Another vaccine reported in 2004 links hCGβ with a human anti-DC antibody, B-11, at genetic level.80 This vaccine is reported to elicit cell-mediated immune response to tumor-associated antigen(s) in a human in vitro model. Monocytes of a normal human donor were incubated with B-11-hCGβ, activated with CD40 ligand mixed with autologous lymphocytes and tested for their ability to mount hCGβ-specific proliferative and cytotoxic T-lymphocyte response. The procedure led to the generation of tumor-specific HLA class AZD6738 datasheet I- and class II-restricted T-cell response (including CTLs) capable of killing human cancer cell lines expressing hCGβ.

According to the authors, this is the first time that cellular immune response has been induced by a vaccine in a human in vitro system in contrast to the other vaccines inducing primarily antibody response. Immunological interventions against

hCG, whether by vaccines or by recombinant human/chimeric antibodies, have entered an exciting new phase. They may provide therapeutic options for advanced-stage cancers, which are often metastasized and refractory to available drugs. These would also be useful for the control of fertility for which there is a continuing need of additional more acceptable methods. According to WHO (http://www.who.int/en), more than 120 million couples still have an unmet need for family planning and 45 million Liothyronine Sodium selleck kinase inhibitor pregnancies are terminated each year globally. Two recombinant vaccines have been developed. One employs hCGβ linked to either an antibody homing to Dendrocytes or linked to a mucosal carrier, and the other has β subunit of hCG fused to B subunit of heat labile enterotoxin of E. coli (hCGβ-LTB). The former has been tested in vitro; it induces a cell-mediated immune response against hCG. The second vaccine, hCGβ-LTB, given along with a non-pathogenic human use approved Mycobacterium indicus pranii

generates several fold higher antibody response in mice than titers established by previous clinical trials to prevent pregnancy. The third vaccine employs an engineered hCGβ with glutamic acid replacing arginine at position 68, conjugated to a human antibody for delivery to dendrocytes. It is in clinical trials in bladder cancer patients with encouraging results. Corresponding Author Dr G. P. Talwar Talwar Research Foundation, New Delhi, India. “
“Regulatory T cells play a crucial role in normal gut homeostasis, as well as during infection with microbial or parasitic pathogens. Prior to infection, interactions with the commensal microflora are essential to differentiation of a healthy steady-state level of immunoregulation, mediated through both Toll-like receptor-dependent and -independent pathways.

Results:  In the ocular waveforms, significant differences in power spectra were observed in frequency band 4 (corresponding to frequencies between 6.25 and 12.50 Hz)

between groups (p < 0.05). No differences in RI occurred. No association was observed between waveform parameters and fasting glucose or insulin resistance. Pioglitazone had no effect on waveform structure, despite significantly reducing insulin resistance, fasting glucose, and triglycerides (p < 0.05). Conclusions:  Analysis of ocular Doppler flow waveforms using the discrete wavelet transform identified microvascular abnormalities that were not apparent using RI. Pioglitazone improved glucose, insulin sensitivity, and triglycerides Osimertinib in vitro without influencing the contour of the waveforms. “
“The pathophysiology underlying hyperthyroidism-induced left ventricle (LV) dysfunction and hypertrophy directly involves the heart and indirectly involves the neuroendocrine systems. The effects of hyperthyroidism Small molecule library manufacturer on the microcirculation are still controversial

in experimental models. We investigated the effects of hyperthyroidism on the cardiac function and microcirculation of an experimental rat model. Male Wistar rats (170–250 g) were divided into two groups: the euthyroid group (n = 10), which was treated with 0.9% saline solution, and the hyperthyroid group (n = 10), which was treated with l-thyroxine (600 μg/kg/day, i.p.) during 14 days. An echocardiographic study was performed to evaluate the alterations in cardiac function, structure and geometry.

