An opposite pattern was observed for progression of nephropathy

An opposite pattern was observed for progression of nephropathy. The authors note that the findings of the study are consistent with CVD studies and the role that SFAs may play in insulin sensitivity and other factors affecting diabetes control. Nonetheless, the authors consider that control of BP and blood glucose and cessation of smoking should remain the therapeutic objectives for modifiable risk factors. When these objectives are obtained, other measures such as encouraging PUFA and MIFA over SFA Sunitinib research buy may help prevent micro and macroalbuminuria.118 Table A5 presents a summary of the relevant studies found by the search strategy

in relation to dietary fat. With the exception of the study by Cardenas et al.118 discussed above, the studies are either of short duration and thus provide little useful evidence for the role of dietary fat in the progression of CKD. Relevant details of the studies are provided in Table A12. In summary, there are insufficient reliable studies to support a recommendation in relation to the prevention and management of CKD in people with type 2 diabetes. Intake

of protein in the usual range does not appear to be associated Selleckchem Sorafenib with the development of CKD. However, long-term effects of consuming >20% of energy as protein on development of CKD has not been determined. Although diets high in protein and low in carbohydrate may produce short-term weight loss and improved glycaemic control, it has not been established that weight loss is maintained in the long term. There have been few prospective controlled studies of low protein diets in people with type 2 diabetes and kidney disease. The studies that have been performed have generally been deficient in experimental design, in methods for measuring kidney function and/or in duration of follow-up. Furthermore, the level of compliance with a low protein diet has not always been assessed objectively by urinary urea

nitrogen excretion. A particular criticism is that changes in the creatinine pool Interleukin-3 receptor and creatinine intake seen in low protein diet studies render measurements of creatinine clearance or the reciprocal of serum creatinine unreliable for the assessment of GFR.119 The objective of the systematic review was to assess the effects of dietary protein restriction on the progression of diabetic nephropathy in people with diabetes (type 1 and type 2 diabetes).120 The review identified 11 studies (9 RCTs and 2 before and after trials) where diet modifications were followed for at least 4 months. Before and after trials were included as it was considered that people could act as their own controls. Of these studies 8 were of people with type 1 diabetes, one type 2 diabetes and two included both type 1 and type 2 diabetes.

CBA data was analysed using fcap Array software (BD Biosciences)

CBA data was analysed using fcap Array software (BD Biosciences). TGF-beta inhibitor Statistical analyses were performed with GraphPad Prism software (Graphpad Software, Inc., La Jolla, CA, USA). Significance was determined using Kruskal–Wallis analysis with

Dunn’s multiple comparisons post-test and Wilcoxon tests. We analysed NKT cells isolated from fresh human thymus, spleen, cord blood and adult peripheral blood. The mean NKT cell frequency of donor tissues were similar for peripheral blood (0·1 (mean) ± 0·02 [standard error of the mean (s.e.m.)], cord blood (0·06 ± 0·01) and spleen (0·08 ± 0·03), but significantly lower in thymus (0·007 ± 0·001). Most (> 90%) thymus and cord blood NKT cells were CD4+, with CD4− NKT cells seen mainly in peripheral blood and spleen (Fig. 1). In contrast to findings in mice that blood NKT cells provide a poor measure of NKT cell frequency in spleen [18], we found that human spleen and blood had similar mean frequencies of NKT cells and of CD4+ and CD4− NKT cell subsets, although this applies

to group analysis, rather than to each individual donor. A recent publication identified diversity within CD4+, CD4− and CD8+ NKT cell subsets, but these cells had been expanded prior to analysis. We analysed cell surface antigen expression by CD4+ and CD4− NKT cell subsets without in-vitro expansion and compared blood-derived NKT cells to those from Selleckchem Lapatinib cord blood, thymus and spleen (Fig. 2). Many antigens were expressed differentially by the CD4+ and CD4− NKT cell subsets (Fig. 2a–j), including CD56 and CD161 (confirming these as ineffective surrogate markers for human NKT cells), with CD161 expressed more highly in peripheral blood and spleen HSP90 than cord blood or thymus. This confirms CD161′s status as a marker of NKT cell maturity [19, 22, 23]. Interestingly, CD161 was expressed by more CD4− than CD4+ NKT cells (Fig. 2a), which supports the hypothesis that comparatively immature precursors

