ライフサイエンスコーパス: ATL

1 ATL is a highly virulent cancer that is resistant to che

2 ATL is classified into 4 distinct clinical diseases: acu

3 ATL is highly refractory to current therapies, making th

4 ATL is needed to not only form, but also maintain, the E

5 ATL leukemia cells were characterized by an increase in

6 ATL tethers and fuses tubules stabilized by the Rtns, an

7 ATLs harness the energy of GTP hydrolysis to initiate a

8 The Met-1 ATL model was established by intraperitoneal injection o

9 500 sera, ELISA using rLb6H detected all 219 ATL samples (sensitivity of 100.0%) with an overall spec

10 ues and finds effective local control across ATL subtypes.

11 t oncolytic activity against HTLV-1 actuated ATL cells.

12 Acute ATL is the most aggressive form, representing 60% of cas

13 40 substrate-binding domain in 8 of 32 acute ATL patients (25%).

14 ent complication and cause of death in acute ATL patients is the presence of lytic bone lesions and h

15 tive Notch1 signaling in patients with acute ATL.

16 Additional ATLs, including miltefosine and perifosine, also displac

17 xis provides new therapeutic targets against ATL and might explain genomic instability leading to the

18 ctor (HBZ) protein which is expressed in all ATL cases physically interacts with NRF-1 and inhibits t

19 oral lobectomy with amygdalohippocampectomy (ATL), but the utility of interictal epileptiform dischar

20 sformed T cell lines, MT-2, MT-4, SLB-1, and ATL-2.

21 tween HTLV-I asymptomatic carriers (ACs) and ATL and HAM/TSP patients.

22 cluding HTLV-I-seronegative donors, ACs, and ATL and HAM/TSP patients.

23 more, despite recent claims that both AG and ATL are semantic hubs, the two areas responded very diff

24 ly activated in HTLV-I-transformed cells and ATL cells, and activating STAT3 mutations were detected

25 o understand the link between HTLV-1 HBZ and ATL in infected individuals.

26 en they judged conceptual size, both LOC and ATL stimulation eradicated the otherwise robust effect.

27 disparate functional profiles of the LOC and ATL, providing the first evidence of a malleable network

28 onstrated increased fMRI activity in OFC and ATL at the onset of the odor cue itself, followed by res

29 nuclear cells (PBMCs) from ATL patients, and ATL patient sera contain higher concentrations of BDNF t

30 tudies indicated that HTLV-I-transformed and ATL cells, but not normal peripheral blood mononuclear c

31 break TRAIL resistance in HTLV-1-associated ATL by transcriptional down-regulation of c-FLIP, a key

32 So far, HTLV-1-associated ATL is incurable by presently known therapies.

33 nt of select patients with HTLV-I-associated ATL and HAM/TSP.

34 s of dynamin-like GTPases known as atlastin (ATL).

35 ulum (ER) membranes is mediated by atlastin (ATL), which consists of an N-terminal cytosolic domain c

36 well as the membrane-fusing GTPase atlastin (ATL) and the lunapark protein (Lnp).

37 The dynamin-related GTPase atlastin (ATL) catalyzes membrane fusion of the endoplasmic reticu

38 fusion of tubules mediated by the atlastin (ATL) guanosine triphosphatase (GTPase).

39 nt on the guanosine triphosphatase atlastin (ATL).

40 triphosphatases (GTPases) called atlastins (ATLs), which are also required to maintain ER morphology

41 e present the first structure of a bacterial ATL, from Vibrio parahaemolyticus (vpAtl).

42 Because ATL patients are unresponsive to chemotherapy, this mali

43 Maintenance requires a balance between ATL and Rtn, as too little ATL activity or too high Rtn4

44 odal semantic cognition, including bilateral ATL, inferior frontal gyrus, medial prefrontal cortex, a

45 NE assembly requires fusion by both ATL and ER-soluble N-ethyl-maleimide-sensitive factor ad

46 We show that both ATL proteins bind with high affinity to oligodeoxyribonu

47 was reduced by ATL, and engagement of ALX by ATL on both neutrophils and platelets was necessary to p

48 ults indicate that fusion of ER membranes by ATL and interaction of ER with growing MT ends and dynei

49 NPA formation in vitro, which was reduced by ATL, and engagement of ALX by ATL on both neutrophils an

50 We further show that Wnt5a secreted by ATL cells favors osteoclast differentiation and expressi

51 L and this may be used for finally capturing ATL.

52 Smoldering/chronic ATL cells produced IL-2 and IL-9 in 6-day ex vivo cultur

53 ere, we demonstrated that smoldering/chronic ATL peripheral blood mononuclear cells spontaneously pro

54 feration in patients with smoldering/chronic ATL that could be targeted for treatment.

