Consider withholding dialysis if a patient over 75 years of age has two or more of the following: Nephrologist response to the Surprise Question of ‘No, I would not be surprised if my patient died within the next 12 months’. High comorbidity score (e.g. MCS ≥ 8). Marked functional

impairment (e.g. Karnofsky performance status score < 40). Severe chronic malnutrition (serum albumin < 25 g/L Ivacaftor using the bromcresol green method). This guideline will review the current prediction models and survival/mortality scores available for decision-making in patients with advanced kidney disease who are being considered for a non-dialysis treatment pathway. Risk prediction is gaining increasing attention with emerging

literature suggesting improved patient outcomes through individualized risk prediction.[1] Predictive models help inform the nephrologist and the renal palliative care specialists in their discussions with patients and families about suitability or otherwise of dialysis. Clinical decision-making in the care of end-stage kidney disease (ESKD) patients on a non-dialysis treatment pathway is currently governed by several observational trials.[2] Despite the paucity of evidence-based medicine in this field, it is becoming evident that the survival advantages associated with renal replacement therapy in these often elderly patients with multiple comorbidities and limited functional status may be negated by loss of quality of life,[3, 4] further functional decline,[5, 6] increased complications CX-4945 and hospitalizations. Here we review the pertinent predictive models and risk calculators for ESKD and highlight the advantages and disadvantages associated with

each. It is important to recognize that there is currently no consensus for conducting or reporting the development and validation of multivariate prediction models. Prediction models for chronic kidney were often developed using inappropriate methods and were generally poorly Rucaparib in vivo reported.[7] A ‘c-statistic’ is a measurement of how well the model predicts the event. A c-statistic of 0.5 = no better than chance; a c-statistic of 1.0 = perfect prediction and is acceptable if ≥0.7. Models considered to be well reported include the Journal of the American Medical Association (JAMA) Tangri et al. model.[1] The patient population in which the score was developed should be taken into account. Decision-making for ESKD patients are currently being guided by existing mortality prediction models developed and validated in dialysis patients.[5, 8, 9] When considering treatment choices it is important to consider the following facts. There are around 800 kidney transplant operations performed annually. As at 4 January 2012 there were 1135 people waiting for a kidney transplant in Australia, which represents approximately 11% of the people receiving dialysis.

Efficacy as well as safety and tolerability of this regimen were evaluated. Result:  Thirty-two patients with nephrotic IMN (56% male, age 51.5 ± 12.6 years, estimated Roxadustat price glomerular filtration rate 73.7 ± 20.0 mL/min per 1.73 m2) were included in our study. During the median follow-up duration of 30.0 (12.5–42.8) months, 40.6% of patients achieved complete remission, while 40.6% achieved partial remission. Relapse occurred in five patients in a median of 16 (11.5–26) months after cessation of immunosuppressive treatment. No patients developed renal insufficiency during

the follow up, while 16 side-effects were noted in 10 patients. Complete remission rates at 3, 6 and 15 months were 0%, 12.5% and 40.6% and remission rates were 21.9%, 68.8% and 81.2%, respectively. Complement 3 deposition was significantly associated with the probability of non-remission. Conclusion:  Monthly i.v. pulse cyclophosphamide plus oral steroids may be an alternative treatment option in Chinese patients with nephrotic IMN. “
“T AZD6244 ic50 helper

(Th) cells are an integral part of the host’s immune response to eliminate invading pathogens. However, autoimmune or ‘autoinflammatory’ diseases can develop if Th cell responses are not effectively regulated. Several subsets of Th cells exist, including the Th17 subset that produces interleukin-17A, important in experimental models of organ-specific autoimmune inflammation. Its discovery has explained paradoxical observations in model systems thought to be

