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1 ithout increased vascular inflammation (ED1+ tissue macrophages).
2 ction can be sustained for several months by tissue macrophage.
3 s of peripheral blood monocytes and resident tissue macrophages.
4 bone marrow precursors, blood monocytes, and tissue macrophages.
5 finition, not terminally differentiated like tissue macrophages.
6 nctly and universally associated with mature tissue macrophages.
7 1(op/op) mice, which have reduced numbers of tissue macrophages.
8 electively expressed PPARgamma among resting tissue macrophages.
9 rences and expression pattern in the pool of tissue macrophages.
10 asis and thus represent a central feature of tissue macrophages.
11 severe depletion of resident osteoclasts and tissue macrophages.
12 solated mouse monocytes compared with mature tissue macrophages.
13 KKepsilon) in liver, adipocytes, and adipose tissue macrophages.
14 1), such as plasmacytoid dendritic cells and tissue macrophages.
15  but not monocytes, dendritic cells or other tissue macrophages.
16  was required to rapidly replenish destroyed tissue macrophages.
17 ynthesized and secreted by liver, brain, and tissue macrophages.
18 igh-fat diet showed no reductions in adipose tissue macrophages.
19 and restraining the inflammatory products of tissue macrophages.
20 apacity to infect non-dividing cells such as tissue macrophages.
21 reas, and heart but decreased iron levels in tissue macrophages.
22 sociated with storage of glucocerebroside in tissue macrophages.
23  positive, and a small percentage are mature tissue macrophages.
24 ammatory monocytes, and increased numbers of tissue macrophages.
25 ctivating factor acetylhydrolase (PAF AH) in tissue macrophages.
26 nificantly increased replicative capacity in tissue macrophages.
27 hancement of viral spread within nondividing tissue macrophages.
28 CSF-1 dependent, bone marrow-derived adipose tissue macrophages.
29 ting monocytes or from migration of resident tissue macrophages.
30 pe responses and/or deactivating parasitized tissue macrophages.
31 pe that impart high replicative capacity for tissue macrophages.
32 the establishment of persistent infection in tissue macrophages.
33 ls and lymphocytes, but not to B-1a cells or tissue macrophages.
34 ithelial cells, and a subsequent increase in tissue macrophages.
35 e 1 (HIV-1) infects CD4(+) T lymphocytes and tissue macrophages.
36 ted reservoir of infectious HIV-1 virions in tissue macrophages.
37  and precursors of resident and inflammatory tissue macrophages.
38 dentify yolk sac EMPs as a common origin for tissue macrophages.
39 hemoattractant activity for F4/80(+)CD11c(-) tissue macrophages.
40  embryonic-derived but not postnatal-derived tissue macrophages.
41 pilosebaceous follicles and colocalized with tissue macrophages.
42 s in the frequency of M1- or M2-like adipose tissue macrophages.
43 e pathophysiology is manifested primarily in tissue macrophages.(1) In this issue of Blood, Campeau a
44    HIV-expressing cells were associated with tissue macrophages, a target of HIV infection.
45               Mechanisms involved in adipose tissue macrophage accrual continue to be elusive.
46 nce regarding dietary cholesterol on adipose tissue macrophage accrual, systemic inflammation and its
47 ay for erythrophagocytosis in the context of tissue macrophage accumulation and inflammation involvin
48 Stat3 in T cells in DIO mice affects adipose tissue macrophage accumulation and M2 phenotype.
49  and IL-13, in the induction of inflammatory tissue macrophage accumulation and/or hemophagocytosis.
50 eas overexpression of SirT1 prevents adipose tissue macrophage accumulation caused by chronic high-fa
51 t decreases blood glucose levels and adipose tissue macrophage accumulation in a high-fat, diet-fed m
52 ctors that potentially contribute to adipose tissue macrophage accumulation in obesity.
53 ice transgenic for IL-4 production developed tissue macrophage accumulation, disruption of splenic ar
54 i-IL-4 complexes, lead to substantial YM1(+) tissue macrophage accumulation, erythrophagocytosis with
55 lesterol added resulted in increased adipose tissue macrophage accumulation, local inflammation and c
56 s influence diet-induced obesity and adipose tissue macrophage accumulation, mice that were either wi
57 tion, indicating a possible role for adipose tissue macrophage activation.