of CD4− NKT cells are present within the CD4+ subset [22] [19, 23]. Our analysis did not identify any preferential surface antigen expression by either of the CD4+ or CD4 NKT cell subsets. CD8, CD45RA and CD94 were expressed typically by more CD4− NKT cells (Fig. 2i,j and data not shown), whereas CD62L, CD127 and LAIR-1 (Fig. 2c,d,b) were expressed by a higher proportion of CD4+ NKT cells. CD25, CD56, CD16, CD45RO, CD84, CCR7 and signalling lymphocyte activation molecule (SLAM) were expressed differentially by both CD4+ and CD4− NKT cell subsets, but the pattern of expression was similar for each subset (Fig. 2a–j and data not shown). NKT cells from thymus, cord blood, peripheral blood and spleen expressed similar levels of most antigens, although there were exceptions: CD4 was expressed by more NKT cells in thymus and cord blood, CD161 was higher in peripheral blood, CCR7 expression was lowest in peripheral blood and CD25 was highest in cord blood.


study reported that 745T and 1083C were associated with


study reported that 745T and 1083C were associated with increased IFN-γ or IL-2 levels after BCG vaccination [84], but the mechanism is still unclear (Table 1). TLR8 is located on X chromosome and able to recognize single-stranded RNA from pathogens such as RNA viruses. According to the literature, Davila et al. [85] first reported TLR8 SNPs, and they have analysed 149 SNPs from Indonesian and Russian pulmonary TB patients, of these four SNPs were significantly associated with the pulmonary TB among Indonesian and Russian males. Three of the associated TLR8 variants are −129 C/G, −2167 A/G and −1145 A/G present in the regulatory regions, and one variant 1 A/G (Met1Val) at the start codon. Indonesian males were carriers of Met1Val, allele A showed an increased susceptibility to pulmonary TB, While G allele shows protection from TB. Another study reported in Dinaciclib Turkish children [86] also showed an association with susceptibility to pulmonary TB among male children, but found no associations with −129 C/G SNP for TB susceptibility in children, whereas Davila et al. found a strong allelic association with minor allele C in susceptibility to pulmonary TB in males, but the mechanism through which

TLR8 recognizes M. tb and intracellular signalling remains unknown (Table 1). TLR9 composed of 2 exons and encodes 1032 amino acids [87]. It recognizes unmethylated CpG motifs in bacterial DNA. It Ferroptosis inhibitor drugs was found to be essential for cellular responses to mycobacterial CpG DNA [88]. In vitro studies showed that DCs release IL-12 in response to M. tb through TLR9 [89, 90]. A report demonstrates that TLR9-deficient mice are susceptible to Mtb infection, and mice lacking both TLR2 and TLR9 are more susceptible [89] to TB. Four SNPs, C-1486T, C-1237T, G+1174A and G+2848A, have been reported to show high heterozygocity among three major US ethnic groups [91]. C-1237T, a polymorphism Endonuclease located within the putative promoter region that may influence transcriptional regulation of the TLR9 gene.

SNP G+1174A, located in the intron of TLR9, showed a significant association with TB in Indonesian females [92]. Promoter polymorphisms, namely −1237C/T and −1486C/T, are not associated with pulmonary TB in south Indian population [93]. TLR9 activation is essential for the maintenance of M. tb Ag elicited pulmonary granulomatous response; however, the underlying mechanism is not known. SNPs in promoter region potentially affect gene expression levels by altering the binding of gene transcription factors and SNPs in introns, affecting mRNA splicing and/or enhancement of gene transcription. Carvalho et al. [94] reported that peripheral blood mononuclear cells (PBMCs) harbouring the -1237 TC genotype shown higher expression of both TLR9 and IL-6 and increased B-cell proliferation in response to CpG DNA, but the mechanism is not known (Table 1).

1c) As CD56dim NK cells are the major population

1c). As CD56dim NK cells are the major population MLN0128 cost of NK cells, it was not surprising to find

reduced numbers in the HIV-1 mono-infected group, mirroring the results obtained for total NK cells (Fig. 1b). Although previous studies have indicated an increase in the frequency of CD56neg NK cells in HIV-1-infected subjects,23 we did not observe either an elevated number (Fig. 1c) or an elevated frequency (data not shown) in this population of Brazilian subjects, either with or without concomitant HSV-2 infection. It is well established that NK cells are important in the immune response controlling herpesviruses. In particular, HSV pathogenesis in both humans and mouse models is enhanced in the absence of NK cells, when NK cell function is inhibited, or when innate accessory cells required for activation of dendritic cells (DCs), plasmacytoid DCs and macrophages IWR-1 chemical structure are absent or dysfunctional. In HIV-1 infection, alterations in the number and function of NK cells have been described previously.1,24–29 We evaluated the function of NK cells from HIV-1 mono-infected subjects,

