ライフサイエンスコーパス: TAM

1 TAM (Tyro3-Axl-Mer) receptor tyrosine kinases and Met ar

2 TAM and protein S immunostaining was performed on kidney

3 TAM expression and shedding by tubular epithelial cells

4 TAM family receptor tyrosine kinases (Mer and Axl) play

5 TAM PD-1 expression correlates negatively with phagocyti

6 TAM PD-1 expression increases over time in mouse models

7 TAM receptors (Tyro-3, Axl, and Mertk) are a family of t

8 TAM receptors (Tyro3, Axl, and Mer) have been implicated

9 TAM receptors are up-regulated postnatally and maintaine

10 TAMs are recruited to the glioma environment, have immun

11 TAMs integrate levels of hypoxia and lactate into progre

12 TAMs were generated by coculturing primary human macroph

13 Here, we use optical tissue clearing and a TAM-targeting injectable fluorescent nanoparticle (NP) t

14 transcriptomic and proteomic analyses of (a) TAM-abundant and -deficient tumor tissues and (b) sorted

15 providing a first glimpse of what an active TAM receptor kinase may look like and suggesting a poten

16 Additionally, TAMs in the hypoxic niches within the tumor are known to

17 microglial response to brain damage is also TAM-regulated, as TAM-deficient microglia display reduce

18 urden, improving normalization, and altering TAMs.

19 promote association between tumor cells and TAM.

20 e that is independent of the BAM complex and TAM.

21 ality mechanisms: malignant cell killing and TAM-based immunomodulation.

22 ecreased or increased the numbers of TAN and TAM, respectively, accompanied by corresponding changes

23 hich functioned as an attractant for TAN and TAM.

24 Human TIM and TAM family proteins were recently found to serve as phos

25 However, a role for ZEB1 in macrophages and TAMs has not been studied.

26 ated that the decrease in M2 macrophages and TAMs, concomitant with the reduction of cytokine and che

27 on of patients with tenofovir resistance and TAMs was 0.64 (p<0.0001), and the odds ratio for tenofov

28 se to brain damage is also TAM-regulated, as TAM-deficient microglia display reduced process motility

29 response to LPS by restoring and augmenting TAM receptor and ligand expression, as well as by preven

30 Because TAM receptors restrict pathogenesis of neuroinvasive vir

31 , we have shown a strong correlation between TAM-associated spheroids and the clinical pathology of o

32 molecules that bind to the interface between TAM Ig1 domain and Gas6 Lg1 domain can inhibit TAM activ

33 We detected associations between TAMs and drug resistance mutations both between and with

34 vered a critical molecular crosstalk between TAMs and GSCs through the PTN-PTPRZ1 paracrine signallin

35 dult neurogenesis is normally driven by both TAM receptor ligands Gas6 and protein S.

36 Both TAMs and their ligands are expressed in the vasculature,

37 pression of collagen XIV and I is reduced by TAM deficiency.

38 fibroblasts are significantly outnumbered by TAMs in this model and that their expression of collagen

39 Moreover, EGF secreted by TAMs activated EGFR on tumor cells, which in turn upregu

40 ation of Ccr2 In turn, expression of ZEB1 by TAMs induced Ccl2, Cd74, and a mesenchymal/stem-like phe

41 In human ovarian carcinomas, TAM infiltration and CCR2 expression correlated with ZEB

42 promoting melanoma cell growth and CD163(+) TAM in the tumor microenvironment, with potential therap

43 ositively correlates with increased CD163(+) TAM infiltration.

44 lates with infiltration of CD11b(+)/CD163(+) TAMs and poor prognosis of GBM patients.

45 ceptor 1 (S1pr1) alone in CD11b(hi) CD206(+) TAMs infiltrating mouse breast tumors prevents pulmonary

46 Here we find that the central TAM most likely are elevated by a non-thermal, flexural

47 ed extension (rift necking) near the central TAM range front but with negligible thermal encroachment

48 c geophysical soundings spanning the central TAM was acquired.

49 Circulating TAM receptor soluble forms (sTyro3, sAxl, sMer) are rela

50 Correspondingly, TAM depletion reduces intratumoral TNP accumulation and

51 macrophage PPARgamma and Gpr132 as critical TAM modulators, new cancer therapeutic targets, and esse

52 CYP4A(+) TAM infiltration was positively associated with metastas

53 ion in tumors, as characterized by decreased TAMs (CD206+) and MDSCs (Gr1+ CD11b+), increased dendrit

54 lammasome component Nlrp3 in S1PR1-deficient TAMs.

