Cells In Perivascular Adipose Tissue Research Articles

Inflammatory Cells in Adipose Tissue and Skeletal Muscle of Patients with Peripheral Arterial Disease or Chronic Venous Disease: A Prospective, Observational, and Histological Study.

The main goal of this study was to assess whether the presence of peripheral arterial disease (PAD) correlates with increased inflammatory cell infiltration. An observational, single-centre, and prospective study was conducted from January 2018 to July 2022. Clinical characteristics and anthropometric measures were registered. Consecutive PAD patients with surgical indications for a common femoral artery approach and patients with varicose veins with an indication for surgical ligation of the saphenofemoral junction were included. In both groups, samples of sartorius skeletal muscle, subcutaneous adipose tissue (SAT), and perivascular adipose tissue (PVAT) were collected from the femoral region. We analysed the characteristics of adipocytes and the presence of haemorrhage and inflammatory cells in the samples of PVAT and SAT via haematoxylin-eosin staining. We found that patients with PAD had significantly more inflammatory cells in PVAT [16 (43.24%) vs. 0 (0%) p = 0.008]. Analysing SAT histology, we observed that patients with PAD had significantly more CD45+ leucocytes upon immunohistochemical staining [32 (72.73%) vs. 3 (27.27%) p = 0.005]. Upon analysing skeletal muscle histology with haematoxylin-eosin staining, we evaluated skeletal fibre preservation, as well as the presence of trauma, haemorrhage, and inflammatory cells. We registered a significantly higher number of inflammatory cells in patients with PAD [well-preserved skeletal fibres: PAD = 26 (63.41%) vs. varicose veins = 3 (37.50%) p = 0.173; trauma: PAD = 4 (9.76%) vs. varicose veins = 2 (25.00%) p = 0.229; haemorrhage: PAD = 6 (14.63%) vs. varicose veins = 0 (0%) p = 0.248; inflammatory cells: PAD = 18 (43.90%) vs. varicose veins = 0 (0%) p = 0.018]. Patients with PAD had a higher number of inflammatory cells in skeletal muscle and adipose tissue (PVAT and SAT) when compared with those with varicose veins, emphasizing the role of inflammation in this group of patients.

S-40-4: ANGIOTENSIN II-INDUCED BLOOD PRESSURE ELEVATION WAS POTENTIATED TOGETHER WITH INCREASES IN INTERFERON-GAMMA PRODUCING T CELLS IN INTERLEUKIN-23 RECEPTOR-DEFICIENT MICE

Objectives: We previously demonstrated a role for γδ T cells in hypertension and vascular injury. In inflammatory conditions γδT17 are a prominent producer of IL-17A, which has been shown to contribute to hypertension. The development and expansion of γδT17 cells is regulated in part through IL-23 receptors (IL-23R). We hypothesized that angiotensin (Ang) II-induced blood pressure (BP) elevation and vascular injury would be blunted in mice with dysfunctional IL-23R. Design and method: Wild-type (WT) and Il23r knock-in (Il23r gfp/gfp) mice were infused or not with Ang II (490ng/kg/min, SC) for 7 or 14 days. BP was monitored via telemetry, mesenteric artery function and remodeling using pressurized myography, and T cell profiling in mesenteric artery perivascular adipose tissue (PVAT) by flow cytometry. Results: Il23r gfp/gfp mice exhibited a greater BP elevation in response to Ang II than WT by day 3 (152 ± 5 vs 144 ± 7 mm Hg, P < 0.05), which was sustained through day 9 (169 ± 2 vs 155 ± 5 mm Hg, P < 0.05), but eventually similar to that of WT mice by the end of the Ang II infusion (167 ± 2 vs 167 ± 4 mm Hg). Il23r gfp/gfp mice were not protected from vascular dysfunction and remodeling after 14 days of Ang II. Il23r gfp/gfp mice had less γδT17 cells in PVAT than WT mice (40 ± 8 vs 108 ± 15 cells/PVAT, P < 0.05). Ang II increased interferon-γ producing γδ T cells in WT (13 ± 3 vs 5 ± 1 cells/PVAT, P < 0.05) and Il23r gfp/gfp mice (14 ± 3 vs 3 ± 1 cells/PVAT, P < 0.05), and interferon-γ producing CD4+ (125 ± 27 vs 38 ± 13 cells/PVA, P < 0.05) and CD8+ T cells (76 ± 13 vs 33 ± 8 cells/PVA, P < 0.05) only in Il23r gfp/gfp mice. Conclusion: Functional IL-23R deficiency exaggerated BP elevation during the initiation of Ang II-induced hypertension, potentially due to the increased number of interferon-γ producing T cells.

