17,19 In the C57BL/6 background, it was even shown that aged μMT

17,19 In the C57BL/6 background, it was even shown that aged μMT animals finally accumulate plasma cells in the MALT despite the apparent absence

of lymphocytes carrying a BCR, suggesting that B-cell progenitors can undergo CSR to IgA and differentiate into IgA-secreting B cells (ASCs) in the absence of mIgM/mIgD.17,18 To date, little is known regarding the potentially specialized function www.selleckchem.com/products/PLX-4032.html of mIgA that could eventually confer specific properties on mucosal or memory mIgA+ cells in comparison with naive mIgM+ cells. It is often assumed that about half of the IgA-producing B cells are involved in T-cell-independent B1 responses, so that alongside the BCR, their development would rely in a large part on signals given by Toll-like receptors and other cytokine receptors in the MALT microenvironment. Cross-linking of mIgA raises the intracellular calcium concentration and supports B-cell

activation so that mIgA+ B cells residing in the MALT can mediate IgA responses to local immunization.20,21 In addition, we have recently shown that replacing IgM expression with IgA expression in naive B cells results in the IgA BCR actively promoting plasma cell differentiation.22 We intended to check whether, as in ε and γ1 chains, expression of the membrane form of the α immunoglobulin heavy chain was required for generating OSI-906 nmr IgA-ASC. This experiment also allowed us to check whether expression of the α class BCR was responsible for the plasma cell accumulation that normally characterizes MALT tissue and if so whether this knock-out would eventually result in the attrition of the gut plasma cell compartment. Consequently, we generated mutant mice in which the membrane exon downstream of the constant α region (Cα) was replaced by a floxed neomycin gene (αΔtail mice). Animal experimentation was in accordance with international guidelines. Etofibrate EIIa-cre transgenic mice were a kind gift from Dr Heiner Westphal, used under a non-commercial research license agreement from Dupont Pharma (Wilmington, DE). The αΔtail construct included an 8-kb α mouse genomic fragment as a 5′ arm

(from a SalI site 3 kb upstream of the Sα region to a HindIII downstream of CH3 secreted-form transcript polyadenylation signal) and a 3 kb long 3′ arm (a genomic fragment originating from downstream of the Cα gene membrane exon). A 1·5-kb NotI–NotI fragment encompassing a neomycin resistance gene flanked by loxP sites was fixed between both arms. E14 ES cells were transfected with linearized vector and selected using G418 (200 μg/ml). Recombinant clones were identified by Southern blot with an external 5′ probe (570 bp, a BamHI/EcoRI fragment located upstream of Sα). After the injection of recombinant ES clones in C57BL/6 blastocysts, the male chimeras were mated with C57BL/6 females and germline transmission of the mutation was checked by Southern blot with an internal probe (500 bp, CH3 fragment, Fig. 1, middle).

14 As for the SP, availability of seminal material has not been a

14 As for the SP, availability of seminal material has not been an issue because volumes are sufficient for analyses for either human or animal studies. Moreover, sampling methods can be refined for examination of other portions than the bulk ejaculate, Ceritinib mouse such as specific fractions or even specific accessory glands (for instance after massage expression of prostate, seminal vesicles, etc.). Neither does the protein content matter, because proteins are a major component, throughout species. Major SP proteins belong to one of three main groups: proteins carrying fibronectin type II (Fn-2) modules, spermadhesins

or cysteine-rich secretory proteins (CRISPs).30 However, differences in type

and source of proteins are present among species, owing BMS-777607 to the already named differences in glands and/or the sequence they are emptied or the type of ejaculate they have. In most species, proteins are mainly of vesicular gland origin, and in ungulate mammals (boar, stallion, bull, buck), most proteins are Fn2 and/or spermadhesins.30,31 Spermadhesins have been most thoroughly studied in pig SP, as a family built by the following three members: the Alanine–Glutamine–Asparagine proteins AQN (−1 and −3), the Alanine–Tryptophan–Asparagine proteins (AWNs) and the porcine seminal plasma proteins I and II (PSP-I and PSP-II).32 Spermadhesins are multifunctional 12- to 16-kDa glycoproteins whose biological activities depend on their sequence, grade of glycosylation or aggregation state, as well as on their ability to bind heparin [AQN-1, AQN-3 and AWN, grouped as O-methylated flavonoid heparin-binding proteins (HBPs)] or not (PSPs), as they attach in varying

