80 The study was large (736 patients) with a mean follow up of 3 years (range: 6 months to 18 years). At last follow up, 11.5% of patients were obese and obesity was more common in women (17% vs 6%). Obese donors, when compared with the non-obese donors, had significantly higher rates of diabetes (13.5% vs 3%) and hypertension (24% vs 10%). There was a non-significant trend to lower GFR (<60 mL/min) and a higher prevalence of proteinuria in obese donors. This data are concerning and the median follow-up time is short. There is limited ZVADFMK detail

given in terms of screening donors for diabetes, or presence of family history for diabetes and baseline BMI. There are cultural reasons cited for the high rate of weight gain post donation, and the population studied is one that is ethnically more at risk of developing diabetes.

This study highlights that the safety data drawn from predominantly Caucasian populations, do not necessarily hold true for populations with a greater risk of diabetes and/or kidney disease. A report from the OPTN/UNOS registry81 records 102 individuals as waiting for transplant who have previously been living donors, in which African Americans are over-represented. There is no information on the Selleckchem GSK 3 inhibitor prevalence of obesity in the group or other identifiable risk factors that may have been present at donation, however, hypertension and diabetes are listed as the cause of ESKD in roughly one third. The histology of implantation biopsies in obese living donors is subtly different from non-obese donors.82 Increased glomerular planar surface area (GPSA), glomerulomegaly and minor tubular abnormalities are more common in obese donors and there

GNAT2 is a trend to increased arterial hyalinosis. There was no difference in the number of segmental sclerotic lesions or degree of interstitial fibrosis. GPSA was correlated with albuminuria, although all donors had 24 h urinary albumins that were within the normal range. Donor follow up was less than 1 year and no difference in serum creatinine was seen between obese and non-obese donors. A retrospective analysis of 73 patients examined the outcome of unilateral nephrectomy done for clinical indication (i.e. not donors).83 At the time of nephrectomy, patients had normal creatinine and urinalysis, no multisystem disease such as diabetes and no morphological abnormality of the remaining kidney examined by ultrasound. Median follow up was 13.6 years (range: 18 months to 35 years). Twenty of 73 patients developed abnormalities of renal function (proteinuria ± renal insufficiency). Average time to proteinuria was 10 ± 6 years and was slowly progressive in most patients. Thirteen of 73 patients developed renal impairment (serum creatinine > 1.4 mg/dL and creatinine clearance < 70 mL/min per 1.73 m2). Time between development of proteinuria and onset of renal impairment was 4.1 ± 4.3 years.

8-fold), Hmox1 (heme oxygenase 1; 3.4-fold), Folr2 (folate receptor-2; 2.6-fold), Prdx6 (periredoxin-6; 2.5-fold), find more and Spsb4

(SPRY domain and SOCS box containing protein 4; 2.5-fold) (Fig. 5) [43-49]. If Arg1+ cells do have the potential for neuroprotection following TBI, this may be overwhelmed by Arg1− cells, which are greater in number and are less transient. Our findings demonstrate a heterogeneous macrophage response to TBI that changes over time. Expression profiling of Arg1+ and Arg1− macrophage subpopulations demonstrate that they do not exemplify previously described in vitro derived macrophage subsets [17]. They also differ from macrophages that accumulate in skin wound macrophages [50]. Skin wound macrophages, such as TBI-induced Arg1+ cells, both express Arg1 and Mrc1. However, skin macrophages additionally upregulated Clec7a, and do not express Nos2, features that distinguish them from TBI-induced Arg1+ cells. FDA-approved Drug Library It may not be surprising that the macrophage response to TBI differs from macrophage polarization induced in vitro

or in other organs and other in vivo conditions. It is likely that macrophages can assemble their functions and products in a variety of combinations with great diversity. Our findings do demonstrate the heterogeneity of the macrophage response to TBI and they suggest that Arg1 should not in isolation be used as a marker for M2 cells. In this regard, Arg1 expression can be induced by pathways independent of IL-4/STAT6 [51]. Although we were able to identify macrophage subsets by using Arg1 as a marker in YARG mice, we could not detect robust expression of IL-12p40 by flow cytometry on days 1, 4, 7, or 14 in any macrophages or microglia by using Yet40 very mice or by gene expression profiling comparing Arg1+ and Arg1− macrophages, as assessed by gene profiling. This suggests that IL-12p40 may not be a major effector cytokine promoted by brain macrophages or microglia in TBI, and that early in TBI, IL-12p40 is not inversely proportional to Arg1 expression.