55 cells from patients with smoldering/chronic ATL.

56 s, the arsenic/interferon combination clears ATL through degradation of its Tax driver, and this regi

57 utive patients with pathologically confirmed ATL treated with radiotherapy were reviewed.

58 ssion of WT FBXW7 in several patient-derived ATL lines demonstrated strong tumor-suppressor activity

59 potent oncolytic activity in patient-derived ATL transplanted into NSG mice and facilitated a signifi

60 ple worldwide, about 5% of whom will develop ATL.

61 n effective treatment in patients displaying ATL.

62 We found that two duplC-ATL genes underwent pseudogenization and that, in one ca

63 onary basis of a cluster of six genes, duplC-ATLs, which arose from segmental and tandem duplication

64 5%) achieving an excellent outcome following ATL.

65 nhibitors may exert therapeutic benefits for ATL and HAM/TSP patients.

66 (1983-1991) assessed local radiotherapy for ATL.

67 y, there is no accepted curative therapy for ATL.

68 There is no accepted curative therapy for ATL.

69 n of this pathway may improve treatments for ATL.

70 ients from ACs (odds ratio = 14.12) and from ATL patients (odds ratio = 7.00).

71 s at a true-positive rate of 85.42% and from ATL patients at a true-positive rate of 75.00%, and mode

72 However, in infected cells from ATL patients, the viral genome is frequently modified to

73 vivo spontaneous proliferation of PBMCs from ATL and HAM/TSP patients by 67.1% and 86.4%, respectivel

74 ipheral blood mononuclear cells (PBMCs) from ATL patients, and ATL patient sera contain higher concen

75 We then assessed rLb6H against sera from ATL patients infected with different species of Leishman

76 Functionally, ATL FBXW7 mutants lost their ability to interact with in

77 with alemtuzumab in a murine model of human ATL (MET-1).

78 manized anti-Tac) in a murine model of human ATL.

79 tration predicts neural changes in the human ATL and task performance during semantic processing.

80 ither the C-terminal helix or the TMs impair ATL's ability to generate and maintain ER morphology in

81 er, supporting a role for IL-9/IL-9Ralpha in ATL, a neutralizing monoclonal antibody directed toward

82 fector, Pim1, is constitutively activated in ATL cells.

83 the combination of YM155 with alemtuzumab in ATL.

84 diesterase 1 (TDP1), a DNA repair enzyme, in ATL cells.

85 or cell proliferation and tumor formation in ATL-engrafted mice.

86 revent or reduce osteolytic lesions found in ATL patients and improve therapy outcome.

87 onsistent with the loss-of-function found in ATL patients, expression of WT FBXW7 in several patient-

88 ytic bone lesions and hypercalcemia found in ATL patients.

89 1 expression by inhibiting NRF-1 function in ATL cells.

90 sible for its tumor-suppressive functions in ATL cells.

91 ced and 264 repressed genes during growth in ATL compared to that in GM17 laboratory culture medium.

92 fold-greater cell densities during growth in ATL than the dairy-associated strain L. lactis IL1403.

93 lant-inducible genes for L. lactis growth in ATL, xylose metabolism was targeted for gene knockout mu

94 reducing activation of adaptive immunity in ATL patients.

95 (BIRC5) demonstrated a striking increase in ATL, and its expression was increased in patient ATL cel

96 Genes induced in ATL included those involved in the arginine deiminase pa

97 as a target for therapeutic intervention in ATL patients.

98 oth strains grew to similarly high levels in ATL, indicating redundancy in L. lactis carbohydrate met

99 However, the role of Tax loss in ATL response is disputed, and the molecular mechanisms d

100 Depletion of or mutations in ATL cause an unbranched ER morphology and hereditary spa

101 equency of constitutively activated Notch in ATL patients.