HSV-2 co-infected subjects, and healthy HIV-1-seronegative controls. We stimulated PBMCs from these individuals by co-culture with the MHC class I-deficient K-562 erythroleukemia cell line.30 K-562 cells do not express MHC class I proteins (HLA-A, HLA-B, HLA-C, HLA-E or HLA-G) on their surface; therefore, they fail to express any known ligands for the inhibitory and activating KIRs. We detected an increased absolute number of degranulating NK cells, as indicated by levels of CD107 antibody staining (Fig. 2). The number of CD107+ NK cells in HSV-2 co-infected subjects was Vasopressin Receptor increased relative to HIV-1 mono-infected subjects in stimulated cultures (263 cells/μl versus 195 cells/μl, respectively; P = 0·018) and was not different from that in HIV-1-seronegative healthy control subjects. Furthermore, in cultures with no stimulation, the number of functional

NK cells was significantly depressed in HIV-1 mono-infected subjects compared with healthy control subjects (121 cells/μl versus 198 cells/μl, respectively; P = 0·007). We assessed the relationship between HIV-1 plasma viral load and the number of NK cells expressing the natural cytotoxicity receptors NKp30 and NKp46 in HIV-1 mono-infected and HSV-2 co-infected subjects (Fig. 3). Although there was no difference in the mean number or frequency of NKp30- or NKp46-positive cells between groups (Fig. 3a), or in HIV-1 plasma viral load (Fig. 1a), an inverse correlation was observed in HIV-1 mono-infected subjects for both NK cells receptors (Fig. 3b,c). This correlation was not observed in HSV-2 co-infected subjects. In HIV-1 mono-infected subjects, this inverse correlation was significant for NKp46 (P = 0·046).

Overall, these results suggest that mCRAMP also functions in the

Overall, these results suggest that mCRAMP also functions in the regulation of Th2 IL-4-producing cell differentiation. The role of mCRAMP during an antibody response

to TI and TD antigens has not been fully investigated. Since B cells express Camp/mCRAMP and Camp is rapidly upregulated following B-cell activation, the possibility exists that mCRAMP directly regulates B cells during an antibody response. Furthermore, since LPS induces class switching to IgG3 34 and IL-4 induces class switch recombination (CSR) to IgG1 and IgE 31, and IFN-γ induces CSR to IgG2a/2c 35, respectively, we hypothesized that mCRAMP mRNA upregulation during activation with these factors might affect the levels of specific antibody isotypes produced. Resting splenic B cells were sort-purified from WT and Camp−/− mice and activated in vitro in the presence of LPS, CD40L/IL-4, selleck compound AZD2014 in vitro and CD40L/IFN-γ. WT and Camp−/− B cells produce similar amounts of IgM (Fig. 3A) and IgG3 (Fig. 3B) in response to LPS stimulation, while CD40L/IFN-γ induced equivalent amounts of IgG2c (Fig. 3C). However, Camp−/− B cells produced significantly less IgG1 (Fig. 3D) and IgE (Fig. 3E) in response

to CD40L/IL-4 when compared with WT B cells. To determine whether mCRAMP directly mediated these effects in vitro and the optimal peptide concentration, mCRAMP peptide (1 ng/mL–1μg/mL) was added to Camp−/− B-cell cultures on day 0 with CD40L/IL-4 and the level of IgG1 was measured on day 5. The addition of mCRAMP resulted in a dose-dependent increase in IgG1 with an optimal concentration of 100 ng/mL (Fig. 3F). Camp−/− B cells cultures were repeated with the addition of 100 ng/mL of mCRAMP and the level of IgG2c (Fig. 3C) was unchanged while IgG1 (Fig. 3D) and IgE (Fig. 3E) returned to WT

levels. Overall, these results suggest that mCRAMP functions to positively regulate the level of antibody produced by B cells in an IL-4-dependent manner. The mechanism by which Camp−/− B cells produce less IgG1 in comparison to WT B cells could be explained by a number of factors including differences in proliferation, survival, and CSR. To determine the mechanism by which Camp−/− B cells produce less IgG1, resting B cells were sort-purified and activated with CD40L/IL-4 or LPS/IL-4. The total live CYTH4 B-cell number (Fig. 4A), the percentage of surface IgG1+ B cells (Fig. 4B), and the cell cycle analysis (data not shown) were determined, showing no difference between WT and Camp−/− B cells. ELISpot experiments were performed on day 5 B-cell cultures and spots were enumerated to determine the number of IgG1-secreting B cells. Total spot counts were equivalent between WT and Camp−/− B cells (Fig. 4C), suggesting that CSR is not affected. However, visual inspection of the spot size of WT B cells appeared larger than that of Camp−/− B cell spots. Total ASC spots were dissolved with DMSO and the absorbance was measured at 650 nm (Fig. 4D), showing a significant decrease in absorbance in the Camp−/− B cells.