55 Blood-derived TAMs do not universally conform to the phenotype of micr

56 We conclude that blood-derived TAMs significantly infiltrate pre-treatment gliomas, to

57 Blood-derived TAMs upregulate immunosuppressive cytokines and show an

58 The gene signature of blood-derived TAMs, but not microglial TAMs, correlates with significa

59 cally target immunosuppressive blood-derived TAMs.

60 antigen presentation, embryonically derived TAMs exhibited a pro-fibrotic transcriptional profile, i

61 (CRC) model, we found that monocyte-derived TAMs advance tumor development by the remodeling of its

62 Whereas monocyte-derived TAMs played more potent roles in antigen presentation, e

63 noparticle (NP) to examine three-dimensional TAM composition, tumour-to-tumour heterogeneity, respons

64 Hence, disabling TAM signaling may promote engagement of adaptive immunit

65 macrophage subpopulations defined a distinct TAM-induced ECM molecular signature composed of an ensem

66 ting the abundance and phenotype of distinct TAM subsets remain unknown.

67 present a novel signature that distinguishes TAMs by ontogeny in human gliomas.

68 opic expression of miR-29b-1/a did not drive TAM-resistance in MCF-7 breast cancer cells.

69 This E2f3 TAM gene expression signature was sufficient to predict

70 cells, suggesting unique functions for each TAM population.

71 However, what enables TAMs to have a superior capacity to establish pre-metast

72 e outer leaflet of their membranes, enabling TAM receptor activation and downregulation of antiviral

73 CSF-1R blockade is characterized by enhanced TAM penetration throughout and within tumours.

74 Together, these results establish TAM receptors as both controllers of microglial physiolo

75 ide that selectively targets MRC1-expressing TAMs (MEMs).

76 high-density lipoprotein (rHDL)-facilitated TAM PET imaging in a breast cancer model.

77 iruses, these findings have implications for TAM antagonists that are currently in clinical developme

78 ancers, our findings uncover a mechanism for TAM-mediated spheroid formation and provide a potential

79 hese findings suggest that EGF secreted from TAMs plays a critical role in promoting early transcoelo

80 Furthermore, TAMs isolated from IH-exposed mice treated with celecoxi

81 e further development of small molecule Gas6-TAM interaction inhibitors as a novel class of cancer th

82 g blockade shifted the MHC-II(lo)/MHC-II(hi) TAM balance in favor of the latter as observed by the pr

83 iation of Ly6C(hi) monocytes into MHC-II(hi) TAMs.

84 Here we show that both mouse and human TAMs express PD-1.

85 Here, we identify TAM-derived factors and their roles in the development o

86 re abundant in gliomas and immunosuppressive TAMs are a barrier to emerging immunotherapies.

87 rophage colony-stimulating factor (M-CSF) in TAM differentiation and polarization in different mouse

88 Deficiencies in TAM signaling have been associated with chronic inflamma

89 resistance but acts as a tumor suppressor in TAM-resistant cells.

90 EGFR or antibody neutralization of ICAM-1 in TAMs blunted spheroid formation and ovarian cancer progr

91 r the effects of cytochrome P450 (CYP) 4A in TAMs on lung pre-metastatic niche formation and metastas

92 The ABHD5/SRM/spermidine axis in TAMs might represent a potential target for therapy.

93 In summary, CYP4A in TAMs is crucial for lung pre-metastatic niche formation

94 iomas and identify phenotypic differences in TAMs of distinct lineages.

95 uent T cell recruitment, is downregulated in TAMs through Mer tyrosine kinase-dependent recognition o

96 e show that the specific ablation of E2f3 in TAMs, but not in tumor epithelial cells, attenuates lung

97 t E2f3b but not E2f3a levels are elevated in TAMs from PyMT mammary glands relative to controls, sugg

98 Mechanistically, ZEB1 expression in TAMs induced their polarization toward an F4/80(low) pro

99 Reduced 5-LO expression in TAMs was mechanistically coupled to an attenuated T cell

100 entify E2f3 as a key transcription factor in TAMs, which influences the tumor microenvironment and tu

101 Downregulation of 5-LO in TAMs required tumor cell death and the direct contact be

102 Expression and activity of 5-LO in TAMs were reduced upon coculture with cancer cells.

103 tly, upregulation of proto-oncogene c-Myb in TAMs induced a stable transcriptional repression of 5-LO

104 esses SRM-dependent spermidine production in TAMs and potentiates the growth of CRC.

