These sequences were submitted to GenBank and were assigned the a

These sequences were submitted to GenBank and were assigned the accession numbers HM773966–HM775073. One hundred and sixty-two IgG1 sequences were also amplified from Australian samples. A number of VDJ sequences were found that aligned to a recently identified germline IGHV3 gene (HM855939). The IGHV3-NL1*01 gene was seen in seven VDJ rearrangements (accession numbers HM773984, HM774108, HM774124, HM774201, HM774302, HM774729, and HM774738). One of these

is an IgG3 sequence (HM774124) that contains no somatic point mutations. Alignments were also seen to 12 other recently identified IGHV allelic variants, including IGHV1-8*02 (HM855457), IGHV1-18*03 (HM855463), IGHV3-7*03 click here (HM855666), IGHV3-9*02 (HM855577), IGHV3-11*06 (HM855329), IGHV3-21*03 (HM855323), IGHV3-21*04 (HM855688), IGHV3-33*06 (HM855436), IGHV3-48*04 (HM855336), IGHV3-53*04 (HM855453), IGHV4-59*11 (HM855471) and IGHV7-4-1*04 (HM855485).

In total, alignments were seen to 91 different IGHV genes and allelic variants. Despite the use of primers specific for the VH1, VH3 and VH4 gene families, many sequences were also amplified that utilized the IGHV5 family genes. In fact, the IGHV5 family genes as well as IGHV1-69 alleles were over-represented in all data sets, when compared with previously reported rearrangement frequencies [21]. Analysis of the VDJ junctions showed the mean CDR3 lengths of PNG IgG sequences to vary between 14.9 (IgG2) and 16.6 amino acids (IgG3), while the IgE sequences had a mean length of 15.4. These differences were not statistically PLEK2 significant. Within the junctions, all previously reported functional IGHD genes were observed. Alignments were also seen to one or more allele of each IGHJ gene, including both IGHJ3*01 and IGHJ3*02. IGHJ3*01 was originally reported as part of a haplotype that includes IGHJ4*01 and IGHJ5*01. In an earlier bioinformatic study of VDJ rearrangements, we failed to find convincing evidence for the existence of these three alleles [24]. The alignments seen in this study confirm the existence of IGHJ3*01, although no convincing alignments were observed to IGHJ4*01 or IGHJ5*01.

In the PNG data sets, 64 sets of clonally related sequences were seen, involving a total of 175 sequences. Forty-four sets contained two sequences, 12 sets contained 3 sequences, 3 sets contained 4 sequences, 2 sets contained 5 sequences and 3 additional sets contained 6, 7 and 16 sequences, respectively. Seven sets contained clonally related sequences from different isotypes, including three sets of mixed IgG1/IgG2 sequences, three set of IgG1/IgG4 sequences and one set of IgG1/IgE sequences. Clonally related sequences were particularly common amongst the IgG4 sequences. Of the 154 IgG4 sequences, 55 (35.7%) sequences were related to other IgG4 or IgG1 sequences. In contrast, only 69 of the 482 IgG1 sequences, 23 of the 288 IgG2, 16 of the 59 IgG3 and 12 of the 125 IgE sequences were members of clonally related sets.

Therefore the events that govern early B-cell activation followin

Therefore the events that govern early B-cell activation following influenza virus infection are crucial for ameliorating disease outcome. The mechanisms underlying early B-cell activation, however, are incompletely understood. Rapid Ab

production originates from extrafollicular foci developing at the edges of the T- and B-cell zones in secondary lymphoid tissues following antigen exposure. These responses are thought to generate primarily short-lived plasma cells 9. Rapid Ab production at extrafollicular sites is attributed to T cell-independent as well as T-dependent responses 10, 11. RAD001 supplier In contrast, the slower intrafollicular germinal center reactions require cognate CD4 T-cell–B-cell interactions 12, 13. They are regarded as the birthplace of long-lived humoral immunity, providing both memory B cells and long-lived plasma cells 11, 13. Both extra and intra-follicular responses develop strongly in the regional

