Transplantation of Pim1/Myc overexpressing pre-BI cells into B-cell-deficient mice expanded the pre-B-cell

compartments up to 100-fold within 4–8 weeks. Transformation remained dependent on the expression of both oncogenes, as removal of doxycycline in vitro and in vivo terminated proliferation and induced differentiation to IgM+ B cells. In contrast, Pim1/Myc-transduced mature B cells that developed from the oncogene-transduced pre-BI cells in the absence of oncogene overexpression in vivo were not capable of long-term proliferation after induction of Pim Barasertib mw and Myc overexpression, neither in vivo nor in vitro, neither with nor without stimulation by polyclonal activators. During the development of B lymphocytes in the murine fetal liver, DJH/DJH-rearranged pre-BI cells develop shortly before birth. From these cells, long-term proliferating cell lines can be established in vitro on M-CSF-deficient BM stromal cell lines (OP9) in the presence of IL-7. Differentiation of these pre-BI cells can be induced in vitro by removal of IL-7, which culminates in the generation of sIgM+ immature B cells 1. Transplantation of these fetal liver-derived pre-BI cell lines into B-cell-deficient recipient mice leads to one wave of B-cell development detectable in spleen and peritoneum, but not in the BM 1. Using this adoptive transfer system, it is possible to study the effect of transgenes – introduced into the pre-BI cell lines

– on B-cell differentiation, survival and Epigenetics inhibitor Carbachol proliferation at different stages of B-cell maturation. We introduce doxycycline-inducible forms of oncogenes by retroviral vectors into such pre-BI cell lines and, therefore, are able to induce the expression of these oncogenes and study their effects at different stages of B-cell development in vitro and in vivo. The proto-oncogene

Myc (c-Myc), a transcription factor of the basic helix-loop-helix/leucine zipper family, has been shown to be deregulated in different types of B-lymphoid tumors 2–4. The Myc protein influences proliferation, differentiation and apoptosis of a variety of different cell types 5–7. Deregulated Myc expression is known to facilitate transit from G1 into S-phase of the cell cycle by activating, directly or indirectly, the genes of cyclines D1, D2, E and A as well as Cdk2, Cdk4 and Cdc25A 8–12, and by decreasing levels and functions of P21cip1 and P27kip1, two inhibitors of cell cycle progression from G1- to S-phase 13, 14. Transgenic expression of Myc under the control of the immunoglobulin μ enhancer (Eμ) in mice expands the pre-BII cell compartment in BM, while impeding the development of mature B cells 15. The serine/threonine protein kinase Pim1 has been found to cooperate with Myc in the development of pre-B-cell lymphomas of mice 16–19. In humans, overexpression of Pim1 and Myc together has been shown in the leukemic cells of around 20% of acute lymphoid leukemia patients, as well as in the Burkitt’s lymphoma cell lines 20.

In fact, the final curtain is now lowering over the idea of a pathogenic role for Th1 cells in EAE, after the finding that T-bet-deficient mice are likely resistant to EAE, RXDX-106 price not due to their lack of Th1 cells, but rather due to disrupted IL23R expression [58]. Such confusing observations

surrounding the function of Th1 cells and the role of IFN-γ in autoimmune disease appeared to be partially explained after the discovery of the CD4+ “Th17” subset, defined by the expression of IL-17A, the prototype member of the IL-17A cytokine family [59]. Th17 cells were in fact shown to be largely heterogeneous in nature, capable of expressing IL-17F, IL-22, and IL-21 alongside IL-17A. The question was once again asked, as for Th1 cells some years before, whether or not the hallmark Th17 cytokine is a major player in disease pathogenesis. It appeared that a similar approach was being taken with respect to the simplicity of identification solely by IL-17A expression, although the community lacked the proper genetic tools to definitively show that CD4+ T-cell-derived IL-17A was crucial for https://www.selleckchem.com/products/AZD0530.html Th17-mediated pathogenesis. At this point some caution had to be exercised, and the crucial distinction made between “pathogenic” and “IL-17A-expressing”. Another concept

now becoming widely accepted is that IL-23 signaling by no means results in IL-17 expression alone. It seems to be impossible with current protocols to induce EAE or colitis in p40- or p19-deficient animals, which both lack functional IL-23 [25]. However, mice deficient in IL-17RA, IL-17A or both IL-17A and IL-17F show Meloxicam attenuated signs of EAE [60, 61], but develop disease nonetheless, which highlights a disconnection between IL-23 and IL-17. IL-17F deficiency in itself has no impact on the clinical course of EAE, and despite being an IL-23-induced cytokine, IL-17F is largely redundant in EAE pathogenesis [62]. Furthermore, a subset of CNS-invading