Other M1 genes are detected, however, both in Arg1+ and Arg1− cells. Thus, the use of a single marker to define M1 and M2 cells in TBI appears not to be sufficient, and the functional consequences of the Arg1+ and Arg1− cell populations on the course of TBI remain unknown. Our findings do not exclude the possibility that there are more than two subsets of responding macrophages, and this is clearly supported by the bimodal expression of MHCII in Arg1− macrophages. Also, despite the extensive differences in gene expression between these cell subsets, particularly, in the expression of chemokines, it is also possible that Arg1+ and Arg1− macrophages may have a shared lineage and/or be partially polarized and that one subtype could become or becoming the other.

76,89,90 In this regard,

reduced Treg-cell suppression after stimulation with various purified microbial ligands suggests that classical vaccine adjuvants derived from crude microbial preparations may simulate immune activation by overriding Treg-mediated immune suppression. Indeed, the transient ablation of Foxp3+ cells alone during stimulation with purified peptide is sufficient to trigger the robust activation, expansion and formation of memory CD8+ T cells, which confers protection against subsequent Listeria infection in an antigen-specific fashion.88 Similarly, Foxp3+ cell ablation augments the expansion and activation of antigen-specific CD8+ T-cells primed by the live attenuated viral vector modified vaccinia virus Ankara.91 These findings are consistent with the enhanced vaccine-induced immunogenicity Torin 1 price that occurs with Treg-cell ablation using anti-CD25 antibody treatment, and the sustained priming of protective CD8+ T cells by attenuated Listeria even in mice lacking all known signal 3 inflammatory cytokines.92–97

Hence, overriding immune suppression by selleck compound Treg cells probably plays pivotally important roles in stimulating protective T-cell responses in vivo. However, while immune adjuvants and vaccine vectors have traditionally been evaluated for their ability to activate T cells indirectly through stimulation of professional APCs that in turn elaborate defined stimulation signals [T-cell receptor (signal 1), co-stimulation (signal 2), and inflammatory cytokines (signal 3)],95,97,98 overriding active suppression by Treg cells probably represents a more fundamental prerequisite ‘signal zero’ essential for stimulating effector T-cell activation in vivo. Although this term has recently been used to describe the activation of innate immunity or chemokine gradients that each also participate Tyrosine-protein kinase BLK in T-cell activation,99,100 we propose that this descriptor is more appropriate for overriding

the impacts of suppression mediated by Treg cells and other immune suppressive cells, which actively restrains T-cell activation (Fig. 1). Since the identification of Treg cells as a separate and defined lineage of CD4+ T cells, there has been an explosion of studies describing the role these cells play in almost every aspect of the immune response. With the establishment of Foxp3 expression as the lineage-specific marker for Treg cells and the development of transgenic mouse tools for manipulating Foxp3+ cells in vivo, newfound protective roles for these cells in host defence against some infections have been uncovered. In turn, for other infections, the detrimental roles played by Foxp3+ cells in host defence have been reinforced.

Patients believed that success with treatment regimens pre and post transplant was highly contingent on the presence of a supportive carer to assist with management of the complex emotional, physical and financial challenges. Patients in this study strongly believed that additional emotional support was required for patients especially those on home therapies, working patients and carers. The use of frequent pragmatic education at all stages of the patient journey FK506 ic50 was valued highly. Conclusions: Strategies to facilitate peer support and meet the emotional needs of patients and carers at all stages of the patient journey is required. 263 A CLINICAL AUDIT OF THE OCCURRENCE OF DAPSONE

ASSOCIATED METHAEMOGLOBINAEMIA IN RENAL TRANSPLANT RECIPIENTS R MALASINGAM1, D RANGANATHAN1, L JEYASEELAN2, M JACKS1, J OWENS1, GT JOHN1 1The Royal Brisbane and Women’s Hospital, Brisbane, Australia; 2Christian Medical College, Vellore, India Aim: We examined the trend in haemoglobin levels before and after commencement of dapsone, the symptomatology and its correlation with levels of methaemoglobin.