Th1 mediated but were exacerbated in the absence of interferon-γ, the prototypic Th1 effector cytokine. Th17 cells express unique transcription factors and secrete a unique pattern of cytokines. Interleukin-17A induces pro-inflammatory cytokines and chemokines and mediates neutrophil recruitment. Th17 cells have a reciprocal relationship with T regulatory cells and can also mediate suppression of Th1 responses. Recent studies also suggest that Th17 cells are not terminally differentiated but can switch into Th1 cells. Ergoloid Th17 cells have themselves been recently shown to induce antigen-specific cell-mediated proliferative glomerulonephritis. There is increasing evidence implicating Th17 cells in anti-glomerular basement membrane disease, lupus nephritis and pauci-immune glomerulonephritis. This review will review the discovery of the Th17 subset, its properties, its relationship with other Th subsets and assess the current evidence implicating Th17 cells in glomerulonephritis. T helper (Th) cells play a central role in adaptive immune responses. These antigen-specific cells are activated by antigen presenting cells and orchestrate the elimination of invading pathogens. Seminal studies by Mosmann and Coffman1 have led to the categorization of Th cell subsets identified by the cytokines they produce. Th1 cells secrete γ-interferon (IFN-γ) and LT-α, and are important in directing cell-mediated immunity against intracellular pathogens.

Anti-neutrophil cytoplasmic autoantibody (ANCA)-associated vasculitis is a complex disease with a strong underlying autoimmune diathesis. Its precise aetiology remains unknown, but contributions from both heritable and environmental factors seems certain. The pathogenic mechanisms that are then triggered involve diverse cell types, inflammatory mediators and signalling cascades. What NVP-AUY922 have we learned from this bewildering array of altered biological processes about the pathogenesis of the disease over the past 2 years? Turning first to the genome, familial segregation of Wegener’s granulomatosis (WG) with a 1·56 relative risk for first-degree relatives of patients

with WG, suggests a genetic basis [1]. Indeed, new associations between ANCA vasculitis and genetic polymorphisms are reported almost monthly from candidate gene association studies. The pattern that is emerging points to a polygenic contribution from relatively common variants that are found throughout the population, each of which may only provide a modest effect. Many of the genes described so far encode proteins that are involved in the immune response, such as human leucocyte antigen (HLA) proteins, PTPN22, CTLA4 and others (reviewed

in [2]). Genomewide association studies that are in progress will doubtless provide further insights. Environmental factors appear to contribute variously (reviewed in [3]). Multiple reports attest to the abilities of drugs such as the anti-thyroid agent propylthiouracil

ABC294640 to induce myeloperoxidase (MPO)-ANCA and, in a minority of individuals, to trigger overt vasculitis. Environmental toxins have been implicated, with the strongest epidemiological evidence emerging around silica, a potential activator of the inflammasome complex that generates, among other activities, the active cytokine interleukin (IL)-1 [4]. Infections have been linked repeatedly to pathogenesis of vasculitis. Oxymatrine Clinical association studies have shown an enhanced likelihood of relapse in nasal carriers of Staphylococcus aureus; α-toxin from S. aureus is also a potent activator of the NLRP3 inflammasome, suggesting potential links between different environmental agents and their proinflammatory effects in vasculitis [5]. Infection has also been implicated in the formation of the most recently described type of ANCA, namely lysosomal-associated membrane protein 2 (LAMP-2); Kain has suggested that anti-LAMP-2 antibodies are important in the pathogenesis of vasculitis and has provided evidence of molecular mimicry between LAMP-2 and the bacterial adhesion protein Fim-H [6]. Links with infection via homology between the middle portion of the complementary proteinase 3 (cPR3) sequence and S.

672 patients were assessed for management of renal anemia during 12 months. Results 1)  Mean age was 68 years and 69.2% was male gender. Percentages of diabetes and history of cardiovascular disease were 37.9% and 27.8%, respectively. Conclusion: Anemia with ID was associated with a higher risk for CV events than without ID. Compared to increasing prescription of ESA, prescription of iron Metabolism inhibitor did not increase sufficiently. These results suggest that it is necessary to assess ID and use iron supplementation appropriately. JIN KYUBOK, PARK BONG-SOO,

JEONG HEUI JEONG, KIM YANG-WOOK Department of Medicine, Inje University, Haeundae Paik Hospital Introduction: Although control of normal hydration state is a key parameter for cardiovascular mortality in