Abstract 131: Interleukin-23 Receptor Deficiency Increased Interferon-gamma Producing T Cells And Potentiated Blood Pressure Elevation In Angiotensin II-infused Mice

Introduction: We previously demonstrated a role for γδ T cells in hypertension and vascular injury. In inflammatory conditions γδT17 are a prominent producer of IL-17A, which has been shown to contribute to hypertension. The development and expansion of γδT17 cells is regulated in part through IL-23 receptors (IL-23R). Hypothesis: We hypothesized that angiotensin (Ang) II-induced blood pressure (BP) elevation and vascular injury would be blunted in mice with dysfunctional IL-23R. Methods: Wild-type (WT) and Il23r knock-in ( Il23r gfp/gfp ) mice were infused or not with Ang II (490ng/kg/min, SC) for 7 or 14 days. BP was monitored via telemetry, mesenteric artery function and remodeling using pressurized myography, and T cell profiling in mesenteric artery perivascular adipose tissue (PVAT) by flow cytometry. Results: Il-23r gfp/gfp mice exhibited a greater BP elevation in response to Ang II than WT by day 3 (152±5 vs 144±7 mm Hg, P <0.05), which was sustained through day 9 (169±2 vs 155±5 mm Hg, P <0.05), but eventually similar to that of WT mice by the end of the Ang II infusion (167±2 vs 167±4 mm Hg). Il-23r gfp/gfp mice were not protected from vascular dysfunction and remodeling after 14 days of Ang II. Il23r gfp/gfp mice had less γδT17 cells in PVAT than WT mice (40±8 vs 108±15 cells/PVAT, P <0.05). Ang II increased interferon-γ producing γδ T cells in WT (13±3 vs 5±1 cells/PVAT, P <0.05) and Il23r gfp/gfp mice (14±3 vs 3±1 cells/PVAT, P <0.05), and interferon-γ producing CD4 + (125±27 vs 38±13 cells/PVA, P <0.05) and CD8 + T cells (76±13 vs 33±8 cells/PVA, P <0.05) only in Il23r gfp/gfp mice. Conclusion: Functional IL-23R deficiency exaggerated BP elevation during the initiation of Ang II-induced hypertension, potentially due to the increased number of interferon-γ producing T cells.

Abstract 507: Adipocyte-specific Cytokine Signaling Regulates Inflammation And Atherosclerosis

Adipose tissue inflammation has been implicated in various chronic inflammatory diseases and cancer. Perivascular adipose tissue (PVAT) surrounds the aorta as a fourth layer and was previously shown to regulate the function of endothelial and vascular smooth muscle cells. Moreover, PVAT contains various immune cells and therefore could contribute to the inflammatory environment in the aorta during atherosclerosis development via cross-talk with adventitia. We found that Western diet (WD) feeding increases the accumulation of immune cells in PVAT of atherosclerosis-prone Ldlr -/- mice and increases the expression of IL-1β. As IL-1 is essential for atherosclerosis development and its inhibition in patients in CANTOS trial reduced inflammation and cardiovascular events, we further evaluated the potential role of IL1R signaling in adipocytes of PVAT.We found that adipocyte-specific ablation of IL1R in Il1r fl/fl Ldlr -/- AdipoCre + mice fed with Western Diet for 16 weeks led to significant reduction in atherosclerosis when compared to Il1r fl/fl Ldlr -/- AdipoCre - controls. Gene expression analysis of isolated adipocytes revealed a significant reduction of expression of several chemokines, including Ccl2, Ccl5, Ccl7 as well as pro-atherogenic cytokines IL-6 and IL-1β . The analysis of immune cell composition by Flow cytometry and scRNA sequencing further demonstrated reduced representation of key pro-inflammatory cell subsets in PVAT of l1r fl/fl Ldlr -/- AdipoCre + which also reflected in their reduced accumulation in the aorta and atherosclerotic plaques. Our data suggest novel adipocyte-specific mechanisms controlling inflammation in atherosclerosis. IL1R signaling therefore directly regulates pro-inflammatory chemokines and cytokines in adipocytes thereby controlling immune cell recruitment to PVAT and aortic wall, which in turn contributes to the enhanced aortic inflammation and atherosclerosis.