degree, to the sperm plasma membrane, from the testis to the ejaculate. Collectively, they have been related to multiple effects on spermatozoa including membrane stabilization, capacitation and interplay between sperm–oviductal lining or sperm-ZP. The HBPs seem to stabilize the plasma membrane over the acrosome prior to capacitation.33 Detection of AWN epitopes on boar spermatozoa bound in vivo to the ZP strongly suggests that the protein mediates sperm–ZP interaction.34 While HBPs do not seem to promote sperm survival, at least in vitro,35 the non-heparin-binding PSP-I and PSP-II,36,37 which accounts for >50% of all SP proteins and forms a glycosylated heterodimer,38 binds to the sperm surface and displays protective action on highly extended and processed spermatozoa.39,40 The PSPs depict, moreover, clear immunostimulatory activities in vitro and in vivo, presumably in relation to specific cytokines.

[26] On the other hand, TDP-43-immunoreactive structures were not

[26] On the other hand, TDP-43-immunoreactive structures were not detected in the vicinity of highly electron-dense BBs with central clear spaces containing Alectinib research buy filaments (Fig. 3c), corresponding

to an advanced stage of BB formation.[26] Murayama et al.[7] have reported that BB-related ubiquitin-positive structures are more frequently observed in ALS patients with shorter disease duration ranging from 10 to 38 months. Quantitative analysis also showed the highest numbers of ubiquitin-positive inclusions in cases with short duration.[27] By contrast, no significant correlation has been found between the number of BB-containing neurons and disease duration or the number of skein-containing neurons.[11] Previous ultrastructural

studies have shown that BBs were observed in and around the skein-like inclusions.[6, 8, 10] Moreover, Y 27632 bundles of filaments, which resembled those found in the skein-like inclusions were observed inside and around the BBs.[7, 10] We showed that TDP-43-immunoreactive filamentous structures were observed in and around the early stage BBs and that TDP-43 was not associated with advanced stage BBs. It is likely that BB formation is more aggressive at the earlier stage, whereas the formation of TDP-43 inclusions is continuous in the disease process of ALS. Cystatin C, a cysteine protease inhibitor involved in lysosomal and endosomal protein degradation,[15, 28] is a marker of BBs and is localized to the vesicular structures of

BBs.[29] In normal conditions, the amount of cystatin C is enough to inhibit cysteine protease activities, such as cathepsins and caspases. In our previous study, we demonstrated a marked decrease in cystatin C immunoreactivity in the cytoplasm of anterior horn cells in ALS.[29] Since TDP-43 can be proteolytically processed by caspase-3, one of the cysteine proteases,[30] the decrease of cystatin C may cause activation of cysteine proteases in anterior horn cells of ALS, leading to cleavage of TDP-43. Native TDP-43 has nuclear localization signals and nuclear export signals, both of which are important for Montelukast Sodium subcellular transport of this protein.[31, 32] TDP-43 is cleaved to generate C-terminal fragments in degenerating neurons in ALS and FTLD-TDP.[3, 33] As C-terminal fragments of TDP-43 might lose the nuclear localization signal, the fragmented TDP-43 remains in the cytoplasm and then forms protein aggregates. It is possible to consider that an increased sequestration of cystatin C into BBs may cause accumulation and aggregation of pathological TDP-43 in the anterior horn cells in ALS. There is a statistically significant relationship in the occurrence between BBs and TDP-43 inclusions. Although BBs and TDP-43 inclusions are morphologically and antigenically distinct from each other, these two inclusions may participate synergistically in the disease process of ALS. This work was supported by JSPS KAKENHI (F.M., K.W.

Although the overall serum level of T helper type 1 (Th1)-related

Although the overall serum level of T helper type 1 (Th1)-related molecules, such as CD40L and IFN-γ, was restored after treatment, www.selleckchem.com/products/ink128.html Th17-related cytokines, such as IL-17 and IL-23, were down-regulated significantly at 12 months post-treatment compared to pretreatment. Furthermore, these cytokine patterns differed among patient subgroups. Decreased serum concentrations of IL-17 and/or IL-23 were associated

with failure of sputum conversion, the fibrocavitary disease phenotype and M. intracellulare lung disease. Thus, the reciprocal balance between Th1 and Th17 immunity during antibiotic therapy for MAC lung disease is critical for dictating the treatment response. In conclusion, a low level of Th1-related immunomolecules may perpetuate MAC lung disease, and the serum concentrations of Th17-related cytokines can reflect the treatment outcome, disease phenotype