58 atory response, resident and newly recruited tissue macrophages adhere to extracellular matrix and ce
59  is probably life-long since targeted cells (tissue macrophages) allow residual parasites to persist.
60                      Distinct populations of tissue macrophages also acquire context-specific functio
61                        Depletion of visceral tissue macrophages also did not alter central nervous sy
62 nt anti-inflammatory effects with regards to tissue macrophage and neutrophil density following ureth
63 marked reduction in pro-inflammatory adipose tissue macrophages and activated CD8+ T cells.
64 lammatory cytokines in both isolated adipose tissue macrophages and adipocytes.
65                    Microglia are the brain's tissue macrophages and are found in an activated state s
66    First, we show an altered distribution of tissue macrophages and blood monocytes in the absence of
67 y alveolar macrophages, in contrast to other tissue macrophages and blood monocytes.
68 lso show that CD44ICD promotes the fusion of tissue macrophages and bone marrow-derived macrophages.
69                                  HIV infects tissue macrophages and brain microglia, which express lo
70 earance of senescent neutrophils by resident tissue macrophages and DCs helps to set homeostatic leve
71 lia, whereas monocytes, dermal, and lymphoid tissue macrophages and DCs were unaffected.
72     Monocytes are circulating precursors for tissue macrophages and dendritic cells (DCs) but are not
73 tion with, and/or infection of CD4(+)CCR5(+) tissue macrophages and dendritic cells (DCs) play import
74              Furthermore, we determined that tissue macrophages and dendritic cells within the liver
75       Recruited monocytes differentiate into tissue macrophages and dendritic cells, which sample ant
76 ious subsets, which are able to give rise to tissue macrophages and dendritic cells.
77 s used for identifying the complex origin of tissue macrophages and discuss the relative contribution
78                            Its expression on tissue macrophages and epithelial cells suggests importa
79 venger receptor-induced apoptosis in primary tissue macrophages and in macrophage apoptosis in advanc
80 tment reduced peripheral blood monocytes and tissue macrophages and inhibited macrophage function in
81 d plays a role in the maintenance of adipose tissue macrophages and insulin resistance once obesity a
82  an enzyme predominantly expressed in mature tissue macrophages and is implicated in several disease
83                                 In contrast, tissue macrophages and monocyte-derived macrophages in v
84 e characterized by cholesterol deposition in tissue macrophages and prevalent atherosclerosis.
85                              However, unlike tissue macrophages and similar to DCs, they homeostatica
86 row-derived progenitor cells into monocytes, tissue macrophages and some dendritic cell (DC) subtypes
87 f osteopontin in the accumulation of adipose tissue macrophages and the development of insulin resist
88           The selective expression of CR3 by tissue macrophages and the requirement of TLR2 inside-ou
89 type lectin, CD209, known to be expressed on tissue macrophages and to mediate the uptake of M. lepra
90 m for stromal cells (fibrocytes and possibly tissue macrophages) and CD8(+) T and CD21(+) B lymphocyt
91 eplication in fibrocytes (possibly including tissue macrophages) and T and B lymphocytes in the prese
92 een inflammation, cholesterol oxidation, the tissue macrophage, and atherosclerosis.
93  including the osteopetrotic, hematopoietic, tissue macrophage, and reproductive phenotypes.
94 ), CD4(+), CD8(+), and CD25(+)) lymphocytes, tissue macrophages, and dendritic cells (Iba-1(+) and CD
95 IV-1 uses mononuclear phagocytes (monocytes, tissue macrophages, and dendritic cells) as a vehicle fo
96 ving rise to B and T lymphocytes, monocytes, tissue macrophages, and dendritic cells.
97 ransduction in dendritic cells, osteoclasts, tissue macrophages, and microglia.
98 sue inflammation, M1 polarization of adipose tissue macrophages, and the development of insulin resis
99 (SHIVs) during infections of rhesus monkeys, tissue macrophages are able to sustain high levels (>10(
100                                     Resident tissue macrophages are activated by the fungal pathogen
101                                              Tissue macrophages are an important cellular reservoir f
102                                     Although tissue macrophages are anatomically distinct from one an
103                                              Tissue macrophages are critical contributors to HIV path
104                               The origins of tissue macrophages are diverse, with evidence for local
105 ifferentiation of blood-borne monocytes into tissue macrophages are incompletely defined.