The FGF-23 holds some promise as a novel marker of CKD-MBD, parti

The FGF-23 holds some promise as a novel marker of CKD-MBD, particularly in early CKD, and as a potential tool to monitor the efficacy for therapies used to treat this disorder. The significance and potential role of FGF-23 in clinical practice needs to be established, with large, prospective, clinical trials. These will determine whether FGF-23 is a more useful biomarker

of CKD-MBD when compared with phosphate or PTH. MD would like to acknowledge learn more the support of the Royal Australasian College of Physicians Research Foundation and the Jacquot Awards. “
“Aim:  There is limited data concerning the impact of recipient body mass index (BMI) on graft outcome in Asian renal transplant recipients. The aim of this study is to identify whether obesity (BMI ≥25 kg/m2) and overweight (BMI ≥23 kg/m2) can predict graft outcome. Methods:  This is a single-centre retrospective study. All patients who received kidney transplantation between 1997 and 2005 were recruited. Patients were categorized according to two different designated BMI cut-off values. Results:  One hundred and thirty-one patients were recruited with a median follow-up duration of 73 months. If a BMI cut-off mTOR inhibitor value of 25 kg/m2 was used, 86.3%

patients were classified as non-obese and 13.7% as obese. Obesity was significantly ID-8 associated with poor renal graft function and decreased patient and graft survival. On the other hand, 34.3% patients were classified as overweight and 65.7% patients as normal if a BMI cut-off value of 23 kg/m2 was used. Overweight was significantly associated with a lower glomerular filtration rate only. Cox regression analysis showed that obesity (odds ratio (OR) = 3.09), acute rejection (OR = 5.68), pre-transplant diabetes mellitus (OR = 3.21) and age of recipient (OR = 1.06) were all significant independent risk factors associated

with graft failure. Conclusion:  Recipient BMI ≥25 kg/m2 is a significant predictive factor for long-term renal graft outcome in the Asian population. With the introduction of new immunosuppressive agents, the risk of acute rejection in renal transplantation has been significantly reduced. Much of the focus nowadays has shifted to prolong graft survival. Obesity had been linked with an increased incidence of proteinuria, hypertension, hyperlipidaemia, diabetes mellitus (DM) and focal segmental glomerulosclerosis (FSGS) in the general population.1 On the other hand, the impact of recipient obesity on patient and renal allograft survival is controversial. Higher body mass index (BMI) has been shown to be associated with increased risk for graft failure and patient death among white patients with end-stage renal disease who undergo renal transplantation.

22–24 Conversely, skin-derived DCs were shown to induce E- and P-

22–24 Conversely, skin-derived DCs were shown to induce E- and P-selectin ligands that are associated with homing to the skin.24,25 The capacity of DCs to instruct T-cell homing properties is related to their ability to produce active metabolites from tissue-derived factors.

Gut-derived DCs produce retinoic acid, which leads to imprinting of the gut-homing phenotype and suppression of the Opaganib skin-homing phenotype on T cells.26 Similarly, the active form of vitamin D3, 1,25(OH)(2)D(3), which is produced by skin DCs, induces T-cell expression of the skin-selective chemokine receptor CCR10, while inhibiting the expression of gut-homing receptors α4β7 integrin and CCR9.27 Interestingly, recent data also suggest that the DCs are not the starting point but are instructed by local stromal cells.28,29 Albeit the induction of a specific homing phenotype in primed T cells has been occasionally referred to as ‘imprinting’,23 recent data have rather challenged SRT1720 nmr the concept of permanent imprinting and

favour the assumption of flexibility in the expression of homing receptors.25 Hypothetically, organ-specific homing could also be explained by continuing selection or re-induction of a given receptor upon recirculation through selected tissues providing antigen-exposure and organ-specific co-signals.30 Efforts to demonstrate the stability of differentially expressed homing receptors in vivo have been made only recently. The expression of ligands for E/P-selectins that serve medroxyprogesterone as homing receptors for inflamed skin has been shown to persist for at least several weeks in vivo