dialysis patients, the question for biomarkers of volume excess continues. Body composition monitor (BCM; Fresenius Medical care, Bad Homburg, Germany) has been proven as a non-invasive and quantitative method for measuring intracellular and extracellular fluid spaces. In addition, N-terminal pro-B-type natriuretic peptide (NT-proBNP), myeloperoxidase, copeptin and proadrenomedullin are associated with cardiac dysfunction and systemic blood volume. Present study investigated the relationship between body fluid status and volume markers in dialysis patients. Methods: Cohorts EPZ-6438 molecular weight of pre-dialysis (pre-D), hemodialysis (HD) and peritoneal dialysis (PD) patients and age- and gender-matched healthy Korean individuals were recruited in the study (N = 80). In all patients BCM and standard echocardiography were performed. HD patients were measured at the midweek session before dialysis and PD patients were measured with a full abdomen. Also mafosfamide NT-proBNP, myeloperoxidase, cepetin and proadrenomedullin as volume markers were measured. Clinical overhydration was defined as an overhydration-to-exracellular water ratio of >15%. Results: Total

body water, extracellular water and intracellular water were not different in the control, pre-D, HD and PD patients. In the control and pre-D patients, overhydration were 0.6 ± 0.2 L and 1.9 ± 1.0 L, whereas 2.8 ± 0.6 L and 3.0 ± 0.5 L in the HD and PD patients, respectively (p < 0.001). Clinical overhydration was more prevalent in HD and PD patients compared to pre-D patients (35% vs 55% vs 20%, p < 0.05). This was associated with significantly (p < 0.001) higher NT-proBNP and proadrenomedullin levels in HD and PD patients than in the control and pre-D groups. However, no significant difference was found in levels of myeloperoxidase and copeptin in the study groups. Clinical overhydration was associated with cardiac dysfunction markers (LV mass index, LV dimension and ejection fraction, LA diameter and E/E′ ratio). In multivariate models, clinical overhydration was directly related to NT-proBNP and proadrenomedullin concentrations in the study population (r = 0.454 [p < 0.001] and r = 0.505 [p < 0.001], respectively).

Given the results of this study, it seems unlikely that primary immune responses which involve the naive T cell compartment or CD4+ T cell-dependent immune responses in ESRD patients will be affected by their CMV serostatus. At present, such an association has not been reported Doxorubicin research buy and CMV serostatus does not seem to affect the vaccination response in children [32, 33]. In healthy elderly individuals, CMV seropositivity leads to an expansion of effector CD8+ T cells which are CD8+CD28nullCD57+. These CMV-specific T cells were found to be oligoclonal and can constitute to up to one-quarter of the total CD8+ T cell compartment in elderly which makes cells unable to respond to other pathogens [34]. Moreover, these highly

differentiated cells have shorter telomeres and are associated with an increased risk for the development of coronary heart diseases [35]. In conclusion, CMV-positive serostatus is associated with an increased differentiation status of memory T cells and telomere attrition of CD8+ T cells but does not explain the premature T cell ageing associated with the uraemic environment. GPCR Compound Library screening This study was funded by the Dutch Kidney Foundation

(KSPB.10·12). All authors declare no financial or commercial interests. R. Meijers performed the experiments, statistical analysis and wrote the manuscript. N. Litjens designed the study and wrote the manuscript. E. de Wit performed the experiments. A. Langerak contributed to writing the manuscript. A van der Spek performed some of the experiments. C. Baan contributed to writing the manuscript. W. Weimar contributed to writing the manuscript and provided patient data. M. Betjes designed the study and wrote the manuscript. Fig. S1. Gating strategy of the CD4+ and CD8+ T cell subsets. From Nutlin-3 nmr whole

blood we first selected for lymphocytes (a); we then selected the CD3+ lymphocytes (T cells) (b) and made a distinction between the CD4+ and CD8+ T cells (c). On the basis of CCR7 and CD45RO, we divided the different subsets [naive, effector memory (EM), central memory (CM) and end-stage renal disease (EMRA)] for the CD4+ (d) and CD8 (e) T cell compartments. “
“Tuberculosis remains a global health problem, in part due to failure of the currently available vaccine, BCG, to protect adults against pulmonary forms of the disease. We explored the impact of pulmonary delivery of recombinant influenza A viruses (rIAVs) on the induction of Mycobacterium tuberculosis (M. tuberculosis)-specific CD4+ and CD8+ T-cell responses and the resultant protection against M. tuberculosis infection in C57BL/6 mice. Intranasal infection with rIAVs expressing a CD4+ T-cell epitope from the Ag85B protein (PR8.p25) or CD8+ T-cell epitope from the TB10.4 protein (PR8.TB10.4) generated strong T-cell responses to the M. tuberculosis-specific epitopes in the lung that persisted long after the rIAVs were cleared. Infection with PR8.p25 conferred protection against subsequent M.

