Unless otherwise noted, such pairwise comparisons were made between infected pregnant and uninfected pregnant; and between infected pregnant and infected non-pregnant mice within strains; and between infected pregnant mice and infected non-pregnant mice across strains. Pregnancy outcome data were analysed by Fisher’s exact test or chi-squared test as appropriate. Differences with P < 0·05 were considered significant. In agreement with previous studies of virgin mice (15,24), pregnant A/J mice were susceptible to a lethal infection with P. chabaudi AS, whereas B6 mice were resistant (20). Among A/J mice, 100% of infected pregnant mice died by experiment day

12 (n = 7; Figure 1a) whereas B6 mice were resistant, with only 1 of 6 mice succumbing by experiment day 12 (Figure 1a). Because the interest of the study was to evaluate mid-gestational pregnancy outcome in both strains, serial sacrifices were subsequently performed up Ulixertinib supplier to experiment day 11. In A/J mice, a maximum peripheral parasite density of 39 ± 2% (mean ± SEM; n = 21) was observed Sirolimus in vivo in the infected pregnant group at experiment day 11, while the peak parasitemia for infected pregnant

B6 mice occurred on experiment day 10 at 25 ± 3% (n = 16; Figure 1b), a level significantly lower than in A/J mice. Consistent with previous reports (25,26), parasitemia was also significantly higher in infected non-pregnant A/J mice on experiment

day 9 through 11 relative to infected non-pregnant B6 mice (data not shown). Moreover, peripheral PRKACG blood parasite density was significantly higher in pregnant A/J mice relative to non-pregnant mice at experiment day 6 (0·5 ± 0·2% (n = 64) vs. 0·1 ± 0·0% (n = 104), respectively; P = 0·03) and at peak parasitemia (39·1 ± 1·9% (n = 21) vs. 33·4 ± 1·8% (n = 27), respectively; P = 0·04; Figure S1), suggesting that, as in B6 mice (20), pregnancy increases the susceptibility of A/J mice to malaria. While anaemia was not observed in uninfected pregnant A/J and B6 mice, haematocrit was substantially reduced over time in infected pregnant (Figure 1c) and infected non-pregnant (Figure S1 and data not shown; (20) mice of both strains. On experiment day 11, haematocrit in infected pregnant A/J mice was significantly lower than in infected pregnant B6 mice (Figure 1c). As expected in normal pregnancy, uninfected pregnant A/J and B6 mice gained weight over the course of the experiment (Figure 1d). In contrast, infected pregnant mice of both strains did not experience significant weight gain, and starting at experiment day 9, body weights fell steadily with reductions to below starting body weight at experiment day 11 (Figure 1d) (20). From experiment days 9 through 11, mean body weight was significantly lower in infected pregnant relative to uninfected pregnant mice for both strains (P < 0·05).

The responses to stimulation with TLR ligands further revealed the difference between the two groups of differentiated BMDC. The BMDC exposed to rHp-CPI during its differentiation showed significantly lower percentages

of CD40+, CD86+ and MHC-II+ selleck compound cells and IL-6, IL-12p40 and TNF-α cytokine production when stimulated with TLR9 ligand CpG compared with the BMDC that were not exposed to rHp-CPI. Interestingly, the two groups of BMDC generated with or without exposure to rHp-CPI respond in similar manners to stimulation with TLR4 ligand LPS. It is known that a number of cysteine proteases are involved in signalling pathways associated with some TLRs. Proteolytic cleavage of TLR9 by cathepsins is required for TLR9 signalling. The BMDC from cathepsin L-deficient and S-deficient mice

showed impaired responses to stimulation with CpG, but the response to LPS stimulation remained unchanged www.selleckchem.com/products/jq1.html compared with the BMDC from normal wild-type mice.[37] Our results that BMDC generated in the presence of rHp-CPI exhibit impaired responses to CpG stimulation, but showed unchanged responses to LPS stimulation, are consistent with the observations made on BMDC from cathepsin-deficient mice. We then further analysed the modulatory effects of rHp-CPI on differentiated immature BMDC and observed that rHp-CPI treatment alone had no significant effect on DC activation, as shown by the expression of CD40, CD80 and CD86 that was comparable with those detected on control BMDC. In addition, rHp-CPI treatment alone failed to induce production of IL-16, IL-12p40 and TNF-α. These results indicate that the rHp-CPI protein of parasite origin has a negligible effect on differentiated immature

