The hallmark cytokines secreted by the Th17 cells include IL-17A, IL-17F, IL-21 and IL-22.[62] This collection of cytokines can excite B lymphocytes, and trigger local

inflammation and tissue injury in SLE. The role of IL-17 in SLE pathogenesis has been explored in both human and animal models of lupus. In MRL/lpr mice, there was enhanced IL-17 mediated tissue insult after ischemic-reperfusion of the gut.[63] Diminished splenic germinal centre formation as well as suppressed anti-DNA and anti-histone antibodies levels were observed in IL-17R-deficient BXD2 mice.[64] Furthermore, splenocytes from SNF1 mice produced more IL-17 than non-autoimmune B6 mice.[65] LGK-974 clinical trial CD3+CD4−CD8− T cells from MRL/lpr mice secreted abundant IL-17 and the expression of IL-17 and IL-23 receptors in the lymphocytes from these mice were upregulated as the disease progressed.[66] These

lymphoid cells from MRL/lpr mice, after treatment with IL-23 in vitro and transferred to non-autoimmune species, can induce nephritis.[66] Mice lacking IL-17 in FcγR2b-deficient lupus mouse model showed better survival and were largely protected from development of glomerulonephritis.[67] In lupus-prone C57BL/6-lpr/lpr mice, IL-23R deficiency was associated with reduced IL-17-producing cells in the lymph nodes, decreased anti-DNA antibodies and abrogation of lupus nephritis.[68] These findings denote that an aberrantly find more active IL-23/IL-17 axis is responsible for the development of nephritis in lupus-prone mice. Increased circulating IL-17 and IL-23 levels were seen in patients with SLE and such elevation correlates with disease activity.[69] Recent data have suggested that a substantial amount of IL-17 in SLE patients is contributed by the TCR-αβ+CD4−CD8− T lymphocytes.[70] These TCR-αβ+CD4−CD8− T cells and Th17 cells are also detected in kidney biopsies

from SLE patients with renal involvement, hence provide strong evidence for the pathogenic role of IL-17 in lupus nephritis.[70] In addition, IL-17 assumes a crucial role for the survival and proliferation of B lymphocytes and antibody secretion in human SLE.[71] Yang et al. demonstrated the presence of Th17 cells in the PBMC and involved organs of SLE patients and the percentage increased Obatoclax Mesylate (GX15-070) with disease activity.[72] Moreover, the IL-17 from SLE patients can induce adhesion molecule mRNA expression and the adhesion of T cells to endothelial cells.[72] To date, most of the available data of IL-17 and human lupus are derived from observational or correlation studies. Hence, there is limited experience in the manipulation of IL-17 for the treatment of SLE. Therapeutic approaches that limit the cognate interaction between T cells and B cells, prevent inappropriate tissue homing and restore TReg function and the normal cytokine milieu have been explored.

9) EPZ-6438 order attending the urodynamic and voiding dysfunctions meetings were asked to complete the same evaluation of the study before and after a 2-day course on voiding dysfunctions. The median time of urological practice for this senior group was 9.7 ± 4.7 years. The course consisted of stating

basic hydrodynamic principles with interpretation of results and their therapeutic consequences as well as pathophysiology of BPH. Attendants were questioned about the reasons that led them to improve urodynamic knowledge. First, they were asked to point out the main and sole reason to attend the course and after that, to provide as many reasons as they judged important to attend the course. The responses were clustered to five final categories that encompassed all kind of responses. Studied participants were also questioned about the availability of urodynamic studies in their region as well as if Ganetespib mouse they rely on the result of the test performed by a third-part. Paired questionnaires before and after the courses/training period were used to assess the impact of learning the urodynamic exam. Participants were

asked about their confidence in doing the study and interpreting the traces themselves and their capacity to set up the equipment, analyze the flow curves and pressure traces, write down a report and diagnose obstruction. Attendants were also asked if the volume of the prostate gland was decisive for the indication of TURP and what would be the limit to perform TURP or trans-vesical prostatectomy. Similarly, 13 regularly used parameters to indicate surgical therapy were ranked before and after the course as an indication if the course changed the urologist’s perception of the importance of any of these parameters and their weight to the decision to point infravesical obstruction. In the