Th17 cells known to produce IL-22 were also ruled out as potential mediators of disease [63]. In a model of chronic intestinal inflammation, IL-17A deficiency also does not ameliorate colonic inflammation after the transfer of IL-17A−/− naïve T cells to RAG-deficient host animals [64]. IL-17A was even shown to have a protective role in colitis by interfering with the function of pathogenic Th1 cells [65]. Furthermore, if the surplus or absence of IL-17A is modulated using diverse genetic or neutralization approaches, EAE disease can still persist [62, 66]. Collectively, it is clear that IL-23 controls important effector functions beyond the induction of IL-17 production by pathogenic T cells.

There were no major complications, and very satisfactory results have been obtained.

This retrospective study showed that both options of raising a large DIEAP flap for unilateral breast reconstruction, namely unipedicled flap based on large medial perforator/s plus additional venous discharge or double-pedicle flap, are safe. Preoperative examination of the dominant perforator/s with CDS and/or MDCT is mandatory in both cases. © 2010 Wiley-Liss, Inc. Microsurgery 2010. “
“Breast conservation surgery in the treatment of early stage breast cancer has become increasingly utilized as a means to avoiding mastectomy. While partial mastectomy defects (PMDs) may often be cosmetically acceptable, some cases warrant consideration of reconstructive options, and while several reconstructive options have been described in this role, a series of deep APO866 datasheet inferior epigastric perforator (DIEP) flaps www.selleckchem.com/products/Vorinostat-saha.html has not been reported to date. A cohort of 18 patients undergoing PMD reconstruction with a DIEP flap were included. Patient-specific data, operation details, cosmetic results, and complication rates were assessed. Oncologic outcomes, in particular recurrence rates, were also evaluated. In our series there were no cases of partial or total flap necrosis, and overall complications were

low. There were two cases of wound infection (both had undergone radiotherapy), managed conservatively, and one case of reoperation due to hematoma. There were no cancer recurrences or effect on oncologic management. Cosmetic outcome was rated as high by both patients and MycoClean Mycoplasma Removal Kit surgeon. The results were thus comparable with other reconstructive options. Although autologous reconstruction has an established complication rate, our results suggest that the DIEP flap may be of considerable value for delayed reconstruction of selected larger partial mastectomy defects. © 2010 Wiley-Liss, Inc. Microsurgery, 2011. “
“The latissimus dorsi (LD) muscle flap is one of the most versatile flaps used for reconstruction of soft tissue defects. With knowledge of its anatomy, harvest of the segmental LD muscle has been introduced as a reliable technique with

the advantage of muscle preservation. We devised a new harvest technique for the segmental LD flap using a limited transverse incision to elevate a less bulky distal segment of the muscle with a sufficient pedicle length obtained by intramuscular dissection of the vascular pedicle. Two cases, in which this technique was effectively applied to reconstruct plantar defects after wide excision of malignant melanoma with a maximally efficient use of donor and recipient tissues, are presented. Satisfactory results were gained with stability in walking. When the defect size permits use of a segmental muscle and the long pedicle is needed, this pedicle-lengthened segmental LD muscle harvest technique would be a valuable method. © 2013 Wiley Periodicals, Inc. Microsurgery 33:491–495, 2013.

The technique reduces the dissection time and does not require sophisticated Trichostatin A molecular weight surgical devices and skill, when compared to endoscopic LD flap harvesting from the literature. © 2012 Wiley Periodicals,

Inc. Microsurgery, 2013. “
“The purpose of this study was to investigate sensory recovery in 33 patients who underwent conventional mastectomy, skin-sparing mastectomy, or nipple-sparing mastectomy with immediate breast reconstruction using abdominal flaps. Reconstructions included a pedicled transverse (28 cases) or vertical (five cases) rectus abdominis musculocutaneous flap. Sensory reconstruction was performed in 15 cases by neurorrhaphy using intercostal nerve. Patients were classified into six groups according to see more type of mastectomy and use of neurorrhaphy. Sensory recovery was estimated by touch, pain, and hot and cold sensation at the nipple,