The structural capillary density and the expression of angiotensin II AT1 receptor in the Clostridium perfringens alpha toxin LV were analyzed using histochemistry and immunohistochemistry, respectively. Hyperthyroidism was found to induce profound cardiovascular alterations, such as systolic hypertension, tachycardia, LV dysfunction, cardiac hypertrophy, and myocardial fibrosis. This study demonstrates the existence of structural capillary rarefaction and the down-regulation of the cardiac angiotensin II AT1 receptor in the myocardium of hyperthyroid rats in comparison with euthyroid rats. Microvascular rarefaction may be involved in the pathophysiology of hyperthyroidism-induced cardiovascular alterations. “
“Microcirculation (2010) 17, 1–11. doi: 10.1111/j.1549-8719.2009.00005.x We tested the hypothesis that segmental differences in the responsiveness and time course of vasodilation to metabolic signals putatively involved in rapid onset vasodilation (ROV) at the start of exercise exist within the skeletal muscle vasculature. Cannulated first-order (1As) and third-order arterioles (3As) of the rat gastrocnemius (G) muscle were exposed to cumulative doses of KCl, acetylcholine (Ach), or adenosine (Ado). In addition, time course and magnitude of vasodilation to localized application of these agonists were determined. 1As and 3As dilated similarly to incremental doses of the agonists.

Comorbidity data were collected and a modified patient symptom module was completed. Fifty-five patients who were managed without dialysis were reviewed and the symptom burden recorded was high. Using a tool that may lead to assessing more effective symptom treatments, revealed the extent of symptom burden in conservatively managed ESKD. It is also important to emphasize that a conservative, non-dialysis approach to ESKD management should not be a vacuum, but in fact can provide an intensive programme

of multidisciplinary care and support. It also provides the patient and their family with the confidence that there will be no reduction in medical and nursing care.60 A study from Hong Kong assessed and compared the quality of life and symptom burden between patients on haemodialysis learn more and peritoneal dialysis with palliative care ESKD patients with an eGFR <15 mL/min.22 This prospective observational study included 179 patients, 134 who had dialysis and 45 who undertook palliative care. Those that received palliative care had greater comorbidity and were older. There was no significant difference in symptom burden between groups and the quality of life was significantly reduced in both groups. In this setting there was little difference in symptoms

and quality of life whether they had dialysis Cabozantinib ic50 or palliative care. The palliative care process needs to consider acknowledging and dealing with this grieving both in the patient, their family and health-care providers. A study conducted by Badger exploring factors impacting on end-of-life transitions in critical care found two key areas of concern for nurses.61 These were the ‘complex emotions and frank indecisiveness expressed by patients’ families. Grief and loss are issues intertwined throughout Olopatadine the course of CKD and ESKD management.62 Although grief is clearly associated with death, it is also evident and experienced much earlier in the trajectory of an illness and is even felt immediately a new high impact diagnosis is realized. Clinicians may avoid discussing end-of-life decisions with patients for fear of causing undue anxiety.63 This is despite the patients desire to address the issues. Cultural differences in the

approach to end-of-life decisions, advanced care planning and withdrawal from dialysis have been addressed by Davison and Holley.43 Non-Western cultures, significantly represented in the Australian population, may have very different understandings of the medical system, health and disease. These cultural sensitivities need to be taken into account when discussing palliative care and end-of-life decisions. Several studies have indicated that the beliefs and values of health professionals have a clear impact on the integration of palliative care into the management of ESKD patients. Twohig and Byock64 found that the focus of care remained on cure and prolongation of life and that ethical cultural and legal issues impact on the clinical decision to withdraw or withhold dialysis.

SEA possesses a different tropism for the Vβ chain of the TCR, preferentially binding to the Vβ1, 3, 10, 11 and 12 types (75). Intraperitoneal administration of SEA can reactivate MBP-induced EAE after one month of clinical remission (76). Soos et al. have shown that SEA produces new episodes of EAE when given in mice which have previously been immunized with MBP after depletion of Vβ8 cells by SEB pretreatment. As previously mentioned, the explanation relies on the types of lymphocytes that remain in place to be stimulated by SEA. This experiment revealed that it is not only Vβ8 cells that can participate in EAE pathogenesis, as was previously believed (77). To our knowledge, there has been

no study of oral administration of SEA in EAE. In any case, the variable behavior seen after administration of SEB/SEA can be explained by the affinity for certain T cells, different TCR restrictions for effector lymphocytes in different species, and differing selleckchem routes of administration. When administered parenterally, SEA acts as a major stimulant of the systemic lymphocyte compartment. Thus, staphylococcal enterotoxins have the opportunity to reactivate EAE, even in animals which have entered a remission period (78). Insulin is now recognized as the major auto-antigen in type 1 diabetes (79). As a consequence, a number of clinical trials have tested the possibility of producing oral tolerance to insulin,