Venetoclax manufacturer Background: In renal transplantation, dapsone is used as a second line prophylactic agent against Pneumocystis jirovecii. An under recognized adverse effect of dapsone therapy is methaemoglobinaemia. Methods: The details of renal transplant recipients on dapsone therapy was obtained from the renal transplant database. A venous blood gas was done on all patients during routine reviews. Methaemoglobin levels were measured using an abl Radiometer 800 blood Astemizole gas machine. Haemoglobin levels before and 1–3 months after starting dapsone therapy were obtained. Results: There were 11 patients who were on dapsone therapy at 100 mgs daily. One patient was excluded due to serial non-attendance to the

clinic. Following commencement of dapsone, 90% of the patients showed a trend towards a decline in haemoglobin. The methaemoglobin levels were all <5% with the highest level recorded at 4.8% and the lowest level noted at 1.3% (mean 3.01, sd 1.035, median 3). There was a 11–29 g/L rise in haemoglobin levels seen with all patients who had stopped dapsone (mean 16.77, sd 6.87, median 18.00). However, these results did not reach statistical significance; P = .06 in the simple segmented regression analysis. The bootstrap regression analysis has shown a significant improvement in haemoglobin values (26.7, 95%CI: 22.44, 32.06, P < .001) after stopping dapsone. Conclusions: These findings suggest methaemoglobinaemia is a common adverse effect of dapsone therapy. A countrywide screening of the causes of anaemia in renal transplant recipients receiving dapsone would be useful. Further studies are required to evaluate the efficacy of dapsone at lower doses, for prophylaxis of PJP.

Transformation of human B cells by EBV infection in vivo might, however, require not only these EBV latent antigens, but also the low level of lytic EBV replication that has been observed in B cells. EBV, which can no longer switch into lytic infection by virtue of a deficiency in BZLF1, the main transactivator that induces EBV replication, was reported in one study to cause less EBV-associated lymphomas

after infection [45]. Therefore, hallmarks of EBV infection, such as persistence and tumorigenesis, can be recapitulated in mice with reconstituted human immune system components, selleckchem but it remains unclear if all latency stages, which are finely attuned to human B-cell differentiation [48], can be modeled in this system. In addition to HIV and EBV, several other viral infections have been tested in mice with reconstituted human immune system

components. Among these, dengue virus was also found to establish infection in this in vivo model and a third of the infected animals developed weight loss and skin rash [49-51]. However, the identity of the infected human cells could not be clearly determined, but might be DC precursors [50]. Nevertheless, around half of the infected animals developed viral loads, which reached 103–105 viral copies/μg RNA in the spleen, 104–107 viral copies/μg MAPK Inhibitor Library cell assay RNA in the blood, and 104–109 viral copies/μg RNA in the liver [49-51]. Similarly, i.p. injection of JC virus resulted in an infection of reconstituted mice, which could be followed by JC virus DNA in blood and urine up to 100 days after infection, but the identity of the infected cells in this study remained

unclear as well [52]. Furthermore, HSV-2 infection was observed in reconstituted BRG mice by intravaginal inoculation [53]. In contrast, ex vivo infection of hematopoietic progenitor cells with HTLV-1 and in vivo reconstitution from these cells produced CD4+ T-cell lymphomas [54]. From this study, the authors concluded that human hematopoietic progenitor cells could constitute a HTLV-1 reservoir in the BM, from which HTLV-associated T-cell lymphomas can develop. Similarly to HTLV-1, infection with HCMV cannot simply be achieved by injecting the virus into reconstituted mice [55]. Instead, HCMV-infected fibroblasts Methamphetamine had to be transferred into the peritoneal cavity of reconstituted mice. G-CSF treatment to mobilize monocytes was then able to increase HCMV viremia and systemic dissemination, and viral antigen expression was found exclusively in human monocytes and macrophages of these mice [55]. Finally, i.v. HCV infection has been attempted in mice with reconstituted human immune system components; these mice were then additionally injected with human hepatocyte progenitors [56]. HCV infection caused liver inflammation, hepatitis, and fibrosis in the infected mice.