105 Importantly, ZEB1 in TAMs was a factor of poorer survival in human ovarian ca

106 tivation of ERalpha, which in turn increases TAM-dependent anti-estrogen chemosensitivity in vitro an

107 antibodies or siRNA knockdown of individual TAMs, we show that the uptake is mediated by endothelial

108 st IL-33 in mice also blocks PDGF-BB-induced TAM recruitment and metastasis.

109 M Ig1 domain and Gas6 Lg1 domain can inhibit TAM activation, and support the further development of s

110 ling by a soluble ST2 significantly inhibits TAMs and metastasis.

111 s 1.29 (1.13-1.47; p<0.0001) INTERPRETATION: TAMs are common in patients who have failure of first-li

112 controlling the differentiation of MDSC into TAM, and its regulatory pathway could be a potential tar

113 monstrate that although differentiating into TAMs, monocytes up-regulate matrix-remodeling programs a

114 We investigated TAM and their ligand protein S in patients with diabetes

115 We isolate TAMs from patient biopsies and compare them with macroph

116 Transcriptome analysis of isolated TAMs from both entities revealed reduced expression of t

117 PD-L1(+) TAMs are enriched for contacts with T cells, and PD-L1(+

118 e a unique topology of cHL in which PD-L1(+) TAMs surround HRS cells and implicate CD4(+) T cells as

119 tionships among PD-L1(+) HRS cells, PD-L1(+) TAMs, and PD-1(+) T cells remain undefined.

120 he TME is expressed by the abundant PD-L1(+) TAMs, which physically colocalize with PD-L1(+) HRS cell

121 TAMs and malignant cells but not to M1-like TAMs.

122 ith good selectivity over anti-tumor M1-like TAMs.

123 exhibited selective toxicity to both M2-like TAMs and malignant cells but not to M1-like TAMs.

124 One of the challenges in targeting M2-like TAMs is a lack of high affinity targeting ligand with go

125 ntially to murine M2 macrophages and M2-like TAMs.

126 M2 macrophage-like TAMs were localized in the center of spheroids and secre

127 that M-CSFR signaling shapes the MHC-II(lo) TAM phenotype.

128 etic and functional signatures of MHC-II(lo) TAMs were downregulated upon M-CSFR blockade, indicating

129 the loss of accumulating M2 and increased M1 TAMs.

130 are linked with tumor-associated macrophage (TAM) and myeloid-derived suppressor cell (MDSC) infiltra

131 on also induced tumor-associated macrophage (TAM) recruitment and acquisition of an M2 tumor-promotin

132 Tumor-associated macrophage (TAM) significantly contributes to cancer progression.

133 and MHC-II(lo) tumor-associated macrophage (TAM) subpopulations that originate from Ly6C(hi) monocyt

134 es to display a tumor-associated macrophage (TAM)-like phenotype, with increased expression of the ch

135 roinflammatory tumor-associated macrophages (TAM) and intratumoral immune infiltration, thereby dimin

136 Tumor-associated macrophages (TAM) and myofibroblasts are key drivers in cancer that a

137 Tumor-associated macrophages (TAM) are important components of the multiple myeloma (M

138 Tumor-associated macrophages (TAM) contribute to all aspects of tumor progression.

139 ccumulation of tumor-associated macrophages (TAM) correlates with malignant progression, immune suppr

140 lastoma (GBM), tumor-associated macrophages (TAM) represent up to one half of the cells of the tumor

141 hils (TAN) and tumor-associated macrophages (TAM) versus females, and they both showed protumor gene

142 ypes, such as tumour-associated macrophages (TAM), can be strong prognostic indicators.

143 e signature on tumor-associated macrophages (TAM), which favors expression of inhibitory rather than

144 s and CD163(+) tumor-associated macrophages (TAM).

145 on of MDSCs to tumor-associated macrophages (TAMs) and DCs.

146 Tumor-associated macrophages (TAMs) are abundant in gliomas and immunosuppressive TAMs

147 Tumor-associated macrophages (TAMs) are essential components of the cancer microenviro

148 In cancer, tumor-associated macrophages (TAMs) are recruited to the tumor stroma in response to c

149 erentiation of tumor-associated macrophages (TAMs) are the major factors contributing to tumor progre

150 ccumulation of tumor-associated macrophages (TAMs) associates with malignant progression in cancer.