same manner they were asked if they would use urodynamic studies before any surgical therapies for BPH. One hundred percent of the junior urologists completed the pre- and post-fellowship questionnaires due to close proximity of the candidates with the authors. Although the same direct effort was done for the meeting urologists, 45 questionnaires were not totally completed (27 cases did not complete the post-meeting questionnaires, nine did not answer one or more item, eight ranked nearly the parameters incorrectly and one was missed). The fellowship-urologists elected to have urodynamic specialization for different reasons (Fig. 1) with 54.7% of them referring to voiding dysfunctions as an inappropriately learned issue of urology and perceived it as “too important to be overlooked” (45.3%), while 26.5% stated they did not feel confident to interpret the graphics. When more than one option was allowed the scenario became even worse as confidence in performing the exam revealed a higher rate of perception of inappropriate training (85.5%) as the main reason to extend learning besides the lack of confidence to interpret the graphics (81.

This may suggest that while high levels of FoxP3 expression are required to prevent Th2 differentiation, a reduced level of FoxP3 expression is still sufficient to prevent the emergence of Th1 and potentially Th17 responses. Indeed, mature Tregs

in which FoxP3 expression has been ablated (due to an induced cre-mediated deletion of a floxed FoxP3 allele) develop a capacity to produce considerable amounts of IL-2, tumour necrosis factor (TNF)-α, IFN-γ and IL-17 [36]. Furthermore, upon transfer to lymphopenic hosts, Tregs in which FoxP3 had been deleted failed to show suppressive function, but rather contributed to inflammation and predominated among tissue infiltrating lymphocytes. Any scientific readout is only as robust as the assay used to achieve it, and the assays used to measure suppressive potential in vitro and in vivo have different strengths and weaknesses. Neratinib in vitro This must be borne in mind because, like many biological phenomena, Treg activity in vivo cannot always be predicted accurately from their behaviour in vitro and vice versa [37–39]. The techniques used to interrogate Treg activity Selleckchem beta-catenin inhibitor have changed over time, reflecting our changing understanding of how Tregs function. The initial identification of the role of Tregs in preventing autoimmunity came from observations of autoimmune pathology in mice lacking CD25+ T cells [13]. Subsequently, assaying the capacity of CD25+

Tregs to suppress the proliferation of their CD25– counterparts in vitro became the gold standard measurement of suppressive potential (see below [40]) and antibody-mediated depletion of CD25+ T cells in vivo was adopted as an imperfect but practical strategy to assess the role Dapagliflozin of Tregs in models of infection, allergy and autoimmunity [41–44]. These in vitro and in vivo experiments identified many of the suppressive pathways utilized by Tregs– IL-2 deprivation [40], expression of CTLA-4 and glucocorticoid-induced TNF receptor-related protein

(GITR) [45,46], cell contact-dependent suppression [40], production of anti-inflammatory cytokines such as IL-10, TGF-β and IL-35 [31,47–51] and the expression of enzymes promoting tryptophan catabolism and adenosine production [52–54]. Throughout this time the role of Tregs was seen primarily as preventing the activation and differentiation of autoreactive T cells and the main arena for suppressive activity was considered to be the draining lymph node during naive T cell priming [39,55,56]. Their potential to modulate ongoing responses, or to display suppressive activity at sites of inflammation, was harder to address using such assays, although promising findings have been reported [57–59]. On this point, it is important to remember that Tregs can have controlling effects on inflammation through actions on a range of immune cell populations, not simply T cells.

In the normal functioning lung, those captured elements are transported to the oropharynx by the mucociliary escalator from where they are swallowed or cleared by coughing. In CF the cilia function is impaired severely due to dehydration of the airway surface liquid (ASL), and the particles and microbes are stuck in the larger airways within the ASL [2]. Microbes within the mucus can be aspirated to the lower or more peripheral parts of the airways – physiologically

termed the respiratory Fulvestrant ic50 zone (respiratory bronchioles and alveoli). Besides being the zone where gas exchange takes place, this part of the lung harbours the alveolar macrophages, type II alveolar epithelial cells and the majority of the pulmonary dendritic cells (DCs). Primarily the alveolar macrophages, but also type II alveolar cells, recognize the pathogen-associated molecular patterns