P2256Aging and inhibition of Nox4 and Nox1 exacerbate perivascular inflammation in spontaneous hypertension

Abstract Introduction Hypertension is associated with enhanced NADPH oxidase activation and increased accumulation of immune cells leading to perivascular inflammation. However, while aging and oxidative stress are a major factor for the development of hypertension, their effect on perivascular inflammation remains unclear. Purpose We aimed to establish the interaction between aging, oxidative stress and perivascular inflammation. We hypothesize that the modulation of oxidative stress, by NADPH oxidase inhibition, could affect perivascular inflammation during the aging. Methods Using flow cytometry, we studied leukocyte infiltration in the perivascular adipose tissue (PVAT) in 1-, 3-, 6- and 12-month-old SHR (Spontaneously Hypertensive Rats) and normotensive WKY (Wistar-Kyoto) rats (n=5–12). Additionally, 1-month-old rats were treated with GKT137831 or ML171 (60mg/kg; NOX1/4 and NOX1 inhibitor, respectively) for 4 weeks. Blood pressure (PB) was measured by tail cuff. Statistical analysis was performed using two-way ANOVA or t-test. Data are presented as means±SEM. Results Aging in SHRs was associated with an increase of BP (139±4 vs. 180±4 vs. 203±3 vs. 209±3, mmHg) and an elevation of PVAT leukocytes (2090±164 vs. 2255±359 vs. 2502±496 vs. 3255±408, cell/mg) in 1-, 3-, 6- and 12-month-old rats, respectively. These effects were not seen in WKY. These were associate with similar changes of NK cells (p int <0.001) and macrophages (p int <0.001) in the SHR PVAT. Within T cell compartment, TH17 cells in PVAT were only elevated with age in SHR (1.04±0.08% vs. 1.89±0.2%, 1.08±0.1% vs. 2.03±0.2%, 1.71% vs. 4.37±0.5%, WKY vs. SHR, 3-,6- and 12-months, respectively, p int<0.001). While an age-related increase of Nox4 mRNA in the vessels was observed in both groups, this increase was more dynamic in SHRs, (p int <0.05). Furthermore, 5-, 6- and 9-fold induction of Nox1 mRNA was observed in the vessels of 3-, 6- and 12-months-old SHRs, respectively (p<0.01). Interestingly, GKT137831 increased BP in both WKY and SHR rats (p<0.01, 2-way ANOVA). This was accompanied by the elevation of leukocytes (988±180 vs 147±188 cell/mg, 1487±945 vs 1878±164 cell/mg) and macrophages (107±14 vs. 153±14 cell/mg, 228±26 vs. 298±42 cell/mg) in PVAT of both WKYs and SHRs treated with GKT137831. Moreover, GKT137831 treatment significantly increased (p int<0.01) percentage of TH17 in PVAT of both normotensive (1.4±0.2% vs. 2.5±0.2%) and hypertensive (2.3±0.1% vs. 2.9±0.1%) animals. On the contrary, ML171 treatment, inhibiting only Nox1, in turn protected against an increase of PVAT leukocytes especially among macrophages, TH17 cells (p<0.01). Conclusion Aging and spontaneous hypertension is associated with a trajectory of BP elevation and perivascular inflammation. This state is hastened after NOX1/4 inhibition, while ML171 treatment protects against perivascular inflammation. Acknowledgement/Funding National Science Centre 2013/11/N/NZ4/00310

Inflammatory cells in perivascular adipose tissue and the integrity of the tunica media in atherosclerotic coronary arteries.

Obstructive coronary artery disease (CAD) is characterized by inflammation within the atherosclerotic coronary arteries. Infiltration of inflammatory cells into muscular media can lead to remodeling and weakening of the arterial wall. We examined the relationship between inflammatory infiltration in perivascular adipose tissue (PVAT), state of the external elastic membrane, and the intensity of inflammatory infiltration in the tunica media of coronary arteries obtained by endarterectomy from symptomatic patients with diffuse CAD. We analyzed endarterectomy sequesters from 22 coronary arteries that contained the intima, media, a part of the adventitia, and PVAT in at least one part of the sequester. The coronary arteries were divided into two groups according to the presence or absence of inflammatory infiltration in PVAT. Staining with hematoxylin-eosin and by the Movat’s method showed atherosclerotic changes in the intima and media. Immunohistochemistry (anti-leukocyte common antigen [LCA] antibody) was used for the detection of leukocytes. We found a significant positive correlation between inflammatory infiltration in PVAT and preservation of the external elastic membrane of coronary arteries. Furthermore, we found a significant negative correlation between inflammatory infiltration in PVAT and the intensity of inflammatory infiltration in the media. It seems that the integrity of the external elastic membrane and the proinflammatory properties of PVAT restrain inflammatory cells within PVAT. Both effects may prevent the migration of inflammatory cells into the media and delay the development of CAD.