and aetiological agent. “
“Serum levels and liver expression of CCL2 are increased in patients with alcoholic hepatitis (AH). In an experimental model of alcoholic liver disease (ALD), CCL2 was implicated in proinflammatory cytokines activation and hepatic lipid metabolism, but its role in NVP-BEZ235 manufacturer human disease is currently unknown. In a large cohort of ALD patients, we analysed plasma levels and liver expression of CCL2 and their association with liver disease severity and histological lesions. We also studied the relationship between −2518 A > G CCL2 and CCR2 190 A/G polymorphisms and severity of ALD. We show that CCL2 plasma levels are increased in ALD patients compared with healthy subjects. AH patients had significantly higher plasma levels and hepatic expression of CCL2 than patients without AH. Plasma levels and hepatic expression of CCL2 were associated with disease severity. CCL2 liver expression was correlated with neutrophil infiltrate and interleukin (IL)-8 expression, Ribose-5-phosphate isomerase but not with steatosis. Moreover, there

were more G-allele carriers of −2518 A > G CCL2 polymorphism in severe AH patients than in other ALD patients. Our results demonstrate that CCL2 is increased in ALD, particularly in severe forms, and suggest a role for CCL2 in the pathogenesis of ALD via neutrophil recruitment. Alcoholic liver diseases (ALD) are the most common cause of cirrhosis in the western world [1]. A subset of ALD patients will develop alcoholic hepatitis (AH) characterized by hepatocellular damage and liver neutrophil infiltrates [2]. Severe forms of AH are associated with poor short-term prognosis [3]. Moreover, AH is an independent predictive factor in liver fibrosis progression [4]. Treatments for ALD are currently limited, and better understanding of the pathogenesis of this disease may provide new therapeutic targets.

It should further be noted that beside help, CD4+ T cells might a

It should further be noted that beside help, CD4+ T cells might also directly contribute, by nonperforin nongranzymes pathways, to skin rejection as shown in the anti-HY TCR-transgenic model [[26, 27]]. Such direct participation would account for the fact that depletion of DBA/2 mHfe KO mice in CD4+ T cells resulted in more complete graft protection than depletion in CD8+ T cells. That other MHC class Ib molecules could directly stimulate αβ T lymphocytes and behave autonomously as transplantation antigens has been shown with TL-transgenic mice

[[28]]. However, the TL-encoding transgene T3b was placed under the control of an H-2 MHC class Ibrutinib Ia promoter and, consequently, tissue expression of TL was considerably broadened. Thus, all MHC class Ib molecules might have the intrinsic potential to behave as autonomous histocompatibility antigens. However, this potential should be modulated by the molecular topology of their polymorphic or mutated residues, their tissue distribution and the Selleckchem Deforolimus level of their cell surface expression. Could other mutated forms of HFE also behave as autonomous histocompatibility antigens? There are two other frequent mutated forms of human HFE molecules (H63D, S65C) that

are associated with human hereditary hemochromatosis, albeit loosely [[29, 30]]. However, unlike the C282Y mutated molecule, these variant forms of HFE are cell-surface expressed [[31, 32]]. Furthermore, the H63 and S65 mutated residues are part of an external loop joining two β strands of the floor of the HFE groove and are distant from the area (top of MHC α helices and aa of the presented peptide) of conventional MHC class Ia molecules contacted by αβ TCRs [[33]]. Assuming that MHC class Ib molecules are similarly contacted by αβ TCRs, it seems unlikely that these structural differences of HFE would, at least directly, stimulate conventional T lymphocytes. Considering the rapidity with which mHFE+ skin grafts were rejected by anti-mHFE TCR-transgenic

mice (whether mHfe KO or mutated) and the efficacy with which anti-mHFE TCR-transgenic CD8+ T BCKDHB cells differentiated in CTL when in vitro stimulated, without CD4+ T cell help in both cases, the absence of GVHD following injection of a large number of anti-mHFE TCR-transgenic CD8+ T cells in Rag 2 KO DBA/2 mHFE+ mice was surprising. However, a similar observation has been reported in the anti-HY TCR transgenic model, where the transferred T cells in male recipient mice, following transient activation, disappeared after a few days [[34]]. In the present anti-mHFE TCR-system, disappearance is even more rapid, suggesting that the anti-mHFE CD8+ T cells are eliminated through apoptosis.