BMDC. However, it was observed that rHp-CPI modulates the responses of immature BMDC to stimulation with LPS and CpG. Treatment of immature BMDC with rHp-CPI reduced the CD40 and CD86 expression and IL-6 and TNF-α cytokine production by immature BMDC induced by stimulation with CpG. Treatment with rHp-CPI also suppressed the expression of CD80 and MHC-II molecules and IL-6 production of heptaminol BMDC induced by LPS stimulation. These results suggest that rHp-CPI modulates the TLR-associated signalling pathways differently at the different stages of BMDC development. In addition to the modulation effects on responses to stimulation with TLR-associated signalling pathways, rHp-CPI treatment also resulted in impaired antigen-presenting function of BMDC. Cysteine proteases in endosomes and lysosomes of antigen-presenting cells are known to be involved in the processing of protein antigens and MHC-II molecule maturation. Cathepsin S plays an important role in stepwise proteolytic degradation of the invariant chain (Ii) that regulates MHC-II molecule intracellular trafficking and protects the MHC-II molecule from premature binding of antigen peptide.

Indeed, the causative or the correlative relation between changes in lung mycobiota and disease onset

needs to be proven by expanding the number of samples and moving forward the study from the species to the strain level. The human Fulvestrant research buy GI tract is known to contain a variable fungal microbiota, but the phylogenetic characteristics of those fungal microorganisms and their specific roles as part of the GI tract ecosystem have not yet been studied extensively. Despite its harsh environment, the stomach harbors a microbiota that can include Lactobacillus, Helicobacter, and Candida spp. [147]. Candida colonization of the GI tract of mice has been shown to drive allergic sensitization to food Ags by affecting the mucosal barrier [148]. In particular, intragastrically inoculated mice were administered with OVA to assess Ag sensitization and GI permeability, and anti-OVA Ab titers and plasma concentrations of OVA were measured weekly. The authors showed that C. albicans promoted allergic sensitization was due to mast cell mediated hyperpermeability in the GI mucosa [148]. In healthy human volunteers, another

group carried out both FK506 concentration culture-independent analyses, based on DNA extraction and PCR targeting of both total eukaryotic 18S rRNA genes and fungal ITS, together with culture-dependent analyses of fungi [19]. This study found that the eukaryotic diversity of the human gut is low, largely temporally stable, and dominated by various subtypes of Blastocystis and Candida [19]. The low diversity is likely an artifact due to the fact that the most abundant species occur in the cultivable fraction, particularly Candida spp. The culture-independent analysis revealed a greater number of genera, such as Gloeotinia/Paecilomyces and Galactomyces,

suggesting the importance of using culture-independent surveys to assess species composition [19]. An example of the large variability of the human gut mycobiota was recently provided by a study Methamphetamine of four children and their respective mothers, which reported that infants harbor Saccharomyces spp. as opposed to Candida as the most frequent fungal species in the gut (36%) with respect to their mothers [149]. Whether S. cerevisiae is present in the human gut at birth remains to be elucidated. It is possible that yeasts simply reach the GI tract through food. Fermented foods and beverages containing eukaryotic species such as bread, beer, and wine are consumed on a daily basis, providing ready inocula for the host [19]. Alternatively, it is possible that differences in fungal colonization are related to differences in the genetic makeup of the host or differences in gut permeability. The numerous and diverse interactions between fungi, bacteria, and immune responses can significantly impact gut health and likely contribute to the pathobiology of GI disorders from irritable bowel syndrome to IBD.

Given the basic assumption that ethnic groups residing in Arctic areas have more general and local cold exposure than ethnic groups who reside in

tropical areas, this may have resulted in genetic or functional adaptations over the course of their ancestry. Therefore, it is worthwhile to look at racial differences in local responses to cold. Many of the early studies on cold tolerance employed a cross-sectional approach comparing nonadapted controls with a population living or working in cold environments. Alternatively, if the control group could be drawn from individuals of similar ethnicity, it CH5424802 price can be assumed that the primary difference is in environmental exposure rather than in genetic differences. In support of CIVD being a protective response, humans living in or native to a cold environment seems to have enhanced CIVD, marked by shortened onset times and higher amplitudes, compared with tropical or nonadapted