only on a subfraction of T cells. However, upon repeated stimulation under ligand-inducing conditions (presence of IL-12), the stable fraction was increased, and ex vivo isolated selectin-ligand-positive effector/memory cells turned out to be almost completely stable.31 This shows that imprinting of a stable homing phenotype appears possible, but requires repeated stimulation under permissive conditions, similar to findings for the imprinting of a cytokine memory in T cells.32 The above-mentioned studies on the mucosal homing receptor α4β7 in CD8+ T cells suggested that expression of this receptor is not permanent after initial induction.25 In CD4+ T cells, repeated stimulations in the presence of retinoic acid were found to result in a largely persistent expression of α4β7, and, again, ex vivo isolated α4β7-high memory CD4+ cells remained positive for weeks after adoptive transfer (B. Szilagyi and A. Hamann, unpublished). In contrast, stable expression of the chemokine receptor CCR9, which is also induced on CD8+ cells by retinoic acid and considered to contribute to mucosal homing, was not observed (Mora et al.23 and B. Szilagyi and A. Hamann, unpublished).

Conclusion:  This registry analysis suggests that IL-2Ra inductio

Conclusion:  This registry analysis suggests that IL-2Ra induction may be associated with

a reduction EX 527 datasheet in rejection risk in cyclosporine-treated intermediate immunological risk recipients, but not in low-risk renal transplant recipients. Renal allograft outcomes have been improving over the last 10 years, perhaps related to improved immunosuppression and reduced acute rejection rates.1 Acute rejection, an important determinant of graft survival, occurs commonly in the early post-transplant period, but the incidence has decreased significantly over recent years.2 Antibodies designed to inactivate interleukin-2 receptor antibody (IL-2Ra) on T cells such as basiliximab are often used as induction therapy in immunosuppressive protocols to reduce the risk of acute rejection or to delay the introduction of calcineurin inhibitor (CNI) in those at high risk of delayed graft function.3,4 The effectiveness of IL-2Ra in reducing the risk of acute rejection is well established in deceased- and live-donor kidney transplantation.5,6 Unlike T-cell depletive therapies, IL-2Ra

is not associated with increased infection- or cancer-related morbidity and mortality.7–9 The use of IL-2Ra has been steadily increasing in Australia such that IL-2Ra induction therapy was used for >50% of new renal transplant recipients in Australia by 2005.10,11 Although the efficacy of IL-2Ra in reducing the risk of rejection is well established in renal transplant recipients, the effectiveness of this agent in renal transplant recipients with differing immunological risk remains unclear.10,12,13 The aim of the present

study is to evaluate the efficacy of IL-2Ra induction on allograft outcomes including acute rejection, glomerular filtration rate (GFR), graft and patient ID-8 survival in renal transplant recipients of low and intermediate immunological risk, and when stratified by initial immunosuppression. Using the Australia and New Zealand Dialysis and Transplant (ANZDATA) Registry, all live- and deceased-donor renal transplant recipients in Australia from 1995 to 2005 were included in this study. Follow up was censored at 31 December 2006. Recipients were arbitrarily divided into low immunological risk (primary grafts with ≤2 human leucocyte antigen (HLA)-mismatches and panel-reactive antibody (PRA) < 10%) or intermediate immunological risk recipients (i.e. subsequent grafts or >2 HLA-mismatches or PRA > 25%). Multiple-organ graft recipients, recipients’ age less than 16 at time of transplant and recipients initiated on corticosteroids or CNI-free immunosuppressive regimens were excluded from the study. In addition, recipients who had received induction monoclonal or polyclonal T-cell depletive agents were also excluded.

A significant increase of newly produced proliferating CD34+ eosi

A significant increase of newly produced proliferating CD34+ eosinophil-lineage-committed cells in vivo after allergen exposure (compared with the saline-exposed animals) was identified. It is noteworthy that almost all lung cells that stained positively for CCR3 FK506 molecular weight also co-expressed MBP, which further argues for the eosinophil-lineage commitment of these CD34+ CCR3+ cells. In addition, we cultured CD34+ lung cells to assess their capacity to form CFUs in vitro after incubation with rmIL-5 alone, rmEotaxin-2 alone, or with the combination of rmIL-5 and rmEotaxin-2. Surprisingly, a significant increase in CFUs