Such documents are peer-reviewed, but not copy-edited or typeset. They FG 4592 are made available as submitted by the authors. “
“We hypothesized that

the aberrant expression of microRNAs (miRNAs) in rheumatoid arthritis (RA) T cells was involved in the pathogenesis of RA. The expression profile of 270 human miRNAs in T cells from the first five RA patients and five controls were analysed by real-time polymerase chain reaction. Twelve miRNAs exhibited potentially aberrant expression in RA T cells compared to normal T cells. After validation with another 22 RA patients and 19 controls, miR-223 and miR-34b were over-expressed in RA T cells. The expression levels of miR-223 were correlated positively with the titre of rheumatoid factor (RF) in RA patients. Transfection of Jurkat cells with miR-223 mimic suppressed Doxorubicin nmr insulin-like growth factor-1 receptor (IGF-1R) and transfection with miR-34b mimic suppressed cAMP response element binding protein (CREB) protein expression by Western blotting. The protein expression of IGF-1R but not CREB was decreased in RA T cells. The addition of recombinant IGF-1-stimulated interleukin (IL)-10 production by activated normal T cells, but not RA T cells. The transfection

of miR-223 mimic impaired IGF-1-mediated IL-10 production in activated normal T cells. The expression levels of SCD5, targeted by miR-34b, were decreased in RA T cells after microarray analysis. In conclusion, both miR-223 and miR-34b

were over-expressed in RA T cells, but only the miR-223 expression levels were correlated positively with RF titre in RA patients. Functionally, the increased miR-223 expression could impair the IGF-1-mediated IL-10 production in activated RA T cells in vivo, which might contribute to the imbalance between proinflammatory and anti-inflammatory cytokines. “
“We set out to determine whether intravenous immunoglobulin (IVIG) improves in vitro fertilization (IVF) success rates in women with a difficult history of multiple (≥2) prior IVF failures and /or ‘unexplained’ infertility. A total of 229 women with multiple IVF failures (3.3 ± 2.1) and/or unexplained infertility (3.8 ± 2.7 years) were given IVIG on the day of egg retrieval, and the subsequent IVF success rates ever were compared with published success rates from the Canadian database (CARTR). The pregnancy rate per IVIG-treated cycle was 60.3% (138/229), and the live birth rate per IVIG-treated cycle was 40.2% (92/229). This is a significantly higher success rate compared to the Canadian average (30% live birth rate; CARTR statistics from 2010; P = 0.0012). In cases where a single embryo was transferred, pregnancy rate using IVIG was almost twofold the CARTR pregnancy rate [(61%(20/33) to 34.9% (428/1225)]. In cases where two high quality (≥Grade 3) day 5 blastocysts were transferred, nearly a 100% pregnancy rate was achieved using IVIG (30/31).

The secretion of cytokines after PBMC challenge was related to the number of months that the patient had experienced symptoms before performing the PBCM challenge. There were significant relationships between the IL-12 secretion induced Selleckchem GDC0068 by P-glucan, chitin and LPS (correlation coefficient 0·783, P < 0·001, 0·656, P = 0·002 and 0·835, P < 0·001, respectively) but not for S-glucan. There was also a relation between the duration of the symptoms and the spontaneous secretion of TNF-α (0·323, P = 0·015) and the LPS-induced secretion of TNF-α (0·490, P =0·020). The relationship between duration of symptoms and the P-glucan-induced

secretion of IL-12 is illustrated in Fig. 1. The serum values of cytokines were higher among subjects with sarcoidosis (data not shown) with significant differences for IL-6 and IL-12 (P < 0·001 and 0·003, respectively). The significant relationships between the in vitro production of cytokines and serum levels of IL-2R and IL-12 in the whole material are reported in Table 3. The serum level of IL-12 was related consistently to the secretion of different cytokines induced

by P-glucan. The relationship to IL-2R was less marked. There was also a relation between the P-glucan-stimulated release of IL-12 and the serum level of TNF-α. There were no significant relationships for PI3K inhibitors ic50 the chitin-induced secretions and serum cytokines. The average level of NAHA in the homes of controls was 12·9 (1·5) U/m3 and among subjects with sarcoidosis 30·9 (6·1) (P = 0·046). Among controls there were no relations between NAHA levels at home and the in vitro secretion of different cytokines. In subjects with sarcoidosis there were significant relationships between NAHA levels and the spontaneous secretion of IL-6, IL-10 and IL-12 (correlation coefficient 0·507, P = 0·027, correlation coefficient 0·725, P < 0·001 and correlation coefficient 0·567, P = 0·011, respectively). There was also an inverse relationship between the chitin-induced secretion of IL-12 and the NAHA levels in the homes and between NAHA and the LPS induced secretion of IL-6 and IL-10 (correlation

coefficient 0·621, P = 0·005 and correlation coefficient 0·457, P = 0·049, respectively). Figure 2 illustrates Oxymatrine the relation between the amount of NAHA in the homes of subjects with sarcoidosis and the spontaneous secretion of IL-12. Subjects with a high fungal exposure at home also had a higher spontaneous secretion of IL-12 from their PBMC. The relations between chest X-ray scores and the secretion of all cytokines after stimulation with P-glucan and LPS for the whole material are shown in Table 4. There were significant relationships between chest X-ray scores and the secretion of all cytokines after stimulation with LPS or P-glucan. The major findings from the study stem from the relation between reactions induced by FCWA in vitro, in vivo and the environment.