102 CD25(+)CD3(-) phenotype commonly observed in ATL.

103 Tax expression because it does not occur in ATL cell lines that lack Tax expression or in Jurkat cel

104 and production of metabolic end products in ATL as measured by gas chromatography-time of flight mas

105 support a role for IL-9 and its receptor in ATL by a paracrine mechanism.

106 ly, miR-150 and miR-223 were up-regulated in ATL patients but consistently down-regulated in HTLV-I c

107 idence that BIRC5 plays an important role in ATL cell viability and provides important insight into A

108 ism underlying the downregulation of TDP1 in ATL cells remains elusive.

109 Ags were higher in HAM/TSP patients than in ATL patients.

110 nalysis to test whether activity patterns in ATLs carry information about conceptual object propertie

111 threonine (PEST) domain in T-ALLs, those in ATLs have, in addition, single-substitution mutations in

112 HTLV-I-infected ATL patients have pronounced immunodeficiency associated

113 Interestingly, ATL cells overexpressed the osteolytic-associated genes-

114 iability and provides important insight into ATL genesis and potential targeted therapies.

115 inhibited STAT5 phosphorylation in isolated ATL T cells ex vivo.

116 i-HIV-1 drug, potently and selectively kills ATL cells.

117 o picture and voice naming in the human left ATL.

118 s placed directly on the surface of the left ATL in human subjects, we demonstrate nearly identical r

119 e dispositions are organized within the left ATL include both a single modality-independent (heteromo

120 is finding has led to the idea that the left ATL is a modality-independent convergence region for pro

121 ct electrophysiologic evidence that the left ATL is heteromodal for proper-name retrieval.

122 Specifically, the left ATL was positively activated for all semantic tasks, but

123 ) dispositions for proper naming in the left ATL.

124 American tegumentary leishmaniasis (ATL) (also known as cutaneous leishmaniasis [CL]) is cau

125 les from American tegumentary leishmaniasis (ATL) patients (especially the ML cases) had significantl

126 infection to lethal Adult T-cell Leukaemia (ATL); a progression that is more likely in Japanese men

127 etiological agent of adult T-cell leukemia (ATL) and HTLV-1-associated myelopathy/tropical spastic p

128 he causative agent of adult T-cell leukemia (ATL) and HTLV-1-associated myelopathy/tropical spastic p

129 ormalities, including adult T cell leukemia (ATL) and HTLV-1-associated myelopathy/tropical spastic p

130 Adult T-cell leukemia (ATL) and human T-cell lymphotropic virus type I (HTLV-I)

131 he etiologic agent of adult T-cell leukemia (ATL) and the neurological disorder HTLV-I-associated mye

132 entified a cluster of adult T-cell leukemia (ATL) cases in Japan, provided conclusive evidence that H

133 ymphocyte cell lines, adult T-cell leukemia (ATL) cells, and in other hematologic malignancies.

134 In most adult T-cell leukemia (ATL) cells, Tax oncoprotein expression is typically low

135 Adult T-cell leukemia (ATL) consists of an overabundance of T cells, which expr

136 Adult T-cell leukemia (ATL) is a fatal malignancy caused by infection with the

137 Adult T cell leukemia (ATL) is a serious form of cancer with a high mortality r

138 Adult T-cell leukemia (ATL) is an aggressive malignancy of CD4(+)CD25(+) lympho

139 Adult T-cell leukemia (ATL) is an aggressive T-cell malignancy caused by human

140 Adult T-cell leukemia (ATL) is caused by human T-cell lymphotropic virus I (HTL

141 he etiologic agent of adult T-cell leukemia (ATL) is human T cell lymphotropic virus type I (HTLV-I).

142 eration of smoldering adult T cell leukemia (ATL) T cells.

143 Adult T-cell leukemia (ATL), a heterogeneous disease, can be divided into smold

144 in the development of adult T-cell leukemia (ATL), a T-cell malignancy caused by HTLV-1 infection.

145 I) is associated with adult T-cell leukemia (ATL), an aggressive lymphoproliferative disease with a d

146 he etiologic agent of adult T-cell leukemia (ATL), an aggressive lymphoproliferative disease.

147 -1) that recapitulate adult T-cell leukemia (ATL)-like leukemic symptoms and display HTLV-1-specific

148 he causative agent of adult T-cell leukemia (ATL).

149 f leukemia designated adult T-cell leukemia (ATL).