areola, and 4 points at a distance of 2 cm from the areolar circumference. For touch sensation, conventional mastectomy with innervated flap provided greater sensitivity than the other groups (P < 0.05). For pain sensation, conventional mastectomy with innervated flap provided greater sensitivity than the other groups (P< 0.05). In terms of short-term postoperative sensitivity, skin- and nipple-sparing mastectomies with abdominal flap appear inferior to conventional mastectomy with innervated abdominal flap. © 2011 Wiley-Liss, Inc. Microsurgery, 2011. "
“The Internal Mammary Artery (IMA) and its perforators play an important role in coronary bypass grafting and reconstructive

breast, head, and neck surgery. This study aimed to obtain anatomic data pertaining to these vessels using Multi Detector Computed Tomography Angiography (MDCTA) and to demonstrate that the MDCTA could be a considerable assessment tool prior to surgery. In 50 outpatients (27 males and 23 females), the above-mentioned arteries were bilaterally evaluated with a 16-detector spiral computed tomography scanner. Based on the obtained images, diameters of the bilateral IMAs were separately measured in each intercostal spaces from 1 to 5 through their traces. IMAPs Venetoclax order greater than 0.5 mm in diameter were bilaterally evaluated in terms of distance from the sternal border to the ramification point under the muscular layer, maximal external diameter at ramification from the IMA, and the length between the ramification point from the IMA and enter point to the subcutaneous fat tissue. Mean diameters of the left and right IMAs were 2.05 ± 0.50 mm and 2.20 ± 0.57 mm, respectively. Mean diameters, distances, and lengths of the perforators were 1.30 ± 0.30 mm, 6.80 ± 3.40 mm, 17.05 ± 6.07 mm on the left side and 1.32 ± 0.25 mm, 6.71 ± 3.43 mm, 17.35 ± 3.48 mm on the right side, respectively. No statistically difference was found between the sides (P > 0.05).

[35, 44] The recommended target dose for MMF during the induction phase is 1.5–2 g daily in Asian patients, and it is advisable not to reduce

the daily dose of MMF to below 1.5 g within the first year, and not to go below 1 g daily within the second year. When MMF is used as induction treatment, caution should be exercised when its treatment duration is shorter Selumetinib research buy than 24 months in view of the reported association with increased risk of relapse.[35] Preliminary data suggest that dual immunosuppression with corticosteroids and tacrolimus or triple immunosuppression with corticosteroids, MMF at reduced dose, and tacrolimus may be effective treatments for Class III/IV nephritis or concomitant Class III/IV and Class V disease. Long-term data with these treatment regimens are awaited. The safety of calcineurin inhibitors during pregnancy is an added advantage. For the treatment of Class V LN, members of the ALNN agreed on the following: The threshold for immunosuppressive treatment is proteinuria ≥ 2 g/day in patients with normal renal function and inactive lupus serology, while a lower threshold may apply in patients with evidence

of deterioration in proteinuria or renal function or active lupus serology. Immunosuppressive treatment for pure Class V LN with heavy proteinuria should be a combination of corticosteroids and either CYC, AZA, MMF, or a calcineurin inhibitor. In view of individual variations in pharmacokinetics, blood level monitoring is important in patients treated with calcineurin inhibitors

to ensure adequate drug exposure and to prevent drug-induced adverse effects such as nephrotoxicity. Anticoagulation should be considered in KPT-330 chemical structure patients with persistent heavy proteinuria, especially when additional pro-thrombotic risk factors are present concomitantly. Control of hypertension and risk factors such as dyslipidaemia and diabetes mellitus is important to prevent accelerated vascular complications. Progress in the management of LN over the past two decades has translated into improved renal and patient survival rates. With prompt DNA ligase diagnosis and treatment, the long-term outcome of Asian patients appears more favorable than patients of African or Hispanic descent. Different effective immunosuppressive treatment options are now available, which facilitates individualization of treatment to optimize the efficacy-vs-risk balance. Socio-economic factors remain obstacles in the access to optimal care. In addition to immunosuppression, the importance of adjunctive treatment such as blood pressure control, minimization of vascular risk factors, and reno-preservation cannot be over-emphasized. The knowledge gaps include the optimal management of patients with crescentic LN or thrombotic microangiopathy, the role of mycophenolic acid blood level monitoring, the role of biologics, the optimal surveillance and management of infectious complications, and the management of patients who are intolerant to current treatments.