All four genes are cotranscribed from a promoter that is strongly induced by active SaeR (Geiger et al., 1994). A second promoter drives the expression of saeRS alone and is modestly repressed by these regulatory gene products (Geiger et al., 1994). Activation of the Sae system seems to involve sensing changes in the overall integrity of

Proteasome activity the cell envelope and is highly stimulated by hydrogen peroxide and cationic peptides including α-defensins (Geiger et al., 1994; Novick & Jiang, 2003). Active SaeR promotes the induction of a number of virulence genes in S. aureus through binding of a consensus sequence found upstream of promoters for hla, sbi, efb, lukS-PVL, splA, and saeP (Nygaard et al., 2010). Additionally, expression of β-hemolysin, fibrinogen-binding proteins, lactose catabolizing enzymes, and the chromosomal arginine deiminase operon are all highly affected by Sae (Voyich et al., 2009). It has been shown that SaeRS expression is higher in USA300 than in USA400 clones (Geiger et al., 1994; Montgomery et al., 2008), which may be a result of overactive Agr system (see above) because RNAIII is known to positively regulate Sae expression (Novick Selleckchem BMN-673 & Jiang, 2003). Deletion of saeRS resulted in almost complete loss of Hla expression and a significant drop in PVL levels as well (Montgomery et al., 2010; Nygaard et al., 2010). Moreover, ∆sae USA300

was attenuated in murine sepsis, peritonitis, dermonecrosis, and pneumonia Tobramycin models (Voyich et al., 2009; Montgomery et al., 2010; Nygaard et al., 2010; Watkins et al., 2011). This was surprising given that in USA400, Sae was only essential for sepsis and peritonitis

and not for survival within skin abscesses (Voyich et al., 2009; Watkins et al., 2011). However, USA400 clones do not induce the same level of dermonecrosis and do not express high levels of Hla as in USA300 infections (Montgomery et al., 2008; Li et al., 2010). Thus, it appears as though some of the hypervirulence attributed to USA300 clones in skin/soft tissue infections is likely due to Sae-mediated Hla overproduction. However, HA-MRSA USA500 clones also exhibit severe dermonecrosis during skin infections and overproduce Hla and PSMs yet have not disseminated as widely as USA300. While it has not been directly tested, it is tempting to hypothesize that the overactive Agr system inherent to USA300 results in excessive PSMs and Sae expression, the latter of which leads to high Hla expression. However, the mechanism driving high Agr activity in USA300 is not defined. Agr activity can be modulated through the actions of a number of trans-acting regulators including SarA (Cheung & Projan, 1994), Stk1 (Tamber et al., 2010), MgrA (Ingavale et al., 2005), SigB (Lauderdale et al., 2009), CodY (Majerczyk et al., 2008), CcpA (Seidl et al., 2006), Sar-family proteins other than SarA (Schmidt et al., 2001; Manna & Cheung, 2003, 2006; Tamber & Cheung, 2009), ArlRS (Liang et al.

Also it resulted in reduced tubulointetrsistial hypoxia.[91] In rats with subtotal nephrectomy (5/6) and increased expression of DDAH has lead to ADMA decrease,

which was related to the reduction of proteinuria, as compared to rats that received hydralazine aiming at the Maraviroc same restoration of their blood pressure.[92] Also in rats (Munich-Wistar rats) the administration of standard salt diet (0.5% Na) and the NOs inhibitor NG-nitro-L-arginine methyl ester (L-NAME) for 30 days resulted in moderate albuminuria. The fractional clearance 70 kDalton neutral dextran rose moderately. Rats given L-NAME and high salt diet (3.1% Na) for 30 days exhibited massive albuminuria, whereas the fractional clearance of 70 kDalton neutral dextran was nearly tripled. Depletion of glomerular basement membrane (GBM) anionic sites was seen in both groups.[88] A recent study in non-diabetic CKD stage 1 patients indicated a significant association between ADMA and the levels of proteinuria.[11]Another study showed that ADMA was higher in nephritic proteinuric patients as compared with non-nephrotic range proteinuric patients with the same glomerular filtration rate.[93] Moreover, increased ADMA levels were indentified in children with steroid-resistant nephrotic syndrome due to sporadic focal segmental glomerulosclerosis, compared