If this scheme is adapted for DNT, DNT can be classified as non-infiltrating oligodendroglioma, grade I. In order to further clarify these controversial issues regarding DNT, it is necessary to perform a much more strict epigenetic characterization of floating neurons. We thank Dr. Takanori Hirose (Saitama Medical University; presently, Tokushima Prefectural Central Hospital) for FISH testing and Dr. Hiroyoshi Suzuki (NHO Sendai Medical Center) for their valuable comments and discussion.

“
“A microvascular density (MVD) counting method for reversion-inducing cysteine-rich protein with Kazal motifs (RECK) expression, using a digital image analysis tool, has advantages over manual counting by microscope. Thirty glioma cases with RECK staining were photographed at a magnification Dorsomorphin of 200× high power field and the photographs in RGB images were analyzed, and stained vessels were captured and were counted automatically. MVD with RECK expression using a digital image analysis tool showed comparable results to those of the manual method. RECK intensity expression could show linear correlation with grades of glioma by the digital method, which was superior compared to the manual method. The present method is recommended to researchers undertaking MVD study for glioma. “
“Malignant peripheral nerve sheath

tumors (MPNSTs) arising from cranial nerves are rare and RG7420 solubility dmso usually affect adults. Here we report the clinicopathologic features of a young adult patient with a trigeminal nerve MPNST, in whom another tumor involving the oculomotor nerve on the contralateral side was evident. The patient, an 18-year-old woman, had suffered recurrent paroxysmal sharp stabbing pain

over her cheek and forehead on the right side for 1 month. A brain MRI study disclosed a mass, 35 mm in diameter, in the right Meckel’s Farnesyltransferase cave, and another mass, 10 mm in diameter, involving the intracranial portion of the left oculomotor nerve. Following gadolinium administration, the former and latter tumors exhibited strong and weak enhancement, respectively. The patient had no clinical stigmata characteristic of neurofibromatosis type 1. Following a tentative diagnosis of schwannoma, total resection of the trigeminal nerve tumor was performed. Histologically, the tumor consisted of highly cellular, spindle-shaped cells arranged in a fascicular pattern, with occasional mitotic figures, nuclear pleomorphism and necrosis. Immunohistochemically, the tumor cells showed variable intensities and frequencies of reactivity for S-100 protein, myelin basic protein, CD34, podoplanin and p53, but no reactivity for Smarcb1. Thus, the tumor exhibited features of MPNST. This case appears to provide information that is useful for accurate diagnosis and surgical planning in patients with bilateral or multiple cranial nerve tumors. “
“T. G. D’Aversa, E. A. Eugenin, L.

047; Fig. 4B). Therefore, IL-7 secretion by leukemic cells contributes to the survival of CML-specific CTL. Our results in a murine CML model

using LCMV-gp33 as model leukemia antigen suggested that IL-7 signaling maintains CML-specific CTL and may contribute to disease control. LCMV-gp33 is a foreign antigen, which is expressed in the H8 transgenic mice under a relatively strong promoter. Therefore, the model leukemia antigen used has many similarities to the junction peptides derived of BCR/ABL, which are similarly selleck chemical expressed under a strong promoter and are novel antigens without pre-existing self-tolerance. Nevertheless, the H8-CML model might overestimate the contribution of IL-7 signaling and CD8+ T-cell control. To test the physiological role of IL-7 in CML control, IL-7-deficient bone marrow or C57BL/6 bone marrow was transplanted to irradiated C57BL/6 recipient mice. IL-7−/−-CML mice died within 30 days after bone marrow transplantation (Fig. 5A). On the contrary, BMS 907351 C57BL/6-CML mice survived significantly longer