Selleckchem EMD 1214063 individuals. For example, Arctic natives such as Inuit and Lapps generally have higher mean finger temperatures and CIVD responses compared with control populations from more temperate regions [12,45,56]. Negroid subjects are known to have lower finger skin temperatures during CIVD than Caucasians [54]. Leblanc et al. [47] observed no differences in skin thickness or cell size between skin biopsies of fishermen and controls; however, the fishing group had a greater number buy 5-FU of mast cells in the skin. Mast cells are present in several types of tissues, and contain many granules rich in histamine; H2 histamine receptors are located in smooth muscle cells, and cause a strong vasodilation when stimulated. Again, it is not known if these differences were inherited or acquired. Some ethnic groups continued to be exposed to local and whole body cold for centuries, like the Inuit, whereas other ethnic groups were mainly exposed to heat. Early population-based research demonstrated that Arctic residents have a better CIVD response than non-Arctic residents [12,45,56]. Even though the fingers

are relatively shorter and thicker for people living close to the poles [2,48], providing less biophysical [62] surface area for heat exchange, the fingers nevertheless seem to be able to lose more heat to the environment when exposed to severe cold. Locations where CIVD is observed coincide with the presence of AVAs in the human skin [7]. These AVAs contain alpha-2 receptors and are under powerful sympathetic control; when CIVD occurs, the strong muscle wall of the AVA suddenly relaxes. Hale and Burch [39] reported that AVAs form when there is a higher need for blood flow in the finger. However, the magnitude of this response is very small: 95% of the AVAs remain unchanged and the stimulus for AVA formation has to be severe, for instance, strong ischemia followed by hyperemia.

Undoubtedly, the most studied factor in Echinococcus is the so-called antigen B (AgB), a highly immunogenic lipoprotein and major component of hydatid cyst fluid (94). Although

there are several reports on Erastin solubility dmso immunomodulatory properties of AgB in vitro (94), and biochemical investigations that demonstrate binding of different hydrophobic ligands to AgB (95), the precise function of this protein in the biology of Echinococcus or in the immune response during echinococcosis is still unknown. Originally described as a 160 kDa lipoprotein, AgB was later shown to be built up of several 8 kDa monomers that are encoded by a gene family (96), and since the first full description of an AgB-encoding gene by Frosch et al. (97), there has been constant debate on how many of these genes are actually Selleckchem Panobinostat expressed in these parasites. By studies of Fernandez et al. (98), Chemale et al. (99), Arend et al. (100) and Mamuti et al. (101), the number of AgB subunit genes had grown to five in 2007 (named EmAgB1-EmAgB5 in E. multilocularis and EgAgB1-EgAgB5 in E. granulosus), whereas genomic Southern blot analyses indicated that there are at least seven loci

(102). Studies by Haag et al. (103) and Arend et al. (100) even suggested the presence of further AgB genes (up to 10 in E. granulosus and up to 110 copies in the related E. ortleppi) as well as a high degree of genetic polymorphism among those genes (even within protoscoleces that derived from one single cyst). These authors proposed that numerous AgB copies might be involved in gene conversion mechanisms through recombination processes and DNA rearrangements similar to the situation in protozoans such as Plasmodium sp. or trypanosomes (103). This theory was recently contradicted by Zhang et al. (104) who characterized AgB genes in E. granulosus isolates from different geographic origins and proposed the presence of 10 unique genes (or alleles) that are, however, highly homologous between these isolates and did not

show gross polymorphisms. To shed more light on the situation, we have BCKDHA analysed the presence and location of AgB genes in the current assemblies of the E. multilocularis and E. granulosus genomes. As described by Brehm (72), using the first assembly version of the E. multilocularis genome (19 000 contigs), a total of seven AgB loci appears to form a cluster on a distinct region of the genome. In the latest genome version (600 supercontigs), all these copies are now assembled into one continuous sequence fragment of 57 kbp that is present on scaffold_29 (Figures 2 and 3). The antigen B cluster is flanked by two genes, EmLDLR and EmMTA, which are highly conserved among cestodes.