151 Tumor-associated macrophages (TAMs) can influence ovarian cancer growth, migration, an

152 Tumor-associated macrophages (TAMs) expressing the multi-ligand endocytic receptor man

153 filtration of tumour-associated macrophages (TAMs) facilitates malignant growth of glioblastoma (GBM)

154 The role of tumor-associated macrophages (TAMs) in cancer is often correlated with poor prognosis,

155 activities of tumour-associated macrophages (TAMs) in colorectal cancer (CRC) are incompletely charac

156 lar cells and tumour-associated macrophages (TAMs) in promoting metastasis through the IL-33-ST2-depe

157 e dual role of tumor-associated macrophages (TAMs) in tumor development.

158 ls (MDSCs) and tumor-associated macrophages (TAMs) into tumor microenvironments.

159 Tumor-associated macrophages (TAMs) play an essential role in metastasis.

160 In particular, tumor-associated macrophages (TAMs) produce many cytokines which can support tumor gro

161 or progression.Tumor associated macrophages (TAMs) promote cancer progression.

162 Tumor-associated macrophages (TAMs) promote tumor development, invasion, and dissemina

163 this context, tumor-associated macrophages (TAMs) represent key regulators of the complex interplay

164 ression with a tumor associated macrophages (TAMs) shift towards a pro-tumoral M2 phenotype.

165 immune cells, tumor-associated macrophages (TAMs) take a center stage in promoting both tumor angiog

166 olarization of tumor-associated macrophages (TAMs) to alternatively activated M2 phenotype, promoting

167 ronment induce tumor-associated macrophages (TAMs) to differentiate into distinct subpopulations acco

168 y nonmalignant tumor-associated macrophages (TAMs), but the relationships among PD-L1(+) HRS cells, P

169 stic cells are tumor-associated macrophages (TAMs), either of peripheral origin or representing brain

170 ls (NKRs), and tumor-associated macrophages (TAMs).

171 ulation and as tumor-associated macrophages (TAMs).

172 y may have in tumour-associated macrophages (TAMs).

173 nd function in tumor-associated macrophages (TAMs).

174 to changes in tumor-associated macrophages (TAMs).

175 occurrence of tumor-associated macrophages (TAMs).

176 limitations of tumor-associated macrophages (TAMs).

177 e tumor microenvironment and for maintaining TAMs' tumor-promoting functions.

178 In this manner, TAMs facilitate tumor proliferation, survival and migrat

179 l antibody resulted in a reduction of mature TAMs due to impaired recruitment, extravasation, prolife

180 reduces the virus-induced PD-L1(+) DC, MDSC, TAM and Treg, as well as co-inhibitory molecules-double-

181 suggesting that miR-29b-1/a is not mediating TAM resistance but acts as a tumor suppressor in TAM-res

182 ovel topologically-controlled access memory (TAM).

183 se family consisting of Tyro3, Axl, and Mer (TAM) is one of the most recently identified receptor tyr

184 rosine kinase receptors Tyro3, Axl, and Mer (TAMs) and their ligands protein S and Gas6 are involved

185 c 6 (GAS6), a ligand of the TYRO3-AXL-MERTK (TAM) receptor family, in regulating oral mucosal homeost

186 re of blood-derived TAMs, but not microglial TAMs, correlates with significantly inferior survival in

187 an altered metabolism compared to microglial TAMs.

188 x and the translocation and assembly module (TAM), with each containing a member of the Omp85 superfa

189 x and the translocation and assembly module (TAM).

190 The Transantarctic Mountains (TAM) are the world's longest rift shoulder but the sourc

191 tillites along the Transantarctic Mountains (TAMs) have been used to suggest a diminished East Antarc

192 in situ with antibody and/or relied on mouse TAMs but had not injected SIRPalpha-inhibited cells; als

193 Thus, targeted AID-mediated mutagenesis (TAM) provides a forward genetic tool to screen for gain-

194 correlates of thymidine analogue mutations (TAM) in patients with virological failure of first-line

195 as thymidine-analogue resistance mutations (TAMs)) are rare in the virus from HIV-2-infected individ

196 Namely, TAM-mediated efferocytosis, negative regulation of dendr

197 umor-associated macrophages and neutrophils (TAM and TAN) to solid tumors contributes to immunosuppre

198 Here, we outline a novel TAM protumoral function associated with building of the

199 ar tumor infiltrate or relative abundance of TAM subsets.