JNK2 in myeloid cells impairs insulin's vasodilator effects in muscle during early obesity development through perivascular adipose tissue dysfunction.

Reduced vasodilator properties of insulin in obesity are caused by changes in perivascular adipose tissue and contribute to microvascular dysfunction in skeletal muscle. The causes of this dysfunction are unknown. The effects of a short-term Western diet on JNK2-expressing cells in perivascular adipose tissue (PVAT) on insulin-induced vasodilation and perfusion of skeletal muscle were assessed. In vivo, 2 wk of Western diet (WD) reduced whole body insulin sensitivity and insulin-stimulated muscle perfusion, determined using contrast ultrasonography during the hyperinsulinemic clamp. Ex vivo, WD triggered accumulation of PVAT in skeletal muscle and blunted its ability to facilitate insulin-induced vasodilation. Labeling of myeloid cells with green fluorescent protein identified bone marrow as a source of PVAT in muscle. To study whether JNK2-expressing inflammatory cells from bone marrow were involved, we transplanted JNK2-/- bone marrow to WT mice. Deletion of JNK2 in bone marrow rescued the vasodilator phenotype of PVAT during WD exposure. JNK2 deletion in myeloid cells prevented the WD-induced increase in F4/80 expression. Even though WD and JNK2 deletion resulted in specific changes in gene expression of PVAT; epididymal and subcutaneous adipose tissue; expression of tumor necrosis factor-α, interleukin-1β, interleukin-6, or protein inhibitor of STAT1 was not affected. In conclusion, short-term Western diet triggers infiltration of JNK2-positive myeloid cells into PVAT, resulting in PVAT dysfunction, nonclassical inflammation, and loss of insulin-induced vasodilatation in vivo and ex vivo.NEW & NOTEWORTHY We demonstrate that in the earliest phase of weight gain, changes in perivascular adipose tissue in muscle impair insulin-stimulated muscle perfusion. The hallmark of these changes is infiltration by inflammatory cells. Deletion of JNK2 from the bone marrow restores the function of perivascular adipose tissue to enhance insulin's vasodilator effects in muscle, showing that the bone marrow contributes to regulation of muscle perfusion.

A6338 The Resident MSC-like Cells in Perivascular Adipose Tissue During Aging

A6338 The Resident MSC-like Cells in Perivascular Adipose Tissue During Aging

GW29-e1943 The Resident MSC-like Cells in Perivascular Adipose Tissue During Aging

GW29-e1943 The Resident MSC-like Cells in Perivascular Adipose Tissue During Aging

Abstract P338: Aging and Inhibition of Nox1/4 Modulate Perivascular Inflammation in Spontaneous Hypertension

Introduction: Hypertension is associated with enhanced oxidative stress and perivascular inflammation. Although, that aging and oxidative stress are major factors in the development of hypertension their effect on perivascular inflammation remains unclear. Methods: Using flow cytometry we studied leukocytes infiltrating perivascular adipose tissue (PVAT) in 1-, 3-, 6- and 12-month-old SHR (Spontaneously Hypertensive Rats) and normotensive WKY (Wistar-Kyoto) rats. Additionally, 1-month-old rats were treated with GKT137831 (60mg/kg) or ML171 (NOX1/4 and NOX1 inhibitor, respectively) for 4 weeks. Blood pressure (PB) was measured by the tail cuff. Results: Aging in SHRs was associated with elevation of BP (139±4 vs 180±4 vs 202±2 vs 208±2 mmHg; 1 vs 3 vs 6 vs 12-month-old, respectively) when this effect was not seen in WKY rats. While the total number of leukocytes infiltrating PVAT were comparable between 1-month-old WKY and SHR (p=0.8) aging escalated their numbers only in SHRs (2096±164 vs 1994±296 vs 2311±470 vs 3255±408 cell/mg; p int <0.001). Similar effect was observed among NK cells (p int <0.001) and macrophages (p int <0.001). Moreover, spontaneous hypertension was associated with 2-fold elevation of T cells residing in PVAT in comparison to WKY, however, aging did not affect their number in both groups. While the age-related increase of Nox4 mRNA was observed in both groups, this increase was more dynamic in SHRs, (p int <0.05). Furthermore, 5-, 6- and 9-fold induction of Nox1 mRNA was observed in the vessels of 3-, 6- and 12-months-old SHRs, respectively (p<0.01). GKT137831 treatment significantly increased BP (p<0.01, 2way ANOVA) in both WKY and SHR (150±2 vs 164±3 mmHg, 198±4 vs 209±3 mmHg, respectively). This was accompanied by elevation of the total number of leukocytes (988±180 vs 1471±88 cell/mg, 1487±945 vs 1878±164 cell/mg) and macrophages (107±14 vs. 153±14 cell/mg, 228±26 vs. 298±42) in PVAT of WKYs and SHRs treated with GKT137831. On the contrary, ML171 treatment protected against increased accumulation of CD45+ cells in PVAT, without affecting BP. Conclusions: Aging in spontaneous hypertension is associated with elevation of BP and aggravation of perivascular inflammation which are hastened after NOX1/4 inhibitor treatment.

