) or treatm

290 The identification of HBoV1 as a helper virus for AAV2 replication has implications for t

291 Here, we report that HBoV1 is a novel helper virus for AAV2 replication.

292 limit its own replication by diminishing the helper virus reservoir.

293 only a host cell for replication but also a helper virus such as an adenovirus or a herpesvirus.

294 2) depends on the simultaneous presence of a helper virus such as herpes simplex virus 1 (HSV-1) for

295 P) subunit, relying on the polymerase of its helper virus TNV for replication.

296 In this study, we employed a helper virus-based reverse genetics system to identify N

297 ressed through mitosis in the absence of the helper virus.

298 Since its introduction, new helper viruses and reagents that facilitate complementat

299 the interaction between AAV2 and one of its helper viruses, herpes simplex virus 1 (HSV-1).

300 wn to efficiently inhibit the replication of helper viruses.