Critically for clinical value, this vaccine design has also been demonstrated to induce durable epitope-specific CTL responses against tolerized antigens 27–29, and it is now in several clinical trials. The availability of third generation MHC class I-transgenic mice expressing the human HLA-A2 molecule (HHD mice) provides a powerful tool for the investigation

of both induction and performance of CD8+ T cells recognizing human HLA-A*0201-binding epitopes 30, 31. Trametinib cost In the present study, we investigated the ability of three PSMA-derived HLA-A*0201-binding epitopes, delivered as p.DOM-epitope vaccines, to prime CD8+ T cells in the HHD transgenic mice. We show that, in sharp contrast to full-length PSMA-encoding vaccines, all three p.DOM-PSMA epitope vaccines generated CD8+

T-cell responses. However, the key point is that the target peptides must be naturally presented by PSMA-expressing tumor cells. This has not been clear in the past since most strategies have used human CD8+ T cells expanded in vitro with candidate MAPK Inhibitor Library nmr peptides. By this approach, PSMA27-specific T cells showed weak but definite killing of PSMA-expressing LNCap prostate tumor cells 32. The same study reported that PSMA663 and PSMA711-specific CTLs appeared unable to kill the target cells, suggesting that these peptides were not efficiently processed and presented. However, processing of PSMA663 and possibly PSMA711 was observed subsequently 33. The divergent evidence Avelestat (AZD9668) on the processing

status highlights the difficulties in using human CD8+ T cells expanded in vitro, making decisions about potential peptide targets for vaccination difficult. Testing in the “humanized” model now reveals that T cells specific for PSMA27 and PSMA663, but not PSMA711, could specifically kill PSMA-expressing tumor cells in vitro and in vivo, thereby providing evidence for efficient processing and presentation of these two epitopes. Data on p.DOM-PSMA27 provide validation of the clinical trial in patients with PCa, where induction of CD8+ T-cell responses in the majority of vaccinees is evident 34. Three DNA fusion vaccines encoding PSMA-derived peptide epitopes were constructed according to the previously described vaccine design 26. Each vaccine encoded the first domain of FrC from TT, DOM, genetically fused to a discrete human PSMA HLA-A*0201-binding epitope, to create the p.DOM-PSMA27, p.DOM-PSMA663, and p.DOM-PSMA711 vaccines. The DOM sequence encodes the p30 promiscuous helper T-cell epitope that provides linked T-cell help for the vaccine response. DNA vaccines encoding the full-length human PSMA protein which contains all three epitopes were also constructed for comparison, either alone (p.PSMA) or fused to DOM (p.PSMA-DOM) (Fig. 1A).

v. Extremely useful (A) Moderately useful (B) Mildly useful (C) Not useful at all (D) Agammaglobulinaemia XLA Ataxia telangiectasia Chronic granulomatous disease Chronic mucocutanous candidiasis CVIDs Complement deficiency DiGeorge syndrome Hyper-IgM syndromes Hyper-IgE syndrome IgG subclass deficiencies Selective IgA deficiency SCID Severe congenital neutropenia Specific antibody deficiency IFN-γ/IL-12 cytokine axis

defect Wiskott–Aldrich syndrome XLP ____________________________ at a dose of ________mg/kg every ______• PS-341 research buy hours • days ____________________________ at a dose of ________mg every ______• hours and for • days MARK AS MANY AS APPLY MARK AS MANY AS APPLY MARK AS MANY AS APPLY _____________________________ _____ YEAR Please try to answer all questions to the best of your ability based upon your average approach to the ‘typical’ patient with PID. If you have specific additional concerns or comments regarding a particular question you may list them below (or separately). Question concern ____________________________ ____________________________ ____________________________ ____________________________ Geographic distribution of ESID respondents “
“For long-term attack on tumor cells in patients with prostate cancer, induction of cytolytic T cells is desirable. Several lineage-specific

target proteins are known find more and algorithms have identified candidate MHC class I-binding peptides, particularly for HLA-A*0201. We have designed tolerance-breaking DNA fusion vaccines incorporating a domain of tetanus toxin fused to candidate tumor-derived

peptide sequences. Using three separate peptide sequences from prostate-specific Neratinib mw membrane antigen (PSMA) (peptides PSMA27, PSMA663, and PSMA711), this vaccine design induced high levels of CD8+ T cells against each peptide in a HLA-A*0201 preclinical model. In contrast, the full-length PSMA sequence containing all three epitopes was poorly immunogenic. Induced T cells were cytotoxic against peptide-loaded tumor cells, but only those against PSMA27 or PSMA663 peptides, and not PSMA711, were able to kill tumor cells expressing endogenous PSMA. Cytotoxicity was also evident in vivo. The preclinical model provides a powerful tool for generating CD8+ T cells able to predict whether target cells can process and present peptides, essential for planning peptide vaccine-based clinical trials. Prostate cancer (PCa) is the second most common cause of male cancer death in the UK and USA. Although current treatment can cure localized disease, many patients will have occult micrometastases that lead to subsequent relapse and development of detectable metastatic disease 1. Patient groups at risk could benefit from activating immune attack early against undetected, residual cancer cells using specific vaccines.