(PAMPS; e.g. peptidoglycan, lipopolysaccharide, flagella) of the aspirated microbes by their pathogen-recognizing receptors (PRRs) [3,4]. The PRRs include the Toll-like receptors (TLRs) and nucleotide-binding oligomerization domaine (NOD)-like receptors (NLRs) and activation of the PRRs initiates the host response, resulting in release of cytokines [3,4]. Furthermore, the respiratory zones of find more the lung are in close contact with blood supply, as the total blood volume pumped from the right cardiac ventricle passes through the capillaries of the respiratory zone and back to the left cardiac ventricle as oxygenated blood [5]. Due to close contact between the alveolar space and the vascular lumen, this is also the major focus for recruitment of inflammatory cells through the endothelium, basal membrane and

alveolar epithelium into the alveolar lumen [3,4]. The mechanism involves the mobilization of inflammatory cells from the bone marrow, up-regulation of blood cell integrins and selectins and endothelium adhesion molecules, as well as dilatation and leaking of capillaries to allow humoral and cellular components to pass into the pulmonary lumen and the invading microbes. In contrast, the blood to the upper conductive C-X-C chemokine receptor type 7 (CXCR-7) zone is limited to the arterial blood supply, comprising only 1% of the total cardiac output [5]. Despite the presence of a submucosal plexus, recruitment of inflammation to the conductive zone is relatively limited, probably because of the thicker tissue wall, the mucus produced by the goblet cells and the submucosal glands and the non-phlogistic s-immunoglobulin (IgA) in contrast to the phlogistic IgG response in the respiratory zone [6,7]. The majority of animal models applied for studying chronic P. aeruginosa lung infection is based on the embedding of bacteria in beads consisting of agar, agarose or seaweed alginate to prevent rapid clearance of the bacteria from the lungs. Therefore, we speculated whether improved control of the size, when producing P.

The supernatant was stored at −20°C until further analysis. The protein content was measured using Bio-Rad DC protein assay (#500–0116; Promega, Madison, WI, USA). The luciferase activity was performed using a standard luciferase assay (#E4030; Promega) according to the manufacturer’s instructions and measured on a GloMax™ 20/20 luminometer (#E5311; Promega). For statistical evaluation, the Kruskall–Wallis test followed by a post

hoc test was used for comparisons between all groups in each experiment. A P-value ≤ 0·05 was considered significant. To investigate whether raloxifene can influence the induction phase of CIA, OVX DBA/1 mice were treated from 2 days pre-immunization until 10 days postimmunization with either raloxifene (60 µg/day), oestradiol (1 µg/day) or the Miglyol812 vehicle control (100 µl/day), Imatinib as described in Materials and methods. Arthritis scores were evaluated every other day after administration of the booster injection of CII on day 21. In this experiment raloxifene or oestradiol did not hamper the development of arthritis significantly, as measured by frequency (Fig. 1) and severity (data not shown) of arthritis. In addition, we found find protocol no differences in the serum levels of anti-CII antibodies, IL-6 or the cartilage degradation marker COMP

(Fig. 1). To investigate the anti-arthritic properties of raloxifene, female DBA/1-mice were ovariectomized Thiamet G or sham-operated, and CAIA was induced. Ten days prior to receiving the antibody cocktail, administration of raloxifene (60 µg/day), oestradiol (1 µg/day) or vehicle (Miglyol812, 100 µl/day) was started, and continued 5 days per week until termination of the experiment. Figure 2a shows that treatment with oestradiol resulted in a significantly later onset of disease compared to vehicle-treated OVX controls (P < 0·001 on day 7 and P < 0·01 on day 9). The presence of endogenous hormones (sham-operated

mice) also delayed the onset of arthritis (P < 0·01 on day 7), but this effect was not sustained. Raloxifene treatment did not result in delayed onset compared to vehicle controls. Figure 2b shows that oestradiol treatment resulted in less severe arthritic disease, and this effect was sustained throughout the experiment (P < 0·001 compared to vehicle-treated controls). There was no maintained difference in arthritic severity between the OVX and sham vehicle-treated groups, although the groups differed significantly (P < 0·05) on day 7. Raloxifene treatment did not alter disease frequency or severity significantly compared to OVX vehicle controls at any time-point. Histological examination of the paw sections (Fig. 2c and d) revealed the same degree of destruction in joints from OVX and sham-operated controls (median destruction scores of 5·2 and 6·0 of a maximum of 16, respectively).