150 tic malignancy termed adult T cell leukemia (ATL).

151 etiological agent of adult T-cell leukemia (ATL).

152 iologically causal of adult T-cell leukemia (ATL).

153 al T-cell malignancy, adult T-cell leukemia (ATL).

154 etiological agent of adult T-cell leukemia (ATL).

155 this paper, we demonstrate that Sey1p, like ATLs, mediates homotypic ER fusion.

156 Alkyltransferase-like (ATL) proteins in Schizosaccharomyces pombe (Atl1) and Th

157 a group of proteins [alkyltransferase-like (ATL) proteins] showing amino acid sequence similarity to

158 alyses uncover that the CD and AT-hook-like (ATL) motif of Cbx7 constitute a functional DNA-binding u

159 pid edelfosine, a prototype antitumor lipid (ATL), kills yeast cells and selectively kills several ca

160 is metabolized to aspirin-triggered lipoxin (ATL), 15-epi-lipoxin A4.

161 t increased levels of ASA-triggered lipoxin (ATL; 15-epi-lipoxin A4), and blocking the lipoxin A4 rec

162 a balance between ATL and Rtn, as too little ATL activity or too high Rtn4a concentrations cause ER f

163 crucial role for the anterior temporal lobe (ATL) in semantic processing.

164 udies that the human anterior temporal lobe (ATL) is a semantic representational hub.

165 The anterior temporal lobe (ATL) makes a critical contribution to semantic cognition

166 regions, such as the anterior temporal lobe (ATL) or angular gyrus (AG).

167 ng indicate that the anterior temporal lobe (ATL) plays a crucial and necessary role in conceptualiza

168 s to the anterior part of the temporal lobe (ATL) remains to be clarified.

169 we asked whether the anterior temporal lobe (ATL) serves as a hub for a distributed neural circuit th

170 x (OFC) and the left anterior temporal lobe (ATL) was observed in response to words when preceded by

171 t perception, or the anterior temporal lobe (ATL), a "hub" of supramodal conceptual processing.

172 depends on the left anterior temporal lobe (ATL), where lesions can be associated with impaired nami

173 on subregions of the anterior temporal lobe (ATL).

174 ritical role of the anterior temporal lobes (ATLs) in object knowledge, fMRI studies using univariate

175 show that LX and aspirin (ASA)-triggered LX (ATL) inhibit innate immune signaling by inducing suppres

176 d adult T-cell leukemia and T-cell lymphoma (ATL) are aggressive diseases with poor prognoses, limite

177 elopment of adult T-cell leukaemia/lymphoma (ATL), an aggressive blood cancer, and HAM/TSP, a progres

178 notherapy in adult T-cell leukemia-lymphoma (ATL) patients.

179 xpression in adult T-cell leukemia-lymphoma (ATL).

180 en linked to adult T-cell leukemia/lymphoma (ATL) and HTLV-I associated myelopathy (HAM).

181 ction causes adult T-cell leukemia/lymphoma (ATL) and is associated with a variety of lymphocyte-medi

182 tive disease adult T-cell leukemia/lymphoma (ATL) and the neurodegenerative disorder tropical spastic

183 In adult T-cell leukemia/lymphoma (ATL) cell lines and patient T cells, hbz is often the on

184 )-associated adult T cell leukemia/lymphoma (ATL) cells as a model system.

185 Adult T-cell leukemia/lymphoma (ATL) is an aggressive and fatal disease.

186 Adult T cell leukemia/lymphoma (ATL) is an aggressive cancer of CD4/CD25(+) T lymphocyte

187 Adult T-cell leukemia/lymphoma (ATL) is an aggressive malignancy of poor prognosis.

188 Adult T-cell leukemia/lymphoma (ATL) is etiologically linked to infection with the human

189 1-associated adult T-cell leukemia/lymphoma (ATL) typically has survivals measured in months with che

190 formation in adult T-cell leukemia/lymphoma (ATL), a highly aggressive chemotherapy-resistant maligna

191 ive agent of adult T-cell leukemia/lymphoma (ATL), a malignancy of CD4(+) T cells whose etiology is t

192 es including adult T-cell leukemia/lymphoma (ATL).

193 an Arabidopsis thaliana leaf tissue lysate (ATL).

194 icant clinical activity in Tax-driven murine ATL or human patients.