in the hope of preventing or delaying the onset of the disease in non-diabetic relatives at high risk of diabetes. The Diabetes Prevention Trial–Type 1 showed that 7.5 Z-VAD-FMK cost mg of oral insulin daily did not confer a benefit when compared to placebo. In a subgroup

of this trial which included only those relatives who had tested positive on two occasions for anti-insulin autoantibodies, orally administered insulin proved to be useful in preventing the onset of diabetes, compared with placebo (80). Currently, Ureohydrolase the Pre-POINT (Primary Oral/intranasal Insulin Trial) is addressing the group of children who are at high risk of developing type 1 diabetes and who have not yet developed anti-insular autoantibodies. This trial is ongoing (81). There has been no trial in humans or animals that has tested the efficacy of SEA as an adjuvant for augmenting oral tolerance to insulin or any other peptides that function as autoantigens in type 1 diabetes. In animal models the results of SEA usage appear to be in conflict. Kawamura et al. have shown that staphylococcal enterotoxins (SEA, SEC1, SEC2, or SEC3), when injected iv into non-obese diabetic female mice at 4 and 10 weeks of age, significantly reduce the incidence of diabetes at 32 weeks compared with a saline treated group (82). The explanation, according to the authors, originates in the fact that SAs are able to stimulate a CD4+ fraction of T lymphocytes which is capable of immunoregulatory activity. Ellerman et al.

Repair from ischaemic acute renal failure involves stimulation of tubular epithelial cell proliferation. Agents impairing the ability of renal epithelium to proliferate, especially in the face of ongoing injury, may result in prolonged periods of acute renal failure (ARF) or failure in recovery. Several studies of ARF have shown augmented

injury and delay repair when rapamycin is given near the time of injury [19,20]. The mechanism AZD2281 in vitro appears to involve a combination of enhanced necrosis, increased apoptosis and decreased proliferation of renal tubular epithelial cells. In contrast, it has been demonstrated that treatment with rapamycin in the recipient animals attenuated I/R injury in small bowel [21] and kidney I/R injury [22,23]. Also it has been reported that rapamycin has a potent preconditioning effect in an animal model of heart I/R injury [24]. However, it is well known that rapamycin could aggravate ischaemically injured organs, increasing cell apoptosis and negatively affecting post-transplantation recovery [15,20]. Conversely, tacrolimus is a calcineurin inhibitor normally administered to receptors of renal transplant to block the activation

of nuclear factor of activated T cells (NF-AT) [25]. Tacrolimus produces multi-faceted attenuating actions on inflammatory damage occurring after reperfusion. Lastly, pretreatment with tacrolimus has been shown to provide liver https://www.selleckchem.com/products/R788(Fostamatinib-disodium).html and renal protection against I/R injury in rats [26,27]. Although intervention in the preservation solution and the receptor has always been the first choice, because of insufficient

evidence supporting a successful intervention in the donor there has always been research into the administration of immunosuppressive drugs to the donor. Before transplantation, the kidney already contains several infiltrated macrophages and T lymphocytes [28]. This inflammatory process, activated by cold ischaemia as well as brain death, may be explained by changes in the kidney tissue itself [29]. Another potential reason is that these inflammatory mediators could be released from T lymphocytes and macrophages infiltrated in the kidney. Therefore, the administration of rapamycin and tacrolimus to the donor could Cell press be useful to inhibit the release of mediators from the graft [30]. Anticipating the inflammatory process through the administration of immunosuppressive drugs to the donor could be one of the scenarios to reduce the graft immunogenicity. In previous studies, we have used tacrolimus and rapamycin separately, and we observed a reduction in the in-situ generation of proinflammatory mediators and an up-regulation of cytoprotective genes [17]. We hypothesized that the combined use of rapamycin and tacrolimus treatment in donor animals would be associated with the attenuation of I/R injury.

In addition, T cells of the type-1 inflammatory phenotype were present. Clinical data of the patients strongly support the findings that TAMs, together with tumour-infiltrating T cells, exert tumour-suppressive effects. For the first time, we demonstrated the tumour-suppressive properties of TAMs and have begun to dissect the

underlying processes. These findings will help us understand the potential beneficial actions of TAMs, so that future cancer immunotherapy can be developed based on enhancing these tumour-suppressive effects of TAMs to boost anti-tumour immune responses. We co-cultured find more human primary monocytes with a human colorectal cell line, HT29, as MCTSs for 8 days (this set-up will be referred to as ‘co-culture spheroids’