A host of endogenous antimicrobials play an active role in protecting the pregnant uterus. Both alpha (HNPs) and beta (HBDs) defensins have been detected in amniotic fluid, chorion, and placenta (reviewed by Ref. 52). Defensins have also been detected in the cervical mucus plug that, during pregnancy, forms a physical barrier between the vagina and the uterus and prevents the upward movement of harmful pathogens. In addition, HNPs have been detected in the vernix caseosa (substance covering the skin of fetus and newborn), which

has antimicrobial properties and protects the fetus during delivery and immediately after birth. Increases in the levels of alpha and beta defensins in amniotic fluid are strongly indicative of uterine inflammation or infection which this website can result in preterm labor and delivery.52 Both alpha and beta defensins have been detected in vaginal fluids of healthy pregnant women.53 However, changes in vaginal microflora during pregnancy correlate with the presence of alpha defensins in vaginal fluid.54 Asymptomatic trichomoniasis in pregnancy has also been associated with higher HNPs in vaginal fluids.55 Both SLPI and Elafin are present in the healthy pregnant uterus.56 SLPI has been detected in the decidua, amnion epithelium, vernix

caseosa, and at very high concentrations (750 mg/g) in cervical mucus plugs.52 Elafin, in contrast, is confined to fetal membranes and placenta

at term pregnancy. Both SLPI and Elafin possess anti-protease/anti-inflammatory activities beyond their antimicrobial www.selleckchem.com/products/ensartinib-x-396.html capabilities and are believed to regulate inflammation during pregnancy and labor. Both SLPI and Elafin Amobarbital have been reported to decrease significantly in women with premature rupture of membrane (PROM). This correlates with increases in protease activity [matrix metalloproteases (MMPs) and neutrophil elastase] that contribute to rupture and/or infection. Interestingly, although levels of Elafin in amnion epithelium have been reported to rise in chorioamnionitis, SLPI concentrations did not appear to change. It has been suggested that this might occur as SLPI is degraded by certain pathogens (Trichomonas,57Pseudomonas,58Staphylococcus aureus28 and Chlamydia46). In studies using CVL, SLPI was found to be increased in pregnant women,56 but decreased in the presence of bacterial vaginosis (BV).59 Sachdeva et al.60 confirmed these findings and further demonstrated that SLPI is down-regulated in HIV-infected pregnant women. Elafin has also been detected in pregnant CVLs and reported to be diminished by BV.61 In addition to SLPI, Elafin and the defensins, several other natural antimicrobials are also present in the pregnant uterus although most have not been studied in great detail. Lactoferrin is present during pregnancy and has been detected in amniotic fluid, cervical mucus, and vernix caseosa.

1b). The 5 and 25 μg (4×/72 hr) dose regimens

produced ‘saw-tooth’ patterns, where expression of the CD3–TCR complex was quickly down-regulated after each dose but returned to near predose values before the subsequent dose. With each successive dose, the level of modulation of the CD3–TCR complex increased. In the 2 and 1 μg (4×/72 hr) dose regimens, the extent of modulation was considerably less than in other dose regimens and was clearly discernable only after the fourth dose (Fig. 1b). After the fourth dose, the difference in the percentage of modulation of the CD3–TCR complex between the 2 and 1 μg Metformin (4×/72 hr) dose regimens was significant (30·3% versus 19·7% modulation, P < 0·01). Furthermore, in all dose regimens, there was a transient decrease in lymphocyte numbers in the peripheral blood during and shortly after dosing (Fig. 2), consistent with what has been observed in Proteasome inhibitor the spleens of both NOD and non-autoimmune mice administered monoclonal anti-CD3 F(ab′)2.9,10,19 This observation of lymphopenia during dosing could be the result of either depletion of a subset of lymphocytes or retrafficking of monoclonal anti-CD3 F(ab′)2-bound lymphocytes from the peripheral blood. In Study B, the effectiveness of the various dose regimens in inducing remission of diabetes was investigated in new-onset diabetic NOD mice. In order to evaluate whether a shorter duration of modulation of

the CD3–TCR complex or a lower cumulative dose affects efficacy, Study B also included groups given only three doses. Animals were randomly enrolled into one of five monoclonal anti-CD3 F(ab′)2 dose regimens – 50 μg (5×/24 hr), 25 μg (4×/72 hr), 25 μg (3×/72 hr), 5 μg (4×/72 hr), or 5 μg (3×/72 hr) – or placebo. The 25 and 5 μg doses were chosen based