Diseases and complications caused by Chlamydiales are summarized here in order to provide an overview of the global health impact of infections caused Roxadustat purchase by these strict intracellular bacteria. Trachoma caused by C. trachomatis, present in more than 50 developing and emerging countries (Polack et al., 2005), is characterized by a chronic course. Five stages are recognized, starting from the less severe form with five or more follicles up to the final stage of corneal opacity (Thylefors et al., 1987). Currently, there are 40 million persons with active

trachoma, 8.2 million with trichiasis and over 1.3 million blind people (Burton & Mabey, 2009). The World Health Organization has the objective to eliminate trachoma by 2020 by implementing the SAFE strategy, a combination

of Surgery of trichiasis, Antibiotic treatment, Facial cleanliness, and Environmental improvement (Mariotti et al., 2009). Determining the efficiency of this policy has been proven arduous, mainly because only one or two factors were assessed simultaneously (Wright et al., 2008; Burton & Mabey, 2009). Development of a vaccine seems to be the most appropriate solution, although a recent study by Dean et al. (2008) suggested that trachoma may also be caused by genital C. trachomatis JQ1 clinical trial strains, as well as by Chlamydia pneumoniae and Chlamydia psittaci. The different bacterial species or serovars were detected by real-time quantitative PCR from eye swabs of patients with active trachoma. Moreover, strong immunoreactivity of tears to the chlamydial Hsp60 (GroEL) of all three types was measured. Immunoreactivity to Hsp60 was previously correlated to scarring and to the development of trichiasis (Peeling et al., 1998; Hessel et al.,

2001). In the future, it would be cautious to test trachoma lesions for other Chlamydiales, especially because C. trachomatis is not always detected in active trachoma patients. Chlamydia trachomatis can also cause urogenital infections that when not treated lead to severe complications, such as endometritis, tubal infertility, ectopic pregnancy and miscarriage (Fig. 1) (Baud et al., 2008; Wilkowska-Trojniel et al., 2009). Infertility and other long-term Resminostat complications of urogenital C. trachomatis infections are also associated with significant economical and personal burdens (Hu et al., 2004). It is mostly prevalent in young, sexually active individuals and is to a huge extent asymptomatic (women ≥70%, men ≥50%), making the prevention of new infections more difficult (Bébéar & de Barbeyrac, 2009). Other members of the Chlamydiales order, such as Waddlia chondrophila and Chlamydia abortus, have been linked to miscarriage in humans and bovines (Baud et al., 2007, 2008). It is thought that there is a risk of zoonotic transfer of these pathogens, especially under conditions of poor hygiene. Since several of these species were discovered only recently, their role in animal abortion or in human fetal death has to be further assessed.

Vessel diameter was measured with a video caliper (Colorado Video, Boulder, CO, USA). Vessels without leaks were allowed to develop spontaneous tone (≥17% less initial diameter). Ca++-free PSS was superfused at the end of all experiments to determine passive arteriolar diameters. Compounds were introduced via a syringe pump and at concentrations that previously described elsewhere [24]. A23187, a calcium ionophore, was Bortezomib cell line introduced into the lumen of the arterioles at a concentration of 1 μm, as previously described [36]. l-NMMA (Calbiochem,

Gibbstown, NJ, USA) was used at a final tissue bath concentration of 0.1 mm to competitively inhibit NOS activity. The superfusate concentration of phentolamine, an α-adrenergic receptor blocker, was 1 μm. ADO was superfused at the end of all experiments (0.1 mm) to determine passive arteriolar diameters. Compounds were added directly to the superfusate solution as previously described [26, 27]. ACh, Spermine NONOate,

and PE, were added at increasing concentrations of 0.001–100 μm or A23187 1–1000 nm. All chemicals were from Sigma (St. Louis, MO, USA), unless otherwise noted. Arteriolar diameter, D (μm), was recorded during a control, Selleckchem Silmitasertib intraluminal infusion or PVNS period and immediately following AH. Resting vascular tone was calculated by: %tone = [(Dpass − Dc)/Dpass] × 100, where Dpass is passive diameter under ADO and Dc is the diameter measured during the control period. Arteriolar responses were normalized as follows: percent change from control = [(Dss/Dc) − 1] × 100, where Dss is the steady-state diameter following intraluminal infusion, AH, and PVNS. Dc immediately prior to the beginning of any experimental procedure was used to calculate %tone and reported as