106                         To determine whether tissue macrophages are productively infected, we used 3
107 rom adipose tissue demonstrates that adipose tissue macrophages are responsible for almost all adipos
108                                           In tissues, macrophages are exposed to metabolic, homeostat
109 we review evidence on the pathogenic role of tissue macrophages as long-term viral reservoirs in vivo
110                                              Tissue macrophages assume a distinct phenotype, designat
111 ocytes given to MCP-1 KO recipients, adipose tissue macrophage (ATM) accumulation is reduced by ~40%,
112 Obesity is associated with increased adipose tissue macrophage (ATM) infiltration, and rodent studies
113  the expansion of adipose tissue and adipose tissue macrophage (ATM) polarization, in the current stu
114                                      Adipose tissue macrophage (ATM) recruitment and activation play
115 etes has been known for decades, and adipose tissue macrophage (ATM)-associated inflammation has rece
116       Here, we studied whether human adipose tissue macrophages (ATM) modulate cancer cell function.
117 lation of classically activated (M1) adipose tissue macrophages (ATMs) and the expression of proinfla
118                                These adipose tissue macrophages (ATMs) are inflammatory and promote l
119                                      Adipose tissue macrophages (ATMs) are key players orchestrating
120 o-inflammatory cytokines secreted by adipose tissue macrophages (ATMs) contribute to chronic low-grad
121               We further showed that adipose tissue macrophages (ATMs) in lipodystrophy and obesity a
122                   Here, we show that adipose tissue macrophages (ATMs) in obese mice secrete miRNA-co
123 s that NPY regulates the function of adipose tissue macrophages (ATMs) in response to dietary obesity
124                                      Adipose tissue macrophages (ATMs) infiltrate adipose tissue duri
125 We have examined the hypothesis that adipose tissue macrophages (ATMs) interact with and regulate the
126              Polarized activation of adipose tissue macrophages (ATMs) is crucial for maintaining adi
127    Although recent studies show that adipose tissue macrophages (ATMs) participate in the inflammator
128                                      Adipose tissue macrophages (ATMs) play a critical role in obesit
129                                      Adipose tissue macrophages (ATMs) play an important role in the
130 ever, the functional role of IRF4 in adipose tissue macrophages (ATMs) remains unclear, despite high
131 ere we characterized the response of adipose tissue macrophages (ATMs) to weight loss and fasting in
132  and functional characteristics of adipocyte tissue macrophages (ATMs), in obese patients undergoing
133 en into account the heterogeneity of adipose tissue macrophages (ATMs), nor have they examined how ag
134 infiltration of increased numbers of adipose tissue macrophages (ATMs).
135  displayed cytotoxic activity toward adipose tissue macrophages (ATMs).
136 , we demonstrate that in microglia and other tissue macrophages, beta-amyloid initiates a CD36-depend
137 cent paradigm shifts in our understanding of tissue macrophage biology.
138 ired for the development and distribution of tissue macrophages but is involved in the generation of
139  be specified, as they could be monocytes or tissue macrophages, but most likely dendritic cells.
140                                 Infection of tissue macrophages by X4 HIV-1 may be highly relevant in
141 omplexity is added by the new knowledge that tissue macrophages can be derived either from a resident
142                                              Tissue macrophages can be derived from embryonic progeni
143  novel transgenic mouse (CD11b-DTR) in which tissue macrophages can be specifically and selectively a
144                                      Adipose tissue macrophages can contribute to the systemic proinf
145 l adipose tissue macrophage content (adipose tissue macrophages; CD11b(+), CD11c(+), Ly6C(hi)) concom
146 eatment with clodronate liposomes to deplete tissue macrophages, comparing the sites of (99m)Tc-EC20
147                                              Tissue macrophages comprise a heterogeneous group of cel
148              DPP-4i reduced visceral adipose tissue macrophage content (adipose tissue macrophages; C
149 or insulin action is associated with adipose tissue macrophage content (ATMc) and/or markers of macro
150 mice also had increased body fat and adipose tissue macrophage content, elevated plasma interleukin-6
151 e systemic inflammation or increased adipose tissue macrophage content, were reversed when plasma ins
152 a framework in which to consider how adipose tissue macrophages contribute to the remodeling events i
153 eripheral monocytes associated with death of tissue macrophages correlates with AIDS progression in m
154 ques, increasing monocyte turnover reflected tissue macrophage damage by SIV and was predictive of te
155  overt inflammation, constitutively maintain tissue macrophage/DC populations.