on the results of Study A, in which expression of the CD3/TCR complex, 24 hr after dose 4, was approximately 12% and 50% of baseline, respectively. No animals in the placebo group entered Amino acid remission during the 12-week observation of blood glucose levels. In all dose regimens, approximately half of the mice (44–60%) had long-term remission (Table 1). There was no statistically significant difference in remission rates between the various dose regimens. The well-established 50 μg (5×/24 hr) dose regimen resulted in 56% of the mice being in remission for 12 weeks, which is similar to the originally published 67% remission rate.10 There was no apparent relationship between the dose and the rate of remission. As in previous studies,10 the majority of mice in all dose regimens that entered remission did so 1–2 weeks after treatment and all remained in remission for the 12 weeks of follow-up. Study B demonstrated that a total dose as low as 15 μg resulted in long-term remission of diabetes in NOD mice. In Study C, lower doses were examined to determine the minimum effective dose with the 72 hr dose regimen.

Similarly, when randomly analysing fibres from sections containing revertant fibres, either an increased average intensity, or higher standard errors of the mean was seen, implying that revertant fibre(s) had been included in the analysis (e.g. sample 5 in Figure 3). As with any semiquantitative technique, reliable internal controls and standards are vital. We chose β-spectrin as our internal control to account for differences in the integrity of the fibres. We have previously shown that spectrin is an ideal marker of sarcolemmal integrity as it is not a protein of the dystrophin complex [25] and is not affected by dystrophin deficiency,

except on necrotic and regenerating fibres [26]. All measurements were normalized with their corresponding serial section labelled for β-spectrin. All measurements were expressed relative to the normal dystrophin in standard controls in each particular Decitabine manufacturer experiment and should not be considered absolute values, as we confirmed that there is a certain degree of variability even between controls (Figure 4). We believe that this technique

will be an additional useful tool to the techniques currently in place in diagnosis of neuromuscular diseases in which the study of localization and amount of protein is paramount. We also propose this technique as Rapamycin chemical structure an objective method to quantify protein expression when assessing efficacy of experimental therapies aimed at restoring protein expression, such as in the recent trials of antisense oligonucleotides in DMD [27,28]. The Authors wish to thank the Department 3-mercaptopyruvate sulfurtransferase of Health (UK) for the funding of this study and the Muscular Dystrophy Campaign Centre grant. The Biobank of the MRC Neuromuscular Translational Research Centre is also gratefully

acknowledged. J. E. M. was funded by an MRC Collaborative Career Development fellowship in stem cell research and is currently funded by a Wellcome Trust University award. S. C. B. is funded by the AFM and MDA. The authors also wish to thank Mr David Hunt, Mr Jan Lehowsky, Dr Geraldine Edge, Jihee Kim and Darren Chambers for their technical expertise. No competing financial interests exist. “
“Papillary tumor of the pineal region (PTPR) is a recently recognized and rare pineal tumor, presenting as a solitary mass with or without hydrocephalus. Here, we report a case of c-Kit expressing PTPR with leptomeningeal seeding. A 39-year-old woman presented with a 1-month history of headache and decreased visual acuity. MRI showed a large, 4 cm-diameter solid and cystic enhancing mass at the pineal region with associated ventriculomegaly. Smaller nodular lesions were also found at the pituitary stalk and bilateral internal acoustic canal (IAC). The leptomeninges were noted to be enhanced with gadolinium.

, 2000). Chronic P. aeruginosa lung infection is the major cause of morbidity and mortality in cystic fibrosis (CF) patients (Høiby et al., 2005). This infection is highly resistant to antibiotic treatments and to host immune responses (Høiby et al., 2010). Intensive and aggressive antibiotic treatments may help to eradicate the intermittent

P. aeruginosa lung colonization in CF patients, but it is impossible to eradicate the chronic infection once it has become established. The biofilm mode selleck products of growth is proposed to occur in the lungs of chronically infected CF patients and bacterial cells are thus protected from antibiotic treatment and the immune response (Høiby et al., 2001). The mechanism of biofilm formation by P. aeruginosa BGB324 purchase has been investigated