0 PSI diameter measurements in the A23187 experimental series. All data are reported as mean ± SE. Spontaneous tone was calculated by: % tone = [(Dpass − DI)/Dpass] × 100, where Dpass is the maximal diameter recorded under Ca++ free PSS for coronary or mesenteric arterioles, respectively. DI is the initial diameter of the arteriole Dolichyl-phosphate-mannose-protein mannosyltransferase prior to the experimental period. Active responses to pressure changes were normalized to the maximal diameter according to the following formula: % Normalized diameter = [(Dss/Dpass)] × 100, Dss is the steady-state diameter during each pressure step. The experimental responses to ACh, A23187, and Spermine NONOate are expressed using the following equation: % relaxation = [(Dss − Dcon)/(Dpass − Dcon)] × 100, where Dss is the steady-state arteriolar diameter during the experimental period, Dcon is the control diameter recorded immediately prior to experimental period. Responses to PE were calculated by the following formula: % constriction = [(Dss − Dcon)/(Dcon)] × 100.

The use of anthelmintics for the definitive hosts is difficult in most third world countries, and alternative strategies are needed. Interruption of the hydatid life cycle within the intermediate host by vaccination against the larval stage may be a viable supplement to anthelmintics (2,3,6,7). In the 1960s, it was discovered that the secreted proteins of the oncosphere induce protection. EG95 was subsequently identified as a protective antigen

when immunized animals were challenged with E. granulosus eggs (8). In addition, the antibody produced by animals vaccinated with E. granulosus oncospheres or the EG95 protein was shown to be highly effective in a complement-dependent in vitro oncosphere-killing assay (6,9,10). Poxviruses offer an learn more efficient, low-cost means by which foreign antigen can be delivered to target species (11). Recombinant vaccinia virus (VACV) has been successfully

find more used to vaccinate against rabies in Europe and in America (12,13). In this study, we explored the use of VACV as a viral delivery vehicle for the hydatid oncosphere antigen EG95 in a mouse model and in sheep. We show that antiserum produced in mice against the EG95 antigen is effective in killing E. granulosus oncospheres in an in vitro assay. The coding region of the E. granulosus protective antigen EG95 (7,8) was inserted at the thymidine kinase gene of the VACV Lister strain (termed VV399). The construction of VV399 is described in (14,15). Immunization of mice with VV399: Balb/C mice 6–8 weeks of age were anaesthetized with approximately 200 μL avertin [2,2,2, tribromoethanol; 0·2 mL/15 g mouse of 20 mg/mL solution (Sigma-Aldrich, St. Louis, MO, USA)] injected intraperitoneally. Mice were infected intranasally with 50 μL containing 1 × 108 pfu of VV399. Twenty-five microlitre was introduced into each nostril

using a syringe. Intraperitoneal immunization with EG95 protein: Balb/C mice were immunized with 10 μg of EG95-6xHIS (cloning and expression described in 16) in a total volume 250 μL via the STAT inhibitor intraperitoneal route. Alum adjuvant was prepared as described by Herbert (17). Antigen was prepared by mixing equal parts of soluble protein antigen with adjuvant. Groups of mice were held in individual isolator cages during the course of the experiment. Mice were weighed every 2 weeks following primary immunization and booster immunization. Outbred sheep of mixed sex and <1 year of age were first tested for antibodies against EG95 antigen by ELISA. Animals were divided into two random groups. Group 1: Six sheep were immunized by scarification with 108 pfu of VV399 in PBS in a total volume of 100 μL. A 4 × 4 cm scratched area was made on the bare skin on the inside of each back leg, and 50 μL of virus applied. Group 2: Six animals were each immunized with 50 μg GST-EG95 protein (cloning and expression described in 7,8) with 1 mg QuilA.

These mice developed a progressive inflammatory MI-503 mouse encephalopathy with neuropathological features closely recapitulating those observed in AGS. Considering these data, although not proven beyond doubt, we predict that limiting the exposure of the infant brain to an AGS-related type I interferon immune response will attenuate the disease-associated brain damage. AGS is a genetically heterogeneous disease resulting

from mutations in any one of the genes encoding (i) the 3-prime repair exonuclease TREX1 [16] with preferential activity on single-stranded (ss) DNA; (ii) the three non-allelic components of the RNASEH2 endonuclease complex [17] acting on ribonucleotides in RNA : DNA hybrids; (iii) the Sam domain and HD domain containing protein (SAMHD1) [18], which functions as a deoxynucleoside triphosphate triphosphohydrolase; and (iv) adenosine deaminase acting on RNA (ADAR1) [19], which catalyses the hydrolytic deamination of adenosine to inosine in double-stranded (ds) RNA (Table 1). It is possible that at least one further genetic subtype of AGS is yet to be defined. Although most cases of AGS demonstrate an autosomal recessive pattern of inheritance, rare examples due to de-novo dominant TREX1 mutations have been

reported [20-23]. Moreover, the same heterozygous D18N mutation in TREX1 has been Tigecycline price seen to cause both (dominant) AGS and familial chilblain lupus (effectively, ‘non-neurological