156 productive, hematopoietic tooth eruption and tissue macrophage defects of CSF-1-deficient, osteopetro
157                  The recent recognition that tissue macrophages derive from different sources, couple
158  in the steady state, the dogma remains that tissue macrophages derive from monocytes.
159                                        While tissue macrophages derive from one of a small number of
160 and suggest that the relocation of iron from tissue macrophages during infection may contribute to an
161 poietic deletion of Ntn1 facilitates adipose tissue macrophage emigration, reduces inflammation and i
162 earance of infused enzyme by the MR on fixed tissue macrophages, especially Kupffer cells.
163 f diet-induced obesity, we show that adipose tissue macrophages exhibit reduced migratory capacity, w
164                                              Tissue macrophage export of iron occurs concurrent with
165                        Reciprocally, adipose tissue macrophages express IL-17 and IL-22 receptors, ma
166 ba-1(+) and CD83(+)), with a small number of tissue macrophages expressing CD163 and CD204 scavenger
167                    PM(2.5) increased adipose tissue macrophages (F4/80(+) cells) in visceral fat expr
168   Second, aside from being immune sentinels, tissue macrophages form integral components of their hos
169              The differentiation of resident tissue macrophages from embryonic precursors and that of
170               We assessed gene expression in tissue macrophages from various mouse organs.
171                                              Tissue macrophages function to maintain homeostasis and
172 ctional, and phenotypic heterogeneity within tissue macrophages has altered our understanding of thes
173                                      Adipose tissue macrophages have been proposed as a link between
174                    Since then, monocytes and tissue macrophages have emerged as key sentinels of infe
175 Macs is followed by their specification into tissue macrophages, hereby generating the macrophage div
176    Understanding the mechanisms that dictate tissue macrophage heterogeneity should explain why simpl
177 -wide analysis of gene expression in adipose tissue macrophages highlights the transforming growth fa
178  from the marrow through the blood to become tissue macrophages, histiocytes, and dendritic cells.
179 um enzyme levels through M-CSF regulation of tissue macrophage homeostasis without concomitant histop
180  factor-1 receptor (CSF-1R) kinase regulates tissue macrophage homeostasis, osteoclastogenesis, and P
181 irus with in vivo cell tropism primarily for tissue macrophages; however, in vitro the virus can be a
182  of apoptotic cells is an innate function of tissue macrophages; however, its role in disease progres
183 e functional and phenotypic heterogeneity of tissue macrophages in different anatomic sites and as a
184  cells fail to recapitulate the phenotype of tissue macrophages in key respects, including that they
185 Our results reveal an unanticipated role for tissue macrophages in mesoangioblast function.
186  at altering the proinflammatory capacity of tissue macrophages in progressively HIV-infected individ
187 al macrophages represent the largest pool of tissue macrophages in the human body and a critical inte
188 erleukin 4 and the alternative activation of tissue macrophages in the organismal response to diverse
189 vidence suggesting local self-maintenance of tissue macrophages in the steady state, the dogma remain
190 ytes do not show significant contribution to tissue macrophages in the steady state.
191 nounced proinflammatory signature of adipose tissue macrophages in type 2 diabetic obese patients, ma
192 nce, to our knowledge, of HIV persistence in tissue macrophages in vivo.
193 tes engage different complement receptors on tissue macrophages in vivo.
194  CD11c+ and B220+ dendritic cells and F4/80+ tissue macrophages in vivo.
195 report that activation of different types of tissue macrophages, including microglia, by lipopolysacc
196 (IL-37tg) exhibit reduced numbers of adipose tissue macrophages, increased circulating levels of adip
197 ion of several pro-inflammatory cytokines in tissue macrophages, induction of the anti-inflammatory c
198                                      Adipose tissue macrophage infiltration and inflammation were als
199 y cytokine, mediates obesity-induced adipose tissue macrophage infiltration and insulin resistance, i
200                          Kinetics of adipose tissue macrophage infiltration was characterized by fluo
201 tion, adipocyte apoptosis, prevented adipose tissue macrophage infiltration, and protected against th
202 g of the failing myocardium reverses adipose tissue macrophage infiltration, inflammation, and adipon
203 utaneous fat is inversely related to adipose tissue macrophage infiltration.