(p=0.02). A similar retroviral transduction efficiency of IL-7-deficient and C57BL/6 donor bone marrow cells was confirmed by FACS analysis 3 days after spin-transfection (Fig. 5B). Taken together, these results indicate that IL-7 production by leukemic cells improves the immunological control of CML, in the absence of model antigen gp33. Specific CTL participate in the control of CML without eradicating the disease completely 6, 7, 20. In fact, CML disease is characterized by a chronic phase of 3–5 years during which a specific CTL response coexists with the CML and probably controls the disease. This is followed by the transition to blast crisis. The mechanisms which control this delicate balance between the immune system and the leukemia are largely unknown. Adoptive transfer

experiments revealed that a large fraction of specific CTL disappeared from the circulation and from the lymphoid organs. This process has also been documented for chronic viral infections, and is referred to as exhaustion19, 21–26. The phenotype of CTL that resist physical Cisplatin cost deletion in the presence of a chronic infection has been analyzed before. These CTL were characterized by varying degrees of functional impairment, such as the lack of cytotoxic activity and a reduced capacity to produce IFN-γ 21, 22. However, if partially exhausted and dysfunctional T cells still contribute to disease control is less clear and is often difficult to assess in the presence of a chronic infection. Indications that partially exhausted CTL are of importance for disease control come from experiments with rhesus macaques infected with SIV. Animals which were depleted of CD8+ T cells by monoclonal antibody had significantly higher viral loads 27. We now analyzed the relevance of partially exhausted CTL in the control of CML.

tuberculosis and M. bovis BCG (Hanif et al., 2008; Mustafa et al., 2008). In addition, some of these subjects may Z-VAD-FMK in vitro also be latently infected with M. tuberculosis and thus be responsible

for positive responses to RD1 by responding to other immunodominant M. tuberculosis-specific antigens present in this region, i.e. ESAT-6 and CFP10 (Al-Attiyah et al., 2003, 2006b; Mustafa et al., 2008). The peptide pools of RD15 and its individual ORFs induced weak cellular responses in TB patients. However, in healthy subjects, RD15, RD1502, RD1504 and RD1505 induced strong to moderate responses in both assays, whereas other ORFs of RD15 were weak stimulators in one or both assays. Furthermore, the individual responses of both patients and control groups are highly variable, with some being nonresponsive to specific antigens. This has been observed even with immunodominant antigens of M. tuberculosis, in this study as well as previously (Al-Attiyah et al., 2004, 2006b). Therefore, for diagnostic applications, more than one antigen GSK-3 beta phosphorylation should be used, as is the case with the currently used IFN-γ assays using

peptides of ESAT-6 and CFP10 (Liebeschuetz et al., 2004; Liu et al., 2004). These results also demonstrate that RD15 region contains major Th1 cell-stimulating antigens/peptides recognized only by healthy subjects and not by TB patients. As RD15 is present in M. tuberculosis and deleted in all strains of M. bovis BCG, the recognition of RD15 by healthy subjects could be due to latent infection with M. tuberculosis, as has been previously shown

for RD1 (Al-Attiyah et al., 2003, 2006b; Al-Attiyah & Mustafa, 2008; Mustafa et al., 2008). In addition, several genes within the RD15 region, namely, RD1501 (Rv1963c) and RD1504–RD1509 (Rv1966–Rv1971), share more than 70% homology with mce3 genes in other pathogenic mycobacteria (Mycobacterium marinum and Mycobacterium ulcerans) and a nonpathogenic environmental mycobacterium (Mycobacterium vanbaalenini) (data not shown). It remains to be seen whether some of the reactivities in healthy subjects were due to the exposure of the tested individuals to these mycobacteria. It has been established that CMI, which involves the interaction of antigen-specific T cells and macrophages, plays a major role in protection against TB (Flynn, 2004; Mustafa, 2009c). This interaction is reflected in antigen-induced proliferation of GNAT2 T cells and the secretion of high levels of protective Th1 cytokines, mainly IFN-γ, and low levels of anti-inflammatory cytokines IL-4, IL-5 and IL-10 (Bai et al., 2004; Flynn, 2004; Al-Attiyah et al., 2006a). In particular, IL-10 has multiple effects that interfere with the functions of protective cells and cytokines (van Crevel et al., 2002), thereby helping mycobacteria to survive intracellularly despite abundant production of IFN-γ (Murray et al., 1997). On the other hand, the absence of IL-10 accelerates mycobacterial clearance (van Crevel et al., 2002).