The H.c-C3BP is a new entity as it differs biochemically from other known such proteins. The significance of H.c-C3BP is discussed

in relation to host–parasite interaction. Acrylamide, bis-acrylamide, PMSF, diaminobenzidine (DAB), orthophenyl diamine (OPD), CNBr-activated Sepharose 4B and goat anti-human C3 polyclonal antibody were procured from Sigma–Aldrich (Karnataka, India). Lysozyme, protein molecular weight markers, goat anti-rabbit IgG–horse radish peroxidase conjugate, rabbit anti-goat IgG–horse radish peroxidase and isopropyl thio-D-galactopyranoside were purchased from Bangalore Genei (Bangalore, India). Ni-charged resin, nitrocellulose membranes and sodium dodecyl sulphate were purchased from Bio-Rad laboratories this website (Mumbai, India); rabbit anti-human MAC (C5b-9) antibodies were purchased from Calbiochem (La Jolla, CA, USA) and rabbit anti-human glyceraldehyde-3-phosphate dehydrogenase was procured from Santa Cruz Biotechnology Inc. (Dallas, TX, USA). All other chemicals used were of analytical grade. Sheep and goat abomasums (stomach) were procured from local abattoir; the adult worms were picked up manually and washed several times with prewarmed saline. The excretory–secretory products (ES products) were collected

Birinapant nmr by culturing the adult parasites in RPMI 1640 medium without phenol red containing streptomycin 0·1 mg/mL and penicillin 100 IU (~20 worms per mL of the medium) at 37°C for 6–8 h in a candle jar [10, 11]. The ES products and the adult worms recovered after incubation were stored at −40°C. The infective-stage larvae (L3) of H. contortus were

recovered by mild crushing of the adult parasites and layering the extract over a mixture of autoclaved goat faecal matter and powdered charcoal (3 : 2 w/w) kept on a moistened filter paper in a Petri dish. The Petri dish was kept in a bigger Petri dish containing sterilized distilled water. This assembly was covered with a glass jar and kept at room temperature Bay 11-7085 (25–30°C) with provision for aeration. The larvae, which emerged and were collected in the water reservoir after 5–7 days, were concentrated by filtration through a Whatman No.1 filter paper. The adhered larvae were flushed by dipping the paper in small volume of distilled water and stored at −40°C. Complement C3 was purified as described earlier [15] with modifications. Goat blood was collected in citrate saline. About 120 mL of plasma was treated with 14 mL of 40% PEG-8000 drop wise (~4% (w/v) final concentration). The suspension was centrifuged at 10 000 g for 30 min at 4°C. The supernatant was collected, and 30 mL of 40% PEG was added to increase its concentration to 10% (w/v). It was left overnight at 4°C for precipitation of the C3 protein. The precipitates were collected by centrifugation and dissolved in PBS with stirring to break lump pieces. The solution was dialysed against 20 mm sodium phosphate (pH 7·4) containing 5 mm EDTA.

Metabolic parameters at baseline were compared with 20 non-CKD adults. The primary outcome was an improvement in insulin resistance (glucose disposal rate, GDR) at 6 months (quantified by hyperinsulinaemic euglycaemic clamp). Carbohydrate and 26s Proteasome structure lipid oxidation rates were assessed by indirect calorimetry. At baseline, patients were significantly insulin-resistant compared with lean younger non-CKD individuals (n = 9; GDR 3.42 vs 5.76 mg/kg per minute, P = 0.001), but comparable with their age-, gender- and weight-matched non-CKD counterparts (n = 11; 3.42 vs 3.98 mg/kg per minute, P = 0.4). 25-Hydroxyvitamin D did not change in the placebo group, but rose from 95 ± 37 to 146 ± 25 nmol/L with treatment (P = 0.0001).