LN following 5-Fluoracil purchase influenza virus infection 14. The selection events that underlie the establishment of extrafollicular versus germinal center B-cell responses are important events in the initiation of the adaptive immune response. They coordinate the formation of crucial rapidly protective responses, while ensuring long-term protection from re-infection 11. There is evidence that rapid (antiviral) Ab production can be provided by distinct B-cell subsets 1, 11, 15–19. Marginal zone (MZ) B cells are one such subset. They can respond to blood-borne antigens through rapid production of Ab at extrafollicular sites 17, 18. In the mouse these B cells are only found in the spleen, however, and not in LN 20, 21. Thus, MZ B cells are unlikely to play a role in the response to influenza virus infections, as respiratory tract draining MedLN are the main sites of the initial influenza virus-induced B-cell response 14. Whether there are other subsets in the LN that act as functional equivalents to splenic MZ B cells is currently unknown. Recently, BCR affinity-guided selection events have been implicated as a factor that could determine the B-cell fate following protein immunization 22. Paus et al.22 used an elegant

adoptive cell transfer approach with transgenic hen egg lysozyme-specific B cells to provide evidence that BCR affinity thresholds exist that steer B cells toward the a particular response. In that study high-affinity B cell–antigen interactions resulted in predominantly extrafollicular foci responses, whereas hen egg lysozyme-specific B cells binding antigen with weaker overall affinities were predominately selected into the germinal center response. These data are consistent with a study on vesicular stomatitis virus infection-induced B-cell responses, in which Roost et al. observed no improvement on the overall Ab-affinity during the course of vesicular stomatitis virus infection and showed that early induced virus-specific Ab are of relatively high affinities 23.

These differences might be the cause of the observed distinct cyt

These differences might be the cause of the observed distinct cytokine expression patterns (Hackstadt, 1995; Stephens et al., 1998; Greub et al., 2005b, 2009; Corsaro & Greub, 2006). Here, it should be stressed that major differences exist

in the biology of the classical Chlamydiae and the so-called Chlamydia-related organisms including a threefold larger genome size of Parachlamydia (Stephens et al., 1998; Greub et al., 2009) and its R428 ability to resist to the microbicidal effectors of free-living amoebae (Greub et al., 2003b). Immune cells can also be infected by Chlamydiales although not all do so with the same efficiency. For example C. pneumoniae can infect freshly derived monocytes, but cannot replicate in them and is degraded (Airenne et al., 1999; Wolf et al., 2005).

Chlamydia pneumoniae replicated to a lower extent in macrophages derived from human peripheral blood mononuclear cells (PBMC) as compared with HeLa cells or not at all in freshly derived PBMCs (Kaukoranta-Tolvanen et al., 1996; Wolf et al., 2005). To some degree, growth inhibition is probably due to TNF-α, because interference with antibodies causes increased bacterial growth in alveolar macrophages, although the late gene omcB was still poorly transcribed (Haranaga et al., 2003). Thus, in vivo macrophages seem to be refractory to C. pneumoniae replication compared with other Chlamydiales. Chlamydia trachomatis’ ability to perform a productive replication in macrophages depends on the biovar. Only the LGV biovars were able to replicate within macrophages, while

selleck others generally form persistent forms when infecting these phagocytic cells (reviewed in Beagley et al., 2009). Nonetheless, the persistent C. trachomatis are still metabolically active and can induce apoptosis of other immune cells (Jendro et al., 2004). Indeed, C. trachomatis-infected macrophages release TNF-α that with other components induces apoptosis of T cells, but not of the infected macrophages. Moreover, the factors released during apoptosis of T cells induce an immunosuppressing environment (transforming growth factor-β), thus creating a favorable environment for chlamydial persistence (Jendro et al., 2004). Controlled apoptosis may not only be P-type ATPase a mechanism used by some Chlamydiales to prevent bacterial clearance but might also provide enough time to complete a replication cycle or induce persistence. Waddlia chondrophila has a direct cytopathic effect on macrophages, suggesting that they are not the primary host cells for replication (Goy et al., 2008). This characteristic could help the bacteria prevent early infection recognition, display of antigens and attraction of other immune cells. Several Chlamydiales differ in their ability to induce cytokines after exposure to detrimental conditions such as heat or UV light. Thus, P.