195 ion-binding site conservation identifies new ATLs in sea anemone and ancestral archaea, indicating th

196 ating mutations in Notch in more than 30% of ATL patients.

197 G/C tracts remain stable in the absence of ATL-1, CLK-2 (FA pathway activators), FCD-2, BRC-2, and

198 HTLV-1 infection is the etiological agent of ATL and, unfortunately, most patients succumb to the dis

199 ncoprotein, selectively induces apoptosis of ATL cell lines and has significant clinical activity in

200 The dependence of ATL cells to Pim1 activity was demonstrated using 2 Pim1

201 routine use in the serological diagnosis of ATL.

202 c domain but rather mediate the formation of ATL oligomers.

203 ing that this process is a major hallmark of ATL cytotoxicity in yeast.

204 Aspirin also increased the levels of ATL in the lungs of LPS-treated wild-type C57Bl6 mice (v

205 r critical roles in a conserved mechanism of ATL binding to alkylated DNA.

206 In this study, we used a mouse model of ATL and restored expression of the microRNA, miR-124a, t

207 nical testing of AZD1208 in a mouse model of ATL resulted in significant prevention of tumor growth i

208 umor formation in a xenograft mouse model of ATL.

209 ed to improvement in treatment or outcome of ATL.

210 n, T-cell proliferation, and pathogenesis of ATL in HTLV-1-infected individuals.

211 c instability leading to the pathogenesis of ATL.

212 lay an important role in the pathogenesis of ATL.

213 sidered for symptomatic local progression of ATL.

214 ty characterized by reduced proliferation of ATL cells.

215 r there would be autonomous proliferation of ATL leukemic cells, we purified leukemic cells from pati

216 These results reinforce the relevance of ATL in semantic memory, as well as its amodal organizati

217 erently, with results supporting the role of ATL, but not AG, in semantic representation.

218 clinical manifestations, different stages of ATL have different molecular signatures.

219 h plays an important role in early stages of ATL.

220 monomeric pre- and post-hydrolysis states of ATL.

221 ients with smoldering or chronic subtypes of ATL, or from those with HAM/TSP whose PBMCs are associat

222 ) T-cell immunophenotype similar to those of ATL cells, suggesting that HBZ protein has important rol

223 Functionally, transfection of ATL cells with BIRC5 shRNA decreased BIRC5 expression an

224 Clinical treatment of ATL patients with Zenapax or bortezomib decreased BIRC5

225 rial of this combination in the treatment of ATL.

226 shown promising results in the treatment of ATL.

227 ovel therapeutic target for the treatment of ATL.

228 Cytotoxicity of ATLs is mainly dependent on the changes they induce in p

229 of wild-type or mutant ATL1 or depletion of ATLs alters ER morphology and affects store-operated cal

230 pting its repair by human AGT, a hallmark of ATLs.

231 e further evidence for the conserved role of ATLs in this primordial mechanism of DNA repair.

232 nic/interferon-treated HTLV-1 transformed or ATL cells, Tax is recruited onto NBs and undergoes PML-d

233 Hence, the fingerprint of Tax is all over ATL and this may be used for finally capturing ATL.

234 d TCF4; 200 of the most highly overexpressed ATL genes were analyzed by the Pathway Studio, version 4

235 sis by applying rTMS to normal participants: ATL stimulation generates a category-general impairment

236 and its expression was increased in patient ATL cells resistant to the anti-CD52 monoclonal antibody

237 while ATL can be measured in tissue, plasma ATL is not a biomarker of vascular COX-2 expression.

238 -2-knockout mice to establish whether plasma ATL could be used as a biomarker of vascular COX-2 in vi

239 Here we determine Schizosaccharomyces pombe ATL structures without and with damaged DNA containing t

240 ex vivo spontaneous proliferation of primary ATL cells from several patients.

241 mutations were detected in 25.5% of primary ATL patients.

242 aken together, our data suggest that primary ATL cells, via IL-9, support the action of IL-9Ralpha/CD

243 Alkyltransferase-like proteins (ATLs) are a novel class of DNA repair proteins related t

244 Alkyltransferase-like proteins (ATLs) share functional motifs with the cancer chemothera

245 nctional connectivity between left and right ATLs in patients with chronic aphasic stroke has been il

246 ated with better outcomes following standard ATL in magnetic resonance imaging-negative TLE.