Post treatment, there was no difference in GDR between groups (GDR 3.38 vs 3.52 mg/kg per minute, ancova P = 0.4). There was a relative increase in hyperinsulinaemic oxidative disposal of glucose with treatment (within-group P = 0.03). Supplementation with cholecalciferol in CKD 3–4 results in appreciable increases in 25-hydroxyvitamin D concentrations, but does not increase insulin sensitivity. The insulin resistance observed was

similar among age-, sex- and body mass index-matched individuals with and without CKD. Whether renal dysfunction per se has any influence on the insulin sensitivity of an individual should be the subject www.selleckchem.com/products/Trichostatin-A.html of future work. “
“Although asymptomatic gross haematuria (GHU) is relatively common in children, its causes and clinical outcomes are not clearly defined. Children with asymptomatic GHU were examined and work-up was performed. Patients with recurrent GHU with proteinuria, or significant proteinuria, were considered for renal biopsy. The male : female ratio of all patients was 190:75, and the median age at onset of GHU

was 6.4 years. Patients were grouped according to abnormalities on initial evaluation as follows: idiopathic (50%), proteinuria (21%), hypercalciuria (14%), sonographic abnormality (7%), hypocomplementaemia (4%), familial (3%), and bleeding tendency (2%). Of patients with idiopathic GHU, 38% had a single episode, and of these, 34% had persistent microscopic haematuria, which resolved on follow-up. Late onset proteinuria these was accompanied in 11% of patients with recurrent GHU. Nutcracker syndrome was diagnosed in one patient with recurrent idiopathic GHU. Of patients with recurrent GHU, 89% had no proteinuria on follow-up, and GHU and microscopic haematuria resolved in 97% and 89%, respectively. Our work-up protocol was useful for diagnosis and follow-up planning. Asymptomatic GHU in children was most commonly the idiopathic form. Overall, long-term prognosis appears to be benign; however, careful follow-up is essential. “
“New approaches to increase kidney transplantation rates through expansion of live donor kidney transplantation have become necessary due to ongoing shortage of deceased donor organs.

Lately, the importance of regulatory B cells has been implicated in a series of autoimmune disease mouse models

[16, 20, 43, 44]. These studies indicate that different B-cell subsets could have different roles during autoimmune diseases. We have earlier shown that CD25+ B cells in the PBMCs fraction from patients with RA and systemic lupus erythematosus compared with healthy controls exhibit both a more mature and activated phenotype and seem to belong to the memory B-cell pool [4, 45]. It is thus possible that the CD25+ B-cell subset is involved in the pathogenesis of these diseases, but the exact functional role of these cells is still unknown. They could either be a part of the regulatory B-cell subset as they have

the ability to produce IL-10 or belong to the more pathogenic cell pool as they have the ability to present antigen and migrate. More detailed studies are needed Fulvestrant to fully understand the mechanism of action of these cells in autoimmunity and inflammation. In conclusion, we have clearly shown that murine CD25+ B cells have functionally different properties compared with CD25− B cells. These data suggest that CD25+ B cells are a very active and mobile subset of B cells, Compound Library and an important player in immune regulation that might belong to the memory B-cell subset. However, further investigation is needed to understand the pathway and importance of CD25 expression on B cells in vivo. This research was supported by the Swedish Medical Society, King Gustav V 80-years Foundation, the Adlerbertska

Research Foundation, Magnus Bergvalls Foundation, Wilhelm and Martina Lundgrens Science Foundation, Göteborg Medical Society, the Lars Hierta Memorial Foundation, the Swedish Association against Rheumatism, the Swedish Medical Research Council, the Nanna Svartz Foundation, Rune and Ulla Almlovs foundation, Family Kristler and Tholens foundation, CMR, and the Sahlgrenska through Academy at Göteborg University. The authors declare that they have no commercial interest. AT and MB designed the study. SA carried out the experiments, analysed the data and prepared the manuscript. IG contributed to manuscript preparation. “
“Little information is available regarding changes in immune status for patients with Mycobacterium avium complex (MAC) lung disease during antibiotic therapy. Serum immunomolecules from 42 patients with MAC lung disease were assayed comparatively using an array-based system according to (i) patients with MAC lung disease at the time of diagnosis versus healthy controls and (ii) alterations after 12 months of antibiotic therapy in the MAC lung disease group. In addition, cytokine analyses were performed to determine whether cytokine responses were associated specifically with the disease phenotype, treatment outcome and aetiological agent.