The role of

The role of Selleck Atezolizumab D. massiliensis in tick natural history and its influence on tick’s

fitness are unknown. However, a recent study suggests that this bacterium is pathogenic towards humans (Subramanian et al., 2011). Spiroplasmas (class Mollicutes) are helical, motile, wall-less prokaryotes associated with a variety of insects, other arthropods and some plant hosts (Tully et al., 1981). They are usually considered as commensal organisms in their arthropod hosts, but several are pathogenic for insects and plants. Several species were associated with a male-killing phenomenon (Jiggins et al., 2000). Spiroplasmas have been identified in ticks (Haemaphysalis leporispalustris and Ixodes pacificus) and blood-sucking members of the Diptera, including horseflies

(Tabanus spp.), deerflies (Chrysops spp.) and mosquitoes (Aedes spp., Culex spp.). Spiroplasma ixodetis was first isolated from I. pacificus, a principal vector of Lyme disease on the west coast of the USA (Tully et al., 1981). Later, a nearly identical bacterium Maraviroc price was isolated from a pool of Ixodes ticks in North Rhine-Westphalia (Germany) (Henning et al., 2006), and another strain of Spiroplasma spp. (genetically very close to S. ixodetis) was recently isolated on the XTC cell line from a I. ricinus tick sampled in Slovakia, where prevalence of tick infection by Spiroplasma was 2.5% (Subramanian et al., in press). Virtually nothing is known about the relationship between Spiroplasma and ticks. However, several publications support the pathogenic role Selleck Fludarabine of this bacterium towards humans. Thus, Lorenz et al. (2002) found a Spiroplasma

sp. infection causing a unilateral cataract in a premature human baby. Spiroplasmas have been reported to be involved in neurodegenerative diseases such as scrapie or Creutzfeldt–Jakob disease (Bastian et al., 2004, 2011). In addition to the four potential tick endosymbionts discussed above and to established human pathogens known to be transmitted by ticks (Table 3), several other fastidious intracellular bacteria have been shown to be closely associated with ticks, including Candidatus Midichloria mitochondrii (Sassera et al., 2006), Francisella-like bacteria (Sun et al., 2000), Wolbachia spp., and different Rickettsiales. More studies are needed in this emerging field, whose results may have many applications, including the control of vectorborne diseases of humans and animals. Indeed, the concept of targeting endosymbionts as a mean to control ticks and tickborne diseases has been tested using a chemotherapeutic approach (Ghosh et al., 2007). Novel methods for the isolation and characterization of tick-associated bacteria will likely promote new approaches to control ticks by targeting their endosymbionts.

This study provides an evaluation of the systemic response charac

This study provides an evaluation of the systemic response characteristics of female baboons to ligature-induced periodontitis during pregnancy. Our findings support that ligature-induced periodontitis in baboons elicits changes in systemic inflammatory mediators. Moreover, a subset of the population of baboons that

demonstrated a greater clinical response to FDA approved Drug Library cell line ligation during pregnancy exhibited a discrete systemic inflammatory response. This model of periodontitis and pregnancy resulted in alterations in the level of serum inflammatory mediators throughout the pregnancy and will provide an opportunity to delineate risk factors for oral–systemic disease linkages. This work was supported by USPHS grant DE13958 from the National Institute of Dental and Craniofacial Research. We would like to thank Scott Eddy, Robert Ayala and Malini Bharadwaj for technical support in developing and managing these data. We acknowledge the crucial contribution of Drs Kathleen Brasky, Karen Rice and the scientific and technical staff at the Southwest Foundation for Biomedical Research and contribution from USPHS grant 13986 in support of the Southwest National Primate Research Center at the Foundation. The authors

claim no conflict or financial interests related to the research reported. “
“Effective humoral AZD1208 chemical structure immunity depends on B cells, plasma cells and follicular helper T cells (TFH) and secreted high-affinity antibodies. The differentiation of mature B cell into plasma cells is ultimately hardwired in a regulatory network of transcription factors. This circuitry is responding to extracellular stimuli, which leads to production of higher-affinity antibodies after germinal centre (GC) reaction. The understanding of the transcriptional regulation of GCs and the

initiation of plasma cell differentiation is becoming increasingly clear. It is evident that transcriptional repressor Blimp-1 can drive the plasma cell differentiation, but the initiation of plasma cell differentiation in GCs is likely coupled to Teicoplanin the loss of B cell characteristics maintained by transcription factors Pax5 and Bcl6. Upon activation with appropriate stimuli, most notably the antigen recognized by the B cell antigen receptor (BCR), the resting naive B cells start to proliferate. A subset of these cells starts to secrete antibody and are referred to as plasmablasts. These cells may undergo terminal differentiation in tissues, where they continue antibody secretion and stop the proliferation, and are defined as plasma cells. Plasma cells represent the final differentiation stage of the B cell lineage and are the professional antibody-secreting cells constituting a major branch of humoral immunity.