204 correlated with the degree of IR and adipose tissue macrophage infiltration.
205 tissue factor-PAR2 signaling reduced adipose tissue macrophage inflammation, and specific pharmacolog
206                                         Lung tissue macrophage inflammatory protein-2, keratinocyte-d
207 sma lipids, increases autophagy, and orients tissue macrophages into an anti-inflammatory phenotype i
208 pronounced polarization of liver and adipose tissue macrophages into an M1 phenotype.
209                    The reduction of synovial tissue macrophages is a reliable biomarker for clinical
210 y also suggest that its function in resident tissue macrophages is limited.
211  (MoM), we demonstrate that HIV infection of tissue macrophages is rapidly suppressed by ART, as refl
212 clearance is primarily the function of fixed tissue macrophages (Kupffer cells) that line the hepatic
213 CL2(-/-) mice, despite no changes in adipose tissue macrophage levels, suggests that CCL2 has effects
214 ) primarily infects blood monocytes (MO) and tissue macrophages (M phi).
215 n, Fas ligation on circulating monocytes and tissue macrophages may induce proinflammatory cytokine r
216                                     Resident tissue macrophages mediate early innate immune responses
217 f efferocytosis by resident murine and human tissue macrophages (Mo).
218 the origin and differentiation cues for many tissue macrophages, monocytes, and dendritic cell subset
219                                              Tissue macrophages (Mphis) and dendritic cells (DCs) pla
220 cally and functionally distinct from mammary tissue macrophages (MTMs).
221 rmed with DNA isolated from ischemic muscle, tissue macrophages (Mvarphis), and endothelial cells.
222 at monocytes are the immediate precursors of tissue macrophages needs to be refined based upon eviden
223  probably seldom eradicates all parasites in tissue macrophages; nevertheless, most T cell-intact pat
224 acrophage progenitor frequency and decreased tissue macrophage nitric oxide and IL-12 production in r
225       These findings support the theory that tissue macrophage numbers are regulated through local pr
226                                      Adipose tissue macrophage numbers increase in obesity and partic
227                                              Tissue macrophage numbers vary during health versus dise
228 ication-competent virus was rescued from the tissue macrophages obtained from these animals.
229 much less is known about microglia, resident tissue macrophages of the brain that originate from a di
230            Microglial cells are the resident tissue macrophages of the CNS and are widely recognized
231                                       As the tissue macrophages of the CNS, microglia are critically
232                                        Thus, tissue macrophages, once infected, have the characterist
233 light of recent advances in understanding of tissue macrophage ontogeny, their capacity for self-rene
234 ently, it has become evident that most adult tissue macrophages originate during embryonic developmen
235 rain macrophages but are distinct from other tissue macrophages owing to their unique homeostatic phe
236 ence that obesity-related changes in adipose tissue macrophage phenotype could be mediated by adipocy
237           Our investigations reveal that the tissue macrophage phenotype is under discrete tissue-sel
238 s of cells, including mast cells, monocytes, tissue macrophages, platelets, eosinophils, endothelial
239 trated ER stress-induced rewiring of adipose tissue macrophage polarization by IRE1alpha activation,
240 e the nature, functions, and interactions of tissue macrophage populations within their microenvironm
241  properties that distinguish them from other tissue macrophage populations, we have optimized serum-f
242 is required for efficient HIV replication in tissue macrophages present in human spleens and tonsils.
243                  In this study, we show that tissue macrophages present in the fetal mouse lung media
244 rion sequestration and destruction via local tissue macrophages, prion trafficking by B and dendritic
245                                              Tissue macrophages provide innate defense against GAS, a
246 ant and positive correlation between adipose tissue macrophage quantification at MR imaging and P904
247 l variance in mice was correlated to adipose tissue macrophage quantification by using monoclonal ant
248                 With tissue insult, resident tissue macrophages rapidly efflux to lymph nodes where t
249 LR1-positive plasmacytoid dendritic cell and tissue macrophage recruitment to sterile sites of tissue
250 nclude that CCL2 is not critical for adipose tissue macrophage recruitment.
251 may contribute to obesity-associated adipose tissue macrophage recruitment.