SCH727965 purchase hereafter). To mimic tumours with no macrophage infiltration, we cultured tumour cells alone as spheroids (hereafter referred to as ‘tumour spheroids’). To determine if monocytes co-cultured with tumour cells differentiated into macrophages, we checked the expression of CD68 and CD14, markers up-regulated and maintained, respectively, during monocyte-to-macrophage differentiation. In contrast, CD68 and CD14 expression are down-regulated in monocyte-to-dendritic cell (DC) differentiation (Supporting Information Fig. 1A–C). All the monocytes (CD45+) co-cultured with tumour cells for 8 days up-regulated the expression of CD68 (Fig. 1A) and maintained the expression of CD14 (Fig. 1B), compared with freshly isolated monocytes (Supporting Information Fig. 1A), indicating that the monocytes have differentiated into macrophages. Monocyte cultured alone for 8 days under the same conditions, in the absence of tumour cells, do not spontaneously differentiate (Supporting Information Fig. 1D). In addition, from day 4 to 8, CD68+ cells in the co-culture spheroids displayed increase in size, number of cytoplasmic granules and heterogeneity of cell shape characteristic of monocyte-to-macrophage differentiation (Fig. 1C). Together, these observations indicated that the monocytes have differentiated into macrophages after 8 days

of co-culture with tumour cells. To study the interaction between tumour cells and macrophages, we carried out global gene expression profiling on three groups of cells: (I) tumour cells Tenofovir mouse from tumour spheroids; (II) tumour cells sorted out from co-culture spheroids and (III) tumour cells and TAMs from co-culture spheroids (Fig. 2A). To assess the changes induced in the tumour cells upon co-culture with macrophages, we compared the gene expression profiles of (I) and (II), which gave 286 differentially expressed genes (DEGs; Supporting Information Table 1). Sorted tumour cells in (II) had a purity of 92.6±4.2%, with only 0.5±0.2% TAMs remaining (Supporting Information Fig. 2), making the comparison valid. Twenty-eight of the 286 DEGs (10%) were associated with proliferation and apoptosis (Fig. 2B).

Additionally, nephrin and CD2AP decreased and stained intermittently. Through the immunoelectron microscopy, different degrees of foot processes effacement were observed in the hypertensive group. Nephrin and CD2AP decreased and stained weakly along the podocyte basal membrane, while in the control group, they distributed evenly in podocytes. Conclusion: Hypertension induced dysregulation of podocyte cytoskeletal proteins, which may be an important cause that leads to the development of proteinuria and decline of renal function in hypertensive kidney injury patients. BOKUDA KANAKO1,2, MORIMOTO SATOSHI1, RYUZAKI

MASAKI1, MIZUGUCHI YUUKI1, OSHIMA YOICHI1, NIIYAMA MICHITA1, SEKI YASUFUMI1, YOSHIDA NAOHIRO1, WATANABE high throughput screening assay DAISUKE1, MORI FUMIKO1, ANDO TAKASHI1, ONO MASAMI1, ITOH HIROSHI2,

ICHIHARA ATSUHIRO1 1Department of Medicine II, Endocrinology and Hypertension, Tokyo Women’s Medical University, Tokyo, Japan; 2Division of Endocrinology, Metabolism and Nephrology, Department of Internal Medicine, Keio University, School of Medicine, Japan Introduction: The (pro)renin receptor[(P)RR] plays an important role in tissue angiotensin generation and in angiotensin-independent activation of intracellular signaling. Alisikiren, Selleckchem CHIR 99021 the direct renin inhibitor, effectively inhibits the first step of the renin-angiotensin system (RAS). In addition, it affects (P)RR-mediated actions and (P)RR expressions in experimental models. Aliskiren therefore may have organ protective effects, however, effects of single Aliskiren treatment on kidney and vascular functions still remain unclear. The soluble form of (P)RR [s(P)RR] is secreted into the extracellular space and serum level of s(P)RR is supposed to be a biomarker reflecting the status

of the tissue RAS. Herein, we examined the effects of Aliskiren on kidney and vascular functions and serum s(P)RR levels in hypertensive patients with chronic kidney disease (CKD). Methods: Thirty consecutive essential hypertensive patients with CKD in our outpatient clinic were randomly assigned to the Aliskiren (DRI) group or the Amlodipine, a calcium channel blocker, (CCB) group. Changes in parameters associated Selleckchem Erlotinib with renal and vascular functions and indices of RAS components including serum s(P)RR levels were compared between the groups before and after 3- and 6-month treatment periods. Results: Office blood pressure (BP) was not significantly different between the groups before and after treatment. Plasma renin concentration and activity were significantly increased and decreased, respectively, in DRI group, while these remained unchanged in CCB group. There were no significant changes in serum s(P)RR levels throughout the treatment periods in both groups. Urinary albumin excretion was significantly decreased in DRI group, while no significant changes were observed in CCB group. eGFR remained unchanged in both groups.