0001) (Fig 2C) The establishment of functional T-cell memory is

0001) (Fig. 2C). The establishment of functional T-cell memory is vital for the success of an immunization protocol. To assess if functional CTL responses could be generated by a single immunization or if a prime boost regime Sorafenib order were required, C57BL/6 mice were given single or multiple immunizations with TRP2/HepB human IgG1 DNA. No epitope-specific responses were detectable 20 days after a single immunization with TRP2/HepB human IgG1 DNA, but high-frequency responses were detectable after two immunizations (p=0.026) which increased further

with another immunization (p<0.0001) (Fig. 2D). The avidity of responses after two or three immunizations was analyzed. The responses induced in mice receiving two or three DNA immunizations were of high avidity (1.4×10−12 M and 1.8×10−12 M,

respectively). There is no significant difference in avidity between these two groups (p=0.89) (Fig. 2E). As both the frequency and avidity of the CTL response appear enhanced, the question “was avidity related to frequency?” arose. Over 80 mice were immunized with TRP2/HepB human IgG1 DNA and the frequency and avidity of responses measured. The avidity of the TRP2-specific responses ranged from 5×10−8 M to 5×10−13 M peptide. No significant correlation Raf inhibitor between avidity and frequency of TRP2 peptide-specific responses was identified, suggesting they are independent events (Fig. 3A). It is possible that xenogeneic human Fc influences the frequency and avidity of responses induced. Comparison of responses from immunization with human IgG1 or an equivalent murine IgG2a construct reveals similar frequency and avidity (Fig. 3B), suggesting that the xenogeneic human Fc was not influencing the response. Synthetic peptides have short half lives in vivo and are poor immunogens as they

have no ability to specifically target professional Ag presenting cells such as DC. Current therapies are showing DC pulsed with peptide induce an efficient immune response. TRP2/HepB human IgG1 DNA immunization was compared to DC pulsed with HepB/TRP-2 linked peptide. TRP2/HepB human IgG1 DNA demonstrated similar frequency responses compared to those RVX-208 elicited by peptide-pulsed DC, both of which were superior to peptide immunization (p=0.0051 and p=0.0053) (Fig. 4A). Analysis of the avidity of responses reveals that the avidity in TRP2/HepB human IgG1 DNA immunized mice is 10-fold higher than with peptide-pulsed DC (p=0.01) (Fig. 4B). The TRP2 specific responses were analyzed for ability to kill the B16F10 melanoma cell line in vitro. Figure 4C shows that although responses from peptide and peptide-pulsed DC immunized mice demonstrate a good peptide-specific lysis, mice immunized with TRP2/HepB human IgG1 DNA showed better killing of the B16 melanoma cells (p=0.003). The enhancement of avidity could be related to direct presentation of the epitopes by the Ab–DNA vaccine and similar responses may be elicited by a DNA vaccine incorporating the native TRP2 Ag.

Batf3−/− mice displayed enhanced susceptibility with larger lesio

Batf3−/− mice displayed enhanced susceptibility with larger lesions and higher parasite burden. Additionally, cells from draining lymph nodes of infected Batf3−/−

mice secreted less IFN-γ, but more Th2- and Th17-type cytokines, mirrored by increased serum IgE and Leishmania-specific immunoglobulin 1 (Th2 indicating). Importantly, CD8α+ DCs isolated from lymph nodes of L. major-infected mice induced significantly more IFN-γ secretion by L. major-stimulated immune T cells than CD103+ DCs. We next developed CD11c-diptheria toxin receptor: Batf3−/− mixed bone marrow chimeras to determine when the DCs are important for the control of infection. Mice depleted of Batf-3-dependent DCs from day 17 or wild-type mice depleted of cross-presenting DCs from 17–19 days after infection maintained significantly larger lesions similar to mice whose