252                         As immune sentinels, tissue macrophages regulate immune activation and inflam
253                    Here we show that adipose tissue macrophages regulate the age-related reduction in
254 oxide content (r = 0.87, P < .0001), adipose tissue macrophage-related inflammation at immunohistoche
255 itial events of monocyte migration to become tissue macrophages remain poorly understood.
256 ocytes, whereas dendritic cells and resident tissue macrophages remained unaltered.
257 approaches that could promote elimination of tissue macrophage reservoirs.
258              Our results reveal unique intra-tissue macrophage specialization and identify neuro-immu
259                          Factors that govern tissue macrophage specialization are emerging.
260                     We have identified a new tissue macrophage subset in the thymus and have discover
261 fy Ly6C as a marker of functionally discrete tissue macrophage subsets and support a model of selecti
262  but the transcriptional basis for producing tissue macrophage subsets remains unknown.
263 ervations support a model according to which tissue macrophage subtype specification is distinct from
264 eptor of the Ig superfamily (CRIg), found on tissue macrophages such as synovial macrophages, has pro
265 of Siglec-1 in circulating SSc monocytes and tissue macrophages suggests that type I IFN-mediated act
266                                              Tissue macrophages synthesize neutrophil chemoattractant
267                                        Renal tissue macrophages, T cells, and neutrophils produce var
268 light marked heterogeneity in the origins of tissue macrophages that arise from hematopoietic versus
269 addition to CD4 T lymphocytes, HIV-1 infects tissue macrophages that can actively accumulate infectio
270            These results define a lineage of tissue macrophages that derive from the YS and are genet
271 ry X4 HIV-1 isolates can productively infect tissue macrophages that have terminally differentiated i
272 n resulted in a phenotypic change in adipose tissue macrophages that was characterized by upregulatio
273 h lpr/lpr and B6 mice had similar numbers of tissue macrophages, the loss of Fas in M-CSF-deficient m
274  review, we discuss the different origins of tissue macrophages, the transcription factors regulating
275  with the discovery of an important role for tissue macrophages, these new findings are helping to re
276                                    Like many tissue macrophages, they self-maintain locally.
277 IL-4 was sufficient to drive accumulation of tissue macrophages through self-renewal.
278             We postulate that the failure of tissue macrophages to remove senescent erythrocytes led
279  reduced, further confirming polarization of tissue macrophages toward an anti-inflammatory phenotype
280 n adipose tissue and polarization of adipose tissue macrophages toward an M2 alternatively activated
281 formed to evaluate the kinetics and monocyte/tissue macrophage turnover in Indian rhesus macaques (Ma
282 ilin-1 was diminished on blood monocytes and tissue macrophages under proinflammatory conditions.
283 veal that a distinct process exists in which tissue macrophages undergo rapid in situ proliferation i
284 attractive target for delivering antigens to tissue macrophages via Sn-mediated endocytosis.
285                   Activation of NF-kappaB in tissue macrophages was assessed in mice that expressed a
286 b-PI3Kgamma(-/-) mice, the number of adipose tissue macrophages was similar to control, but displayed
287 s demonstrated that both circulating PMN and tissue macrophages were altered under inflammatory condi
288                                      Adipose tissue macrophages were detected and quantified with a 4
289  In contrast, epidermal Langerhans cells and tissue macrophages were largely preserved.
290  anemia of inflammation, iron accumulated in tissue macrophages, whereas a relative paucity of iron w
291 rominent players in this process are adipose tissue macrophages, which are a specialized leukocyte pr
292 d promotes alternative activation of adipose tissue macrophages, which are required for the increased
293                      Moreover, skin-resident tissue macrophages, which encounter S. mansoni excretory
294 y promoted alternative activation of adipose tissue macrophages, which secrete catecholamines to indu
295 okines and decreased accumulation of adipose tissue macrophages, which were also preferentially biase
296 nitors and the independent myeloid system of tissue macrophages, whose regulation by local microenvir
297 y activates the production of NPY in adipose tissue macrophages with autocrine and paracrine effects.
298                  Infiltrating cells included tissue macrophages, with an HLA-DR(+)CD14(+)CD45(+)CD68(
299 g to the accumulation of glucocerebroside in tissue macrophages within multiple organs.
300 ations like neutrophils and F4/80(+) adipose tissue macrophages without any alterations in the freque

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