247 ric patients with TLE who underwent standard ATL between January 1, 1990, and October 15, 2010, were

248 d MRS investigation showed that the stronger ATL BOLD response induced by the semantic task, the lowe

249 t connectivity is identified in the superior ATL, which is connected to auditory and language areas.

250 s to restore the fusion activity of tailless ATL.

251 ile still allowing VSV to effectively target ATL cells.

252 We conclude that ATL regulates neutrophil-platelet aggregation and that p

253 Here we demonstrate that ATL-derived or HTLV-1-transformed cells are dependent on

254 Our study demonstrated that ATL cells do not express high levels of beta-catenin but

255 ling Wnt gene expression, we discovered that ATL patient leukemia cells shifted expression toward the

256 emone and ancestral archaea, indicating that ATL interactions are ancestral to present-day repair pat

257 ulated in HTLV-I cell lines, suggesting that ATL cells and in vitro-established cells are derived fro

258 combined with structural results reveal that ATLs sculpt alkylated DNA to create a genetic and struct

259 The ATL includes several different cortical areas, namely, t

260 embryogenesis in Caenorhabditis elegans, the ATL-1-CHK-1 (ataxia telangiectasia mutated and Rad3 rela

261 They reveal that (i) the ATL is an important element of the ventral semantic path

262 iduals with higher GABA concentration in the ATL showed better semantic performance and stronger BOLD

263 and resting-state GABA concentrations in the ATL.

264 Multiple sensory modalities converge in the ATL.

265 hanism underlying semantic processing in the ATL.

266 lacing retrograde tracer injections into the ATL: the temporal polar (n = 3), perirhinal (areas 35 an

267 r performance and reacted with 100.0% of the ATL and 89.4% of the VL samples.

268 However, the functional connectivity of the ATL and the functional network underlying semantic cogni

269 In addition, subregions of the ATL have distinct functional properties and thus the pot

270 However, the neurochemical nature of the ATL in the semantic processing remains unclear.

271 l to the neurobiological contribution of the ATL to semantic cognition.

272 valuate the consequences that lesions on the ATL have on the neurocognitive network supporting semant

273 Recent structural studies on the ATL soluble domain reveal two dimeric conformers propose

274 ave primarily implicated regions outside the ATL.

275 Together, our results suggest that the ATL is a central hub for representing and retrieving per

276 e and connectivity analyses suggest that the ATL stores abstract person identity representations.

277 igm designed to ensure signal throughout the ATL.

278 reflecting typical object size), whereas the ATL contributes to this computation when the context req

279 We studied the LPFC connections with the ATL by placing retrograde tracer injections into the ATL

280 in contrast, the dLPFC connections with the ATL were weak.

281 ces (MFC) showed dense connectivity with the ATL, namely, A13 with the temporopolar and perirhinal co

282 Despite this, ATL was unchanged in plasma after LPS and aspirin.

283 Thus, ATL and AG do not share a common interest in semantic ta

284 substitutions cluster in regions adjacent to ATL's catalytic site, but the consequences for the GTPas

285 est that activated Notch may be important to ATL pathogenesis and reveal Notch1 as a target for thera

286 re known to increase risks of progression to ATL.

287 d by LOC stimulation but stayed resilient to ATL stimulation.

288 p and its homologues function analogously to ATLs in mediating ER fusion.

289 -9/IL-15)-dependent manner, while acute-type ATL peripheral blood mononuclear cells did not prolifera

290 In the resting-state analysis, the ventral ATL (vATL) and anterior middle temporal gyrus (MTG) were

291 fected cells in vitro and uncultured ex vivo ATL cells.

292 aled significant differences between ex vivo ATL tumor cells and in vitro HTLV-I cell lines.

293 When ATL function is compromised, the morphology of the endop

294 To examine whether ATL proteins play a role in the biological effects of al

295 We suggest a model in which ATL-mediated fusion counteracts the instability of free

296 While ATL patients carrying a wild-type p53 enter remission fo

297 study is the first to demonstrate that while ATL can be measured in tissue, plasma ATL is not a bioma

298 N-alpha with emodin and DHA in patients with ATL refractory to conventional therapy.

299 nical trial of this regimen in patients with ATL.

300 reversed ASA protection, and treatment with ATL in both LPS and TRALI models protected from ALI.