200 The addition of TAM enhances membrane permeability, inducing calcein to

201 lineate the temporal and spatial dynamics of TAM composition during gliomagenesis, we used geneticall

202 these findings uncover the heterogeneity of TAM origin and functions and could provide therapeutic i

203 Inhibition of TAM recruitment using an anti-colony-stimulating factor-

204 strointestinal fluids, and the metabolism of TAM was shown to be reduced 2-fold and 3-fold for NP-4%s

205 ur results suggest that miR-29 repression of TAM-resistant breast cancer cell proliferation is mediat

206 A3A in differential proliferative control of TAMs.

207 Depletion of TAMs disrupted lung pre-metastatic niches and thereby pr

208 We demonstrated that differentiation of TAMs in tumor site from monocytic precursors was control

209 anisms that drive the pro-tumor functions of TAMs are not fully understood.

210 this study, we investigated the ontogeny of TAMs in murine pancreatic ductal adenocarcinoma (PDAC) m

211 Overexpression of TAMs and their major ligand Growth arrest-specific facto

212 by inhibiting IH-induced M2 polarization of TAMs.

213 cuss how the unique functional properties of TAMs are shaped by tumor-derived signals, placing TAM de

214 ed a chemotactic gradient for recruitment of TAMs and NKRs via CXCR3/CXCL10 and CCR6/CCL20 pathways,

215 3 promotes metastasis through recruitment of TAMs.

216 This article reviews the roles of TAMs as tumor drivers and as mediators of chemoresistanc

217 nd tissue-resident macrophages as sources of TAMs.

218 not impact the proliferation or survival of TAMs, but rather controls a novel gene expression signat

219 volume assessment and spatial information on TAM infiltration at the cellular level in entire lungs.

220 gammaR activatory:inhibitory (A:I) ratios on TAM, are appealing candidates to reprogram TAM and curb

221 F, which upregulated alphaMbeta2 integrin on TAMs and ICAM-1 on tumor cells to promote association be

222 taining regimens, 115 (16%) had at least one TAM.

223 Only TAMs that expressed full levels of Zeb1 accelerated tumo

224 r necrosis and no change in TME cytokines or TAM phenotype and highlighting the importance of type 1

225 In contrast to protein S, the other TAM ligand, which was constitutively expressed postnatal

226 s across tumours in the same animal, overall TAM density is different among separate pulmonary tumour

227 However, restoration of functional p53ER(TAM) reinstated sensitivity to IR in only 50% of Th-MYCN

228 model in which the tamoxifen-inducible p53ER(TAM) fusion protein was expressed from a knock-in allele

229 rtk and Tyro3 suggesting they can act as pan-TAM inhibitors that block the interface between the TAM

230 are shaped by tumor-derived signals, placing TAM development in the context of the broader understand

231 oal of this study was to develop more potent TAM depletion constructs by increasing the valency of bo

232 In primary TAMs from human and murine breast tumors, 5-LO expressio

233 tumors restores recruitment of prometastatic TAMs and intravasation, whereas treatment with the CCL5

234 ere, the author show that caspase-1 promotes TAMs differentiation by attenuating medium-chain acyl-Co

235 de KLA (M2pepKLA) was further used to reduce TAM population in vivo but high concentrations and frequ

236 e CCL5 receptor antagonist Maraviroc reduces TAM infiltration.

237 b-1/a overexpression significantly repressed TAM-resistant LCC9 cell proliferation, suggesting that m

238 n TAM, are appealing candidates to reprogram TAM and curb tumor-mediated immunosuppression, thereby e

239 eutic target in GADD45beta for reprogramming TAM to overcome immunosuppression and T-cell exclusion f

240 tiated toward non-phagocytic, high-SIRPalpha TAMs.

241 Surprisingly, TAMs frequently co-express canonical pro-inflammatory (M

242 ponses to an estrogen antagonist, tamoxifen (TAM), via at least in part, epigenetic reactivation of E

243 ated miR-29b-1/a transcription in tamoxifen (TAM)-resistant breast cancer cells, ectopic expression o

244 entify increased cortisol production and TAN/TAM infiltration as primary factors in the gender dispar

245 Higher levels of cortisol, TGFB1, and TAN/TAM infiltration in males were also confirmed in human p

246 Use of CSF1R inhibitors to target TAM is therapeutically appealing, but has had very limit

247 ovel therapeutics that simultaneously target TAMs and tumor hypoxia.