to healthy controls age-matched.[94] In an observational cohort study in type 2 diabetic patients, with normoalbuminuria or microalbuminuria, those with higher ADMA levels had a greater incidence

check details of reaching a more advanced state of albuminuria compared to those with lower ADMA levels.[95] Yilmaz et al. found in stage 1 CKD patients with diabetes mellitus type 2 circulating levels of myostatin and SFas, two cell death mediators were independently related to the degree of the proteinuria, as well as to endothelial dysfunction and circulating ADMA (Yilmaz hypothesis: leakage from the intracellular space caused by necrosis and/or faulty apoptosis during this website proteinuria could contribute to high ADMA levels, since ADMA is mostly intracellular).[96] The possible mechanisms by which ADMA and the other inhibitors of NOs are involved in the pathogenesis of proteinuria are: (i) The impairing of both glomerular size and charge selectivity of GBM. The effects likely reflect functional rather than structural disruption of the glomerular wall.[88] (ii) ADMA compromises the integrity of the filtration barrier by altering the bioavailability of NO and oxygen superoxide O2− (antagonism of the NO with reactive oxygen species-ROS and O2−).[90] (iii) The link between ADMA and proteinuria seems to be due to altered protein turnover or PRMT activity,[97] or other mechanisms involving the renin-angiotensin system (RAS blockade using ramipril, lowers ADMA levels, proteinuria and cell death mediators).

The allergen that is supposed to induce the original allergic responses is named the primary sensitizer, and the others are considered cross-reactive allergens. There are several clinical and laboratory criteria to classify an allergic reaction as cross-reacting, but the condition should be first empirically demonstrated (104). The clinical relevance of IgE cross-reactivity has been described for foods, pollens, mites and other allergen sources (105), but its occurrence between mite and Ascaris allergens, although widely suspected (106), has not been thoroughly investigated. Cross-reactivity

depends on amino acid sequences https://www.selleckchem.com/products/pf-562271.html and conformational structures of the molecules, which explains why it is more frequent (but not exclusive)

among phylogenetically related species. Ascaris and mites are related invertebrates and are expected to share several allergens. Independently of which source is the primary sensitizer, among inhabitants of the tropics, allergenic stimulus this website derived from a persistent inhalation of high concentrations of mite allergens and infections with A. lumbricoides may generate a particular immune response that involves cross-reactivity in both directions. Several antigens of Ascaris have been analysed (50,107,108) and other are under scrutiny, but our knowledge about the allergenic composition of the whole extract is still very limited; in fact, the International Union of Immunology Societies only reports the ABA-1 allergen (Asc s 1) and Forskolin supplier the recently submitted tropomyosin (Asc l 3). Because almost all allergens from domestic mites have been identified, it is now possible to study their cross-reactivity with Ascaris.

We performed dose–response ELISA and immunoblotting inhibition studies with extracts of B. tropicalis, D. pteronyssinus and A. suum, demonstrating that there is a high degree of cross-reactivity between these sources including protein IgE epitopes (24). Although carbohydrate epitopes can be involved (109), inhibition of IgE binding was also demonstrated using deglycosylated extracts and nonglycosylated recombinant allergens. Using sera from patients with asthma, our experiments strongly suggest that mites are the primary sensitizers and that clinically relevant allergens such as tropomyosin and glutathione transferases are involved. Although, as suggested, the clinical relevance of cross-reactivity between parasites and house dust mites in tropical regions needs to be demonstrated (109,110), we postulate that the high prevalence of IgE antibodies to mites observed in tropical populations is partially the result of cross-reactivity with Ascaris allergens. Also, the high prevalence of allergy observed in urban areas of the tropics, even in places with poor hygienic conditions, may be influenced by the same phenomenon.