selleck screening library Batf-3-dependent DCs were depleted from the onset of infection. Thus, we have identified a crucial role Temozolomide in vitro for Batf-3-dependent DCs in protection against L. major. “
“Dendritic cells (DCs) are known as antigen-presenting cells and play a central role in both innate and acquired immunity. Peripheral blood monocytes give rise to resident and recruited DCs in lymph nodes and non-lymphoid tissues. The ligands of nuclear hormone receptors can modulate DC differentiation and so influence various biological functions of DCs. The role of bile acids (BAs) as signalling molecules has recently become apparent, but the functional role of BAs in DC differentiation has not yet been elucidated. We show that DCs derived from human peripheral blood monocytes cultured with a BA produce lower levels of interleukin-12 (IL-12) and tumour necrosis factor-α in response to stimulation with commensal bacterial antigens. Stimulation through the nuclear receptor farnesoid X (FXR) did not affect the differentiation of DCs. However, DCs differentiated with the specific agonist for TGR5, a transmembrane BA receptor, showed an IL-12 hypo-producing phenotype. Expression of selleck inhibitor TGR5 could only be identified in monocytes and was rapidly down-regulated during monocyte differentiation to DCs. Stimulation with

8-bromoadenosine-cyclic AMP (8-Br-cAMP), which acts downstream of TGR5 signalling, also promoted differentiation into IL-12 hypo-producing DCs. These results indicate that BAs induce the differentiation of IL-12 hypo-producing DCs from monocytes via the TGR5-cAMP pathway. Dendritic cells (DCs) are classified as professional antigen-presenting cells and play a central role in both the innate and acquired immune responses. The DCs are a heterogeneous population of cells that can be divided into two major populations: (i) non-lymphoid tissue migratory and lymphoid tissue-resident DCs and (ii) plasmacytoid DCs. Migratory and resident DCs function in the maintenance of self-tolerance and the induction of specific immune responses against invading pathogens.

Serum samples from patients with TB reacted more strongly with MP

Serum samples from patients with TB reacted more strongly with MPB64 antigen than did those from uninfected individuals. In addition, serum samples from TB patients

with active infection reacted more strongly with the antigen than did samples from patients with inactive TB. When urine samples were assessed using this assay, similar results were obtained. Correlations between the data obtained from serum and urine samples were analyzed for all subjects, including uninfected individuals, and a strong positive correlation between the results of serum and urine tests (n = 36, r = 0.672) was found. The sensitivity and specificity of this assay for serum samples was 85.7 % and 85.0 %, and for urine samples 75.0 % and 85.0 %, respectively. These results suggest that dot-blot assay with MPB64 Ruxolitinib in vitro antigen could be a useful screening test for active

TB. Because urine samples can be obtained more easily than serum samples and because urine is less contagious, urine testing should probably be employed for screening purposes. Dabrafenib supplier According to the World Health Organization, about two billion people, approximately one third of the world’s population, are infected with M. tuberculosis. In 2011, around 8.8 million new cases of TB and 1.1 million deaths from this disease were reported (1). This is the greatest number of deaths caused by any single pathogen. From sub-Saharan Africa to Asia, the annual incidence of TB now exceeds 300 per 100,000. In Japan, the number of new cases of TB and its incidence has been increasing since 1997. In 2007, the number of new TB patients reached 25,311, with the total incidence rising to 19.8, which is higher than in many other developed countries (1). In Japan, a high percentage of infected elderly patients develop active TB and, in urban areas, the percentage of immigrants from Southeast

Asian countries with TB is not negligible. The diagnosis of pulmonary TB is based on the presence of respiratory symptoms (cough, sputum, and hemoptysis) and systemic symptoms (fever, malaise, and weight loss), and the findings on chest X-ray films and computed tomography scans. Examination of the patient’s sputum and gastric Glycogen branching enzyme juice, as well as auxiliary diagnostic tests such as the QuantiFERON test, tuberculin skin test, and bronchoscopy, can also be performed (2). For many years, the tuberculin skin test was the standard test for TB infection. However, this test does not become positive until 4–6 weeks after establishment of infection and prior BCG vaccination can influence its results. Accordingly, the QuantiFERON-TB Gold In-Tube, which is based on three tuberculosis-specific antigens (ESAT-6, CFP-10 and TB7.7 proteins), is now recommended as a more specific test for TB (3, 4). There have been many attempts to develop serodiagnostic tests for TB that detect antibodies targeting various structural components of M. tuberculosis.