A New Method to Measure Peripheral Retinal Vascular

Caliber over an Extended Area. Microcirculation17(7), 495–503. Objective:  To describe a new computer-assisted method to measure retinal vascular caliber over an extended area of the fundus. Methods:  Retinal photographs taken from participants of the Singapore Malay Eye Study (n = 3280) were used for this study. Retinal selleck chemicals vascular caliber was measured and summarized as central retinal artery equivalent (CRAE) and central retinal vein equivalent (CRVE) using a new semi-automated computer-based program. Measurements were made at the Standard zone (from 0.5 to 1.0 disk diameter) and an Extended zone (from 0.5 to 2.0 disk diameter). Results:  Reliability of retinal vascular caliber measurement was high for the new Extended zone (intraclass correlation coefficients >0.90). Associations of CRAE with blood pressure were identical between the Extended and Standard zones (linear regression coefficient −2.53 vs. −2.61, z-test between the two measurements, p = 0.394). Associations of CRAE and CRVE with other cardiovascular risk factors were similar between measurements in the two zones. The R2 of regression models for the Extended zone

was slightly higher than that for the Standard zone for both CRAE (R2, 0.324 vs. 0.288) and CRVE (R2, 0.325 vs. 0.265). https://www.selleckchem.com/products/Deforolimus.html Conclusions:  The new measures from Extended zone are comparable with the previous measures, and also more representative of retinal vascular caliber. “
“Please cite this paper as: Blaise, Roustit, Millet,

and Cracowski (2011). Effect of Oral Sildenafil on Skin Postocclusive Reactive Hyperemia in Healthy Volunteers. Microcirculation 18(6), 448–451. Objective:  Sildenafil is a type 5 phosphodiesterase inhibitor that has a theoretical ability to increase hyperemia following a short bout of ischemia. We tested Methisazone if oral sildenafil increases skin PORH in healthy volunteers. Methods:  We assessed forearm skin PORH (occlusion of blood flow for five minutes) in ten healthy volunteers 120 minutes following the oral administration of 50 or 100 mg of sildenafil. Cutaneous blood flow on the forearm was monitored using LDF. Results:  The PORH peak, expressed as a percentage of baseline, was clearly increased with 100 mg sildenafil: 746% (95% CI 447–1044) versus 484% (95% CI 354–613) with 50 mg sildenafil, and 468% (95% CI 347–588) without sildenafil (p = 0.03 for 100 mg versus 50 mg and control). Oral sildenafil at 50 mg increased the AUC of PORH on the forearm compared with control: 4568 PU.sec (95% CI: 2252–6883) with 50 mg sildenafil versus 1030 PU.sec (95% CI 737–1322) without sildenafil (p = 0.006). Likewise, 100 mg sildenafil increased the AUC (5271 PU.sec (95% CI −81–10,623), albeit bordering on significance (p = 0.07). Neither dose increased maximal LTH. Conclusions:  Acute sildenafil administration at 50 and 100 mg enhances skin hyperemia following a short bout of ischemia.

4 ± 0.3 μm/s. Accordingly, mean speeds of ≥4.0 μm/s (speeds 10 times or more faster than that of Brownian motion) were judged as indicating motility; bacterial motility was also judged by direct observation through a phase-contrast

microscope. The data are presented as the mean ± SD of at least three trials. For analysis of bacterial shape, bacterial cells were grown on blood-agar plates for 12–18 hrs at 37°C and examined by scanning electron microscopy GSK1120212 [16]. For this, pieces of blood-agar-block on which colonies had developed were fixed with 2.5% glutaraldehyde in 75 mM PBS (pH 7.4) for 2 hrs at 4°C, washed with PBS, and subsequently postfixed in 1% osmium tetroxide for 2 hrs at 4°C. The fixed samples were dehydrated with 50%, 70%, 90% and 100% acetone for 2 hrs each at room temperature (around 18°C),