Depletion of dendritic cells in perivascular adipose tissue improves arterial relaxation responses in type 2 diabetic mice

BackgroundAccumulation of multiple subtypes of immune cells in perivascular adipose tissue (PVAT) has been proposed to cause vascular inflammation and dysfunction in type 2 diabetes (T2DM). This study was designed to investigate specific roles for dendritic cells in PVAT in the development of vascular inflammation and impaired PVAT-mediated vasorelaxation in T2DM. Methods and ResultsStudies were performed using db/db mice (model of T2DM) and their Db heterozygote (DbHET), lean and normoglycemic controls. Dendritic cell depletion was performed by cross-breeding DbHet with Flt3l−/− (null for ligand for FMS-kinase tyrosine kinase) mice. Using PCR, it was found that the majority of dendritic cells (CD11c+) were located in PVAT rather than the vascular wall. Flow cytometry similarly showed greater dendritic cell accumulation in adipose tissue from db/db mice than DbHET controls. Adipose tissue from db/db mice displayed increased mRNA levels of proinflammatory cytokines TNF-α and IL-6 and decreased mRNA levels of the anti-inflammatory mediator adiponectin, compared to DbHET mice. Depletion of dendritic cells in dbFlt3l−/dbFlt3l− (confirmed by flow cytometry) reduced TNF-α and IL-6 mRNA levels in diabetic adipose tissue without influencing adiponection expression. Moreover, in mesenteric arteries, dendritic cell depletion improved the ability of PVAT to augment acetylcholine-induced vasorelaxation and anti-contractile activity. ConclusionsIn a murine model of T2DM, dendritic cells accumulated predominantly in PVAT, as opposed to the vessel wall, per se. Accumulation of dendritic cells in PVAT was associated with overproduction of pro-inflammatory cytokines, which contributed to an impaired ability of PVAT to augment vasorelaxation and exert anti-contractile activity in T2DM.

Commensal Microbe-specific Activation of B2 Cell Subsets Contributes to Atherosclerosis Development Independently of Lipid Metabolism

The relation between B2 cells and commensal microbes during atherosclerosis remains largely unexplored. Here we show that under hyperlipidemic conditions intestinal microbiota resulted in recruitment and ectopic activation of B2 cells in perivascular adipose tissue, followed by an increase in circulating IgG, promoting disease development. In contrast, disruption of the intestinal microbiota by a broad-spectrum antibiotic cocktail (AVNM) led to the attenuation of atherosclerosis by suppressing B2 cells, despite the persistence of serum lipid abnormalities. Furthermore, pharmacological depletion of B2 cells with an anti-B2-cell surface CD23 antibody also attenuated commensal microbe-induced atherosclerosis. Moreover, expression analysis of TLR-signaling-related genes in the activated B2 cell subsets, assessed using the Toll-Like Receptor Signaling Pathway RT2 Profiler PCR Array, confirmed activation of the B2-cell autoantibody-production axis, which was associated with an increased capacity of B2 cells to bind to intestinal microbiota. Together, our findings reveal the critical role of commensal microbe-specific activation of B2 cells in the development of atherogenesis through lipid metabolism-independent mechanisms.

Role of chemokine RANTES in the regulation of perivascular inflammation, T-cell accumulation, and vascular dysfunction in hypertension.