compared with control was found in all three groups, arguing that eotaxin-2 itself can function as an eosinophilopoietic factor in the lung, expanding the previous findings that lung progenitors

can produce IL-5-dependent CFUs in vitro.9,24 Studies in humans have suggested a role of eotaxin-1 in the differentiation of CD34+ cells towards eosinophils because cord-blood-derived CD34+ cells cultured in the presence of eotaxin-1 differentiate into eosinophils.21 Furthermore, we have previously shown that CD34+ cells release markedly more IL-5 compared with the CD34− eosinophils, suggesting that the airway CD34+ cells may play an autocrine role in their final maturation to eosinophils.9 In contrast, we were unable to detect any colony formation of BYL719 price BM CD34+ cells that were incubated with eotaxin-2 alone, suggesting that this chemokine only has haematopoietic function outside the BM. Taken together, these findings suggest that allergen-induced haematopoietic events do occur in the lung during allergen exposure, and that eotaxin-2 has haematopoietic effects alone or together PDK4 with IL-5, primarily within the airways, whereas IL-5 has haematopoietic effects in the BM as well as in the lung. CD34+ progenitors

that co-express IL-5Rα are considered to be the earliest eosinophil-lineage-committed progenitor cell.4 CD34+ IL-5Rα+ cell numbers are increased in the mucosa of patients with atopic asthma compared with controls and CD34+ IL-5Rα+ as well as CD34+ CCR3+ cells have been shown to increase in BM, circulation and induced sputum in patients with allergic asthma compared with controls.4,12–14,36,37 The present study show that CD34+ CD45+ IL-5Rα+ eosinophil progenitors are increased in the airways after allergen exposure, confirming previous published data in mice and humans.4,22,36,37 However, we also demonstrate a significant increase in the proliferating IL-5Rα+ cells in vivo in the lung after allergen challenge. It is important to note that most of the IL-5Rα+ cells in the airways of allergen-exposed mice also co-expressed CCR3, which implies that these receptors may have complementary functions in the lung CD34+ cells.

For these reasons, useful

For these reasons, useful BTK inhibitor classification tree models and diagnostic models have been promptly built up by this technique in several medical realms such as cancer, autoimmune disease, haematological disease and mental diseases [16–19]. In our study, we used the data of a training set to construct a classification tree model that help accurately discriminate patients with active TB from patients with other respiratory diseases and healthy people, and then we applied this model to a test set to verify its performance of classification. Patients.  According to the case definitions described elsewhere, 75 patients

with active TB (active TB group) and 103 individuals (non-TB group) including 43 patients with common respiratory diseases (CRD subgroup) and 60 healthy controls (HC subgroup) were recruited from 309th hospital of Chinese PLA. These patients were randomly divided into two sets: a training set and a test set. Our study was approved by the ethics committee of Peking Union Medical College Hospital, and informed consent was obtained from each patient and volunteer. Case definitions.  Diagnosis INCB018424 concentration of active TB was based on several criteria as follows: (1) sputum smear positive of

acid-fast bacilli or culture positive of M.tb, (2) positive TST, (3) specific symptoms such as persistent cough, weight loss, and night sweats and (4) characteristic changes of chest X-ray (CXR) like lung with cavities in upper lobes. Sputum smear-positive TB (SPP-TB) and smear-negative TB (SNP-TB) patients were classified according to widely accepted criteria [20], and all patients with SNP-TB were ultimately confirmed if their symptoms and CXR turned better after 3 months of anti-TB treatment. TST was performed on active TB group in their first visit according to standard intradermal

Mantoux test with 5 IU purified protein derivative of Bacillus Calmette-Guerin (BCG) (Chengdu institute of biological product, Sichuan, China) and read after 72 h. An induration of ≥5 mm is considered a positive test [21]. Anyone who met the criteria above or had a history of contact with active TB patients was excluded from the non-TB Dehydratase group. To rule out latent patients with TB from this group, individuals that have received BCG vaccination before should be negative in IGRA (QuantiFERON®-TB Gold in Tube; Cellestis, Carnegie, Vic., Australia), which was performed according to the manufacturer’s instructions (cut-off value ≥ 0.35 IU/ml), and other individuals in the non-TB group should be negative of TST. In CRD subgroup, patients with lung cancer and sarcoidosis were diagnosed according to their biopsy evaluation, while patients with pneumonia, COPD, and bronchiectasia were diagnosed based on their clinical manifestations, radiographic features and prompt clinical response to regular therapy.