by many research groups. Extracellular polymeric substances, including polysaccharides, proteins and extracellular DNA, are important components that hold bacterial cells together, stabilize biofilm architecture and function as a matrix (Stoodley et al., 2002; Flemming et al., 2007). Type IV pili and flagella are required for P. aeruginosa biofilm formation (O’Toole & Kolter, 1998). Interactions between nonmotile and motile subpopulations of P. aeruginosa cells are involved in the formation of mushroom-shaped biofilm structures, which confer resistance to antibiotic treatments (Yang et al., 2007, 2009a, b; Pamp et al., 2008). Type IV pili are required for the motile subpopulation of P. aeruginosa cells to associate with extracellular DNA released from the nonmotile subpopulation of P. aeruginosa cells, and flagella-mediated chemotaxis is required for the movement of motile subpopulations of P. aeruginosa cells to nonmotile subpopulations of P. aeruginosa cells (Barken et al., 2008). Thus, among the factors contributing to P. aeruginosa biofilm formation, type IV pili and flagella have proven to play essential roles. Pseudomonas aeruginosa can perform swimming motility in aqueous environments, which is mediated by its polar flagellum. In addition, two distinct types of surface-associated motility have been defined when

P. aeruginosa grow on agar plates: twitching motility requiring functional type IV pili (Semmler Cepharanthine et al., 1999; Mattick, 2002) and swarming motility requiring functional flagella, biosurfactant production and, under some conditions, type IV pili (Kohler et al., 2000; Deziel et al., 2003). There is a strong interest in finding ways of inhibiting the development of biofilms or eliminating established biofilms. For example, iron chelators are used to prevent biofilm development, especially under low oxygen conditions such as in CF lungs with chronic infections of P. aeruginosa (O’May et al., 2009). Quorum-sensing inhibitors are used to block cell-to-cell communications and reduce biofilm formation by P. aeruginosa (Hentzer et al., 2003; Yang et al., 2009a, b).

, 2005; Scott et al., 2010), and has been found to be secreted by C. concisus UNSWCD (Kaakoush et al., 2010). The capability of bacteria to effectively attach to ECM components is a vital phenomenon as in some bacterial species it may be directly related to virulence (Patti et al., 1994). The secretion and immunoreactivity of this protein are significant in terms of C. concisus UNSWCD, potentially playing a pathogenic role in adhesion to and subsequent colonization of host cells. In this study, 37 proteins

were identified to be immunoreactive in C. concisus-positive CD patients’ sera. We demonstrated that FlaB, ATP synthase F1 alpha subunit, and OMP18 of C. concisus are the predominant antigens recognized by all patients with CD. Furthermore, at least six of the identified immunoreactive proteins were involved in adhesion to the host cell, a finding which suggests https://www.selleckchem.com/products/PD-0332991.html that C. concisus selleck kinase inhibitor can cross the mucus layer and attach to the intestinal epithelium. In conclusion, this study provides important insights into the antibody response of patients with CD to C. concisus infection. This work was made possible by the support of the National Health and Medical Research Council, Australia. No conflicts of interest exist. “
“Chlamydia trachomatis (CT) is the leading sexually transmitted

bacterial infection in humans and is associated with reproductive tract damage. However, little is known about the involvement and regulation of microRNAs (miRs) in genital CT. We analyzed miRs in the genital tract (GT) following C. muridarum (murine strain of CT) challenge of wild type (WT) and CD4+ T-cell deficient (CD4−/−) C57BL/6 mice at days 6 and 12 post-challenge. At day 6, miRs significantly downregulated in the lower GT were miR-125b-5p, -16, -214, -23b, -135a, -182, -183, -30c, and -30e while -146 and -451 were significantly upregulated, profiles not exhibited at day 12 post-bacterial challenge. Significant differences in miR-125b-5p (+5.06-fold

change), -135a (+4.9), -183 (+7.9), and -182 (+3.2) were observed in C. muridarum-infected CD4−/− compared to WT mice. In silico prediction and mass spectrometry revealed regulation of miR-135a and -182 and associated proteins, that is, heat-shock GBA3 protein B1 and alpha-2HS-glycoprotein. This study provides evidence on regulation of miRs following genital chlamydial infection suggesting a role in pathogenesis and host immunity. “
“Laboratorio de Investigación en Inmunología, Hospital Infantil de México, “Federico Gómez”, Ciudad de México, México Myosin 1g (Myo1g) is a hematopoietic-specific myosin expressed mainly by lymphocytes. Here, we report the localization of Myo1g in B-cell membrane compartments such as lipid rafts, microvilli, and membrane extensions formed during spreading. By using Myo1g-deficient mouse B cells, we detected abnormalities in the adhesion ability and chemokine-induced directed migration of these lymphocytes.