248 tatus quo therapeutic strategies that target TAMs indiscriminately and in favor of strategies that sp

249 In this study, we found that TAM and myofibroblasts directly support chemoresistance

250 In vivo, we found that TAM and myofibroblasts were the main sources of IGF prod

251 This method reveals that TAM density was heterogeneous across tumours in the same

252 entational and positional analyses show that TAM exhibits a highly dynamic conformation within the li

253 y (ABT) was investigated, demonstrating that TAMs contribute to prostate cancer disease recurrence th

254 Here we describe that TAMs require ZEB1 for their tumor-promoting and chemothe

255 Further, we have determined that TAMs promote spheroid formation and tumor growth at earl

256 Herein, we report that TAMs secrete abundant pleiotrophin (PTN) to stimulate gl

257 single-cell DNA damage response reveals that TAMs serve as a local drug depot that accumulates signif

258 established by advanced imaging showing that TAMs instruct the deposition, cross-linking, and lineari

259 The TAM (Tyro3, Axl, Mer) subfamily of RTKs in particular fe

260 The TAM also consists of an OMP, designated TamA, and a sing

261 The TAM receptor ligand, growth arrest specific 6, re-establ

262 ces in the conformational dynamics among the TAM family members could potentially be exploited to ach

263 ibitors that block the interface between the TAM Ig1 ectodomain and the Gas6 Lg domain.

264 electivity of substrate interactions for the TAM relative to those of the BAM complex.

265 s observed here beginning to address how the TAM can be more effective than the BAM complex in the fo

266 oteins: BamA in the BAM complex, TamA in the TAM.

267 ith negligible thermal encroachment into the TAM.

268 AXL, a member of the TAM (Tyro3, Axl, MerTK) family of receptors, plays impor

269 liferation promoted by overexpression of the TAM family members AXL or TYRO3 depends on gamma-secreta

270 However, of the three members of the TAM family, the Axl kinase domain is the only one that h

271 that the ATP/inhibitor-binding sites of the TAM members closely resemble each other, posing a challe

272 tion arises is through the inhibition of the TAM receptor, MERTK, and activation of the inflammasome.

273 Here, we review the TAM receptor tyrosine kinases-TYRO3, AXL, and MERTK-as a

274 Here we show that the TAM receptor tyrosine kinases Mer and Axl regulate these

275 r results illuminate a mechanism whereby the TAM phenotype is controlled and identify the cell-surfac

276 ebate about the origin of the diatoms in the TAMs and their link to EAIS history, supporting the view

277 titude winds transported diatoms towards the TAMs, dominantly from extensive emerged coastal deposits

278 Therefore, TAM receptors are critical for downregulating proinflamm

279 iggers their engulfment by microglia through TAM receptor-dependent mechanisms.

280 own therapeutic targeting systems, solely to TAMs or tumor hypoxia, however, novel therapeutics that

281 s constituted approximately 85% of the total TAM population, with resident microglia accounting for t

282 ifferentiation and the occurrence of M2-type TAMs during tumor development.

283 findings suggest a heretofore unappreciated TAM receptor hierarchy in advanced atherosclerosis.

284 ell types can phagocytose PMPs, and by using TAM-blocking antibodies or siRNA knockdown of individual

285 In this study, we investigated how vascular TAMs and their ligands may mediate endothelial uptake of

286 In vitro TAM polarization away from the M2 phenotype induced by C

287 ent, Ile(75) suppress excision activity when TAMs are present in the HIV-2 RT.

288 tanding of the molecular mechanisms by which TAM and fibroblasts contribute to chemoresistance is unc

289 rophages engorged on the human tumors, while TAMs were minimally phagocytic, even toward CD47-knockdo

290 ion) and metastatic burden, accompanied with TAM polarization away from the M2 phenotype in spontaneo

291 erosis or lesional processes associated with TAM receptor signaling.

292 se xenografts, especially when combined with TAM treatment.

293 anotherapeutic drug delivery correlated with TAM heterogeneity, and successful response to CSF-1R blo

294 In crude comparisons, patients with TAMs had lower CD4 counts at treatment initiation than d

295 ir resistance (93 [81%] of 115 patients with TAMs vs 352 [59%] of 597 patients without TAMs; p<0.0001

296 nalyses to compare patients with and without TAMs for the presence of resistance to tenofovir, cytosi

297 sistance comparing patients with and without TAMs was 1.29 (1.13-1.47; p<0.0001) INTERPRETATION: TAMs

298 eatment initiation than did patients without TAMs (60.5 cells per muL [IQR 21.0-128.0] in patients wi

299 th TAMs vs 352 [59%] of 597 patients without TAMs; p<0.0001), NNRTI resistance (107 [93%] vs 462 [77%

300 lls per muL [37.0-177.0] in patients without TAMs; p=0.007) and were more likely to have tenofovir re