and the samples in 3-methylbutyl (isoamyl) acetate were then critical-point dried. The dried samples were coated with gold–palladium and subjected to analysis using a scanning electron microscope. Campylobacter structures in the flagellate polar region were analyzed by transmission electron microscopy [16] and thin-section or negative-stain images obtained. For thin-section images, bacterial cells grown on blood-agar plates for 12–18 hrs at 37°C were carefully suspended in and fixed with 2.5% glutaraldehyde in PBS BGJ398 molecular weight for 2 hrs at 4°C, followed by washing and postfixing with 1% osmium tetroxide, as described above. The fixed samples were dehydrated with 70%, 90%, 95% and 100% ethanol for 10 mins each at room temperature, and embedded in EPOK 812 (Oukenn, Tokyo, Japan). The embedded block was cut with an ultramicrotome (MT-500) with a diamond knife (producing 70 nm thin sections) and stained with 2% uranyl acetate and Sato’s lead staining

solution (containing lead citrate, lead nitrate and lead acetate). The stained thin sections were analyzed using a transmission Uroporphyrinogen III synthase electron microscope. For negative-stain images, bacterial cells grown on blood-agar plates for 12–18 hrs at 37°C were carefully suspended in water. One drop of the bacterial suspension was applied to a collodion-coated grid screen (3 mm diameter), followed by addition of one drop of 1% uranyl acetate for 30–60 s (negative staining). The stained grids were analyzed using a transmission electron microscope. Campylobacter jejuni was grown at 37°C and then examined for motility at various temperatures. As shown in Figure 1, the motility of C. jejuni is strictly regulated by temperature. C. jejuni is highly motile at 37–42°C, whereas motility is immediately lost when the temperature is lowered to room temperature range (<20°C). The motility of C. jejuni, which is lost at 20°C, immediately and completely recovers when the temperature is increased to 37–42°C. Reversibility was observed even in the presence of chloramphenicol (which inhibits protein synthesis) at 100 μg/mL, similarly to H. pylori.

To date, the enhancement of Ab synthesis mediated by IFN-β treatment is not resulting in an excessive Ig production or in an induction of auto-Abs (data not shown and [46]). Rather, this therapy restores via monocyte-mediated bystander mechanisms the correct TLR7 responsiveness of MS-derived B cells, which in this way fully acquire the capacity to mature into Ig-producing cells, similar to HDs. In this

scenario, the study from Warrington et al. [47] is of great interest that demonstrates how naturally occurring polyclonal human Abs (in particular IgM) can strongly promote FK506 concentration remyelination inducing a transient Ca2+ influx in myelin-forming cells. Thus, the ability of IFN-β therapy to induce polyclonal Abs (and in particular IgM) with potential remyelinating activity reveals another mechanism of protection possibly mediated by this drug, that could lead to amelioration of find more neurological symptoms in MS patients. An additional aspect to take into account from our findings is that the deficient TLR7-induced IgM and IgG production observed in MS patients might correlate with worsening of disease or impaired immune responses against infections with TLR7-recognized RNA viruses, such as influenza, or upon vaccination. Many studies have been conducted in this regard. Different groups have reported that the risk of relapse is increased in individuals with MS bacterial or viral infections [48, 49]. In the case of Astemizole influenza,

it was shown that the reduction of infection episodes leads to a lower number of exacerbations in MS sufferers. In a study with 180 RRMS patients, 33% of individuals, who became infected with this virus, developed an acute relapse within 6 weeks [50]. However, randomized, double-blind, placebo-controlled studies during the past decade have shown that influenza vaccination of MS patients neither increases the relapse rate nor worsens the course of disease [51]. Indeed, the administration

of standard vaccines in MS patients is considered safe worldwide, it follows the same recommendations as in healthy adults and actually should be recommended to MS patients in order to avoid attacks of the disease [52]. Having all this in mind, it cannot be excluded that our data on the reduced level of secreted Abs in response to TLR7 stimulation can have a role in the exacerbation of relapses observed in MS-affected individuals along episodes of influenza infection. The increasing recognition that viruses, and in particular EBV, can be etiological factors driving the development of MS or other autoimmune diseases in genetically susceptible individuals further strengthens the potential of administering anti-viral therapies to people affected by these disorders [12]. In line with this view, the increased TLR7 gene expression observed upon IFN-β might be part of a specific antiviral program induced by this cytokine that could counteract dysregulated responses to viral infection in MS patients.