The initial rate of haemoglobin digestion peaked at pH 4·0. Above pH 6·0, the rate was no different to controls, which correlated with gel analysis of the 24-h reaction samples; revealing that the 15-kDa haemoglobin doublet was depleted up to pH 6·1 compared to controls (Figure 2). For reactions with albumin a very similar profile was generated, with the fastest initial rate of digestion observed at pH 3·7 (Figure 3). However, the initial rate values obtained were selleck inhibitor approximately fivefold lower than those for the digestion of haemoglobin and consequently much closer to background control values. SDS PAGE analysis confirmed that there was a decrease in the intensity

of intact albumin, accompanied by an increase in lower molecular weight bands presumed to be partially digested albumin, below pH 5·6. It can also be seen that below pH 4·2, albumin digestion occurred in the absence of H-gal-GP, presumably as a result of the acidic conditions AZD9668 supplier (Figure 3). Similarly for haemoglobin digestion, the doublet in the 24-h samples corresponding to haemoglobin shows decreased intensity compared to corresponding 0-h samples for enzyme-free controls as well as for reactions containing H-gal-GP at pH conditions below pH 4·2 (Figure 2). Reactions

of H-gal-GP with different concentrations of ovine haemoglobin substrate at pH 5·0 were set up and the increase in free amino groups was monitored by taking samples at regular time intervals. It was assumed that the absorbance value obtained after a 24-h digestion represented a complete turnover of all haemoglobin in the reaction and therefore

was equivalent to the total concentration of haemoglobin in the reaction. The absorbance value of each sample from all time points was used to estimate its concentration of haemoglobin. These concentration estimates were then plotted against time to obtain a turnover rate per second (v). This rate was plotted against the total concentration of haemoglobin in the reaction to produce the Michaelis–Menton curve which gave a kcat of 0·03 s−1 and a KM of 29 μm (Figure 4). The rate of digestion of ovine haemoglobin was monitored ADP ribosylation factor as before except that the H-gal-GP was pre-incubated with serum IgG obtained from sheep which had been successfully vaccinated with H-gal-GP (pIgG – see Table 1) or from control sheep immunized with adjuvant alone (cIgG – see Table 1). Different pH conditions under which IgG bound to H-gal-GP (with pre-incubation at pH 7·4 followed by reaction at pH 4·0 and with pre-incubation and reaction both at pH 4·0 as described in the Materials and Methods) were tested before the detection of IgG inhibition at pH 5·0 (data not shown). For inhibition experiments carried out with both the IgG pre-incubation and subsequent reactions held at pH 5·0, H-gal-GP was incubated with either pA, pIgG, cIgG or buffer.

1). It is remarkable that many aspects of systemic autoimmune diseases resemble those of chronic viral infections and that both type I IFNs and IL-17, which contribute to disease pathogenesis, have a crucial role in early innate defense mechanisms. This supports the long-existing idea of an environmental trigger such as infection for systemic autoimmune diseases to develop in genetically susceptible individuals,

who may either display increased immune responses to the initial trigger or lack the ability to abort such responses in time, or both. This, in turn, may explain why polymorphisms in genes involved in the control of innate inflammatory pathways — such as IRFs — are often associated with autoimmune diseases. Data generated in the past few years GSK3 inhibitor point to a role for IL-17 and IL-17-producing cells in the pathogenesis of systemic auto-immune diseases such as SLE. Such studies have, however, focused mainly only on IL-17 and Th17 cells, raising questions about Maraviroc the possible involvement of other immune cell subsets known to produce IL-17, as well as the contribution of other Th17-derived cytokines, in the pathogenic mechanisms and end organ damage. In particular, in light

of recent studies showing that Th17 cells do not represent one defined cell subset but rather a spectrum of cells with different cytokine expression profiles and degrees of pathogenicity, it will be interesting to further define the Th17 cells involved in systemic autoimmune diseases, as well as the cytokines they secrete in addition to IL-17. Financial

support was obtained from the Karolinska Institute, next the Swedish Research Council, the Göran Gustafsson Foundation, the Torsten and Ragnar Söderberg Foundation, the King Gustaf the Vth 80-year foundation, the Swedish Foundation for Strategic Research, the Heart-Lung Foundation, the Magn. Bergvall Foundation, the Lars Hiertas Minne Foundation, the Tore Nilsson Foundation, the Swedish Rheumatism Association, and the Jonas Söderqvist Foundation. The authors declare no financial or commercial conflict of interest. “
“Chlamydia trachomatis infections are a significant cause of reproductive tract pathology. Protective and pathological immune mediators must be differentiated to design a safe and effective vaccine. Wild-type mice and mice deficient in IL-22 and IL-23 were infected intravaginally with Chlamydia muridarum, and their course of infection and oviduct pathology were compared. Local genital tract and draining lymph node immune responses were also examined in IL-23-deficient mice. IL-22- and IL-23-deficient mice exhibited normal susceptibility to infection and oviduct pathology.