Recent studies have emphasized the role of perivascular inflammation in cardiovascular disease. We studied mechanisms of perivascular leukocyte infiltration in angiotensin II (Ang II)-induced hypertension and their links to vascular dysfunction. Chronic Ang II infusion in mice increased immune cell content of T cells (255 ± 130 to 1664 ± 349 cells/mg; P < 0.01), M1 and M2 macrophages, and dendritic cells in perivascular adipose tissue. In particular, the content of T lymphocytes bearing CC chemokine receptor (CCR) 1, CCR3, and CCR5 receptors for RANTES chemokine was increased by Ang II (CCR1, 15.6 ± 1.5% vs. 31 ± 5%; P < 0.01). Hypertension was associated with an increase in perivascular adipose tissue expression of the chemokine RANTES (relative quantification, 1.2 ± 0.2 vs. 3.5 ± 1.1; P < 0.05), which induced T-cell chemotaxis and vascular accumulation of T cells expressing the chemokine receptors CCR1, CCR3, and CCR5. Mechanistically, RANTES−/− knockout protected against vascular leukocyte, and in particular T lymphocyte infiltration (26 ± 5% in wild type Ang II vs. 15 ± 4% in RANTES−/−), which was associated with protection from endothelial dysfunction induced by Ang II. This effect was linked with diminished infiltration of IFN-γ-producing CD8+ and double-negative CD3+CD4−CD8− T cells in perivascular space and reduced vascular oxidative stress while FoxP3+ T-regulatory cells were unaltered. IFN-γ ex vivo caused significant endothelial dysfunction, which was reduced by superoxide anion scavenging. In a human cohort, a significant inverse correlation was observed between circulating RANTES levels as a biomarker and vascular function measured as flow-mediated dilatation (R = −0.3, P < 0.01) or endothelial injury marker von Willebrand factor (R = +0.3; P < 0.01). Thus, chemokine RANTES is important in the regulation of vascular dysfunction through modulation of perivascular inflammation.—Mikolajczyk, T. P., Nosalski, R., Szczepaniak, P., Budzyn, K., Osmenda, G., Skiba, D., Sagan, A., Wu, J., Vinh, A., Marvar, P. J., Guzik, B., Podolec, J., Drummond, G., Lob, H. E., Harrison, D. G., Guzik, T. J. Role of chemokine RANTES in the regulation of perivascular inflammation, T-cell accumulation, and vascular dysfunction in hypertension.

Abstract 19231: Chemotactic Properties of Perivascular Adipose Tissue in Angiotensin Ii Dependent Hypertension

Introduction. Recent studies show that immune system is involved in hypertension (HT). Angiotensin II (AngII) causes accumulation of T cells in perivascular adipose tissue (pvAT) but precise mechanisms of their infiltration remain unclear. Hypothesis. RANTES and it’s receptors recruit T cells towards pvAT. Methods. Expression of chemokine receptors on peripheral blood T cells and chemokine ligands in pvAT was studied by flow cytometry and quantitative RT-PCR respectively. Chemotaxis of T cells towards pvAT, vAT (epidydymal AT) or RANTES was studied in Boyden chambers. Results. 14 day infusion of AngII (490mg/d/kg) was associated with significant increase in T cell content in pvAT with concomitant increase of RANTES mRNA expression (p&lt;0.001). Expression of other CCR5 ligands MCP-1, MIP-1α and MIP-1β was significantly decreased. AngII significantly increased total content of T cells in pvAT expressing receptors for RANTES: CCR1 (27.9±4.6% vs.15.7±1%), CCR3 (17.1±1.4% vs.10.5±1.4%), CCR5 (23.6±0.9% vs.17±0.9%), while having no effect in vAT. T cells showed increased chemotaxis towards pvAT obtained from AngII infused mice when compared to sham animals (4.4±0.7 vs.0.17±0.17; p&lt;0.01). Moreover pvAT attracted higher amount of T cells as compare to vAT (4.4±0.7% vs.0.8±0.1%; p&lt;0.05); there was minimal migration toward subcutaneous fat. Moreover RANTES (10ng/ml) recruited T cells, but not B cells, from blood. Ang II infusion increased chemotaxis of blood derived T cells towards RANTES by 2-fold (p&lt;0.01). However the most prominent chemotaxis potential was observed in pvAT isolated T cells from AngII treated mice (2.4±0.3% vs.0.8±0.2% in sham, p&lt;0.01). CD4-CD8- T cells were characterized by the highest rate of migration towards RANTES. In contrast, migration capability of T cells resident in vAT was of minimal rate. Conclusions. Ang II enhances T cell migration into pvAT but not vAT by increasing local RANTES expression. All known RANTES receptors are involved. And in particular CCR1 and CCR5 on CD3+CD4-CD8- cells.