Phosphoglycerate kinase AGS’), thus highlighting the role of unknown, modifying factors (which might be genetic or environmental) and/or stochastic mechanisms. The proteins defective in AGS are all associated with nucleic acid metabolism. The finding of mutations in TREX1 and the genes encoding the RNASEH2 complex in 2006, in the context of a clinical phenotype mimicking congenital infection, led us to hypothesize that (i) these proteins might be involved in clearing cellular nucleic acid ‘debris’; and (ii) that a failure of such waste removal could result in immune activation, specifically triggering an innate immune response more normally induced by viral nucleic acid [24] (Fig. 2). At least with regard to TREX1, cogent evidence has emerged in support of this hypothesis. Thus, Yang et al. [25] demonstrated that TREX1 deficiency results in the intracellular accumulation of abnormal ssDNA species. This finding was confirmed by Stetson and colleagues [26], who showed that in Trex1-null mice, ssDNA activation of a Toll-like receptor (TLR)-independent cytosolic pathway involving IRF3, TBK1 and STING results in the induction of a type I interferon response, and a recruitment of the adaptive immune system requiring functional lymphocytes.

The attenuated SIV-immunized animals exhibited increased frequencies of tetramer-positive cells in vaginal mucosa equivalent to those seen in monkeys infected with wild-type SIV, with relative enrichment compared with blood ranging from 2- to 11-fold (Fig. 1). Interactions between chemotactic cytokines and receptors expressed on lymphocytes provide important signals for recruitment of lymphocytes into tissues.7 To investigate the possibility of a role for chemokines in directing genital homing of SIV-specific lymphocytes, we studied expression of CXCR3 and CCR5, receptors for chemokines induced during inflammation, on CD8+ T cells in blood and vagina

lymphocytes. CXCR3 was expressed on the majority of CD8+ T cells in both vagina and peripheral blood (representative data are shown in Fig. 2).

CXCR3 was expressed on a significantly Lapatinib molecular weight higher percentage of CD8+ T cells in vagina than in blood (86% versus 51%, P < 0.05, Wilcoxon signed rank test). Mean fluorescence intensity was also significantly higher for CXCR3 on CD8+ T cells from the vagina than for CD8+ T cells in blood (P < 0.05). While most of the CD8+ T cells in vagina were positive for CXCR3, the frequency was significantly higher for tetramer+ cells than for the total CD8+ T-cell population in vagina (91% versus 86%, P < 0.05) and in peripheral blood (71% versus 51%, P < 0.05). CCR5 expression on these selleck chemical cell populations displayed a pattern similar to that of CXCR3, but did not reach statistical significance, a finding that may be related to the fact that fewer animals were included in the analysis (Fig. 2). In contrast, expression of CXCR4, a receptor that participates in homeostatic lymphocyte trafficking and is expressed on most circulating CD8+ T cells, was similar on tetramer+ and bulk CD8+ populations in blood and vagina (Fig. 2). As expected, expression of CCR7, a chemokine receptor that helps to direct migration of central memory T cells into lymph nodes and is low on tissue effector memory cells,14 was largely absent both on bulk CD8+ T cells and SIV tetramer+ cells in vaginal

tissue (Fig. 2). The expression of receptors specific Urease for inflammatory chemokines on nearly all SIV tetramer+ cells in vaginal tissues suggests that expression of chemokines recognized by these receptors may regulate localization of T cells to the female reproductive tract. To investigate whether the inflammatory chemokines that recognized the receptors expressed on CD8+ T cells tracking to vaginal tissues are produced in situ, vaginal tissues from SIV-infected macaques were stained with antibodies against CXCR3 and one of its ligands, CXCL9 (MIG). Large numbers of CXCR3+ cells were detected in the vaginal lamina propria, with high concentrations of positive cells localized to lymphoid aggregates (Fig. 3).