In additional experiments to determine possible postinfection mec

In additional experiments to determine possible postinfection mechanisms of inhibition by Trappin-2/Elafin, TZM cells were infected with HIV-1 IIIB and BaL

at an MOI of 1 and were washed out at 6 and 24 hr postinfection followed by the addition of 10 ng/ml of recombinant Trappin-2/Elafin ITF2357 ic50 (rTrappin-2/Elafin). Assays were developed at 48 hr by addition of the Beta-Glo substrate and measurement of relative light units using a luminometer. Viability of TZM cells upon treatment with Trappin-2/Elafin and CVL was quantified using the CellTiter 96® AQueous One Solution Cell Proliferation assay (Promega) according to the manufacturer’s instructions. Briefly, reagent was added directly to cell cultures B-Raf inhibition and incubated for 1 hr at 37°, after which the absorbance of each well was read at 490 nm in a plate reader. CVL samples from 32 HIV-positive women (12 Black, nine Hispanic and 12 White) were provided by Dr S. Cu-Uvin (Brown University, Providence, RI). Fifteen CVL samples from HIV-negative women (five Black, five Hispanic and five White) were obtained from the Rhode Island HIV Epidemiology Research Study (HERS). All sample collections were carried out in accordance with human experimentation guidelines of Miriam Hospital (Brown University, Providence, RI). CVL from women were catalogued by race based on self-identification.

The HIV-positive and HIV-negative women were in

the same age range (18–50 years). The HIV-positive women were relatively healthy with average CD4 counts of 712 cells/mm3 blood, an average plasma viral load of 12 666 copies/ml and Thiamet G were not on any antiretroviral therapy. Only six out of 32 women showed a detectable genital tract viral load. CVL was collected by washing the cervical-vaginal area with 10 ml of sterile saline (pH 7·0) and collecting the fluid, which was then centrifuged at 10 000 g for 5 min and separated from the cellular fraction. The supernatants were aliquoted and stored frozen at −80° until use. For the HIV-negative samples used in this study, CVL were collected and frozen immediately at −80°. Before assaying the supernatants, samples were thawed, centrifuged at 10 000 g for 5 min and separated from the cellular fraction. A two-tailed paired t-test or a one-way analysis of variance (anova) with Bonferonni’s post-test was performed using GraphPad InStat version 3.0a (GraphPad Software, San Diego, CA). A P-value of < 0·05 was taken as indicative of statistical significance. Epithelial cells were isolated from uterus (UT), Fallopian tube (FT), endocervix (Cx) and ectocervix (Ecx) FRT tissues, grown to confluence and, in the case of epithelial cell (EC) from the upper FRT, high TER (> 500 ohms/well). CM was collected at 24 hr and cells were harvested to isolate RNA.

We note that while our studies are under revision, another recent

We note that while our studies are under revision, another recently published report indicates that Dlg1 is not required for T-cell activation [30]. However, our study for the first time examines the requirement for Dlg1 in functional regulation of T cells with both TCR-fixed and

polyclonal (endogenously generated) T-cell repertoires by employing several experimental approaches in vivo. First, we tested the requirement for Dlg1 during Ag-driven T-cell clonal expansion in vivo. Using this immunization-based approach we found no evidence for Dlg1 involvement in T-cell activation Carfilzomib mw and clonal expansion by cognate Ag in vivo. We also tested if Dlg1 is required for homeostatic proliferation of T cells in lymphopenic hosts. This process is regulated by signals emanating from cytokine receptors and TCR upon its ligation with MHC/self peptide complexes in vivo [31]. IL-7 is produced abundantly in lymphopenic hosts and can drive homeostatic expansion of both naïve CD4+ and CD8+ T cells. In this context, the expansion of CD8+ T cells has been found to be more robust,

as compared with that see more of CD4+ T cells, presumably due to differential expression of IL-7R components [32]. Consistent with this view, homeostatic expansion of OT1 T cells in our experiments was markedly more robust as compared with OT2 T cells, however in both cases, we found no evidence for involvement of Dlg1 in homeostatic expansion of T cells. Thus, taken together, our in vitro and in vivo studies with TCR-transgenic

T cells do not implicate Dlg1 in TCR activation or T-cell proliferation of primary T cells. We also addressed the potential requirement for Dlg1 in the generation of memory T-cell subsets in vivo. Here, we focused on the endogenous polyclonal T-cell response, because the use of TCR-transgenic mouse models in studies of the Liothyronine Sodium kinetics of memory T-cell induction is thought to be nonphysiological. Thus, TCR-transgenic models can give biased results due to the high frequency of responding Ag-specific T cells and the abundance of Ag [33]. However, our analyses of polyclonal T-cell responses demonstrate significantly increased frequencies of IL-2 producing T cells upon boost immunization in KO mice, as compared with WT mice, although we can not rule out that Dlg1 may also be involved in T-cell migration and/or homing in vivo. However, we observe alterations in the frequencies of effector and central CD4+ T-cell memory subsets indicating that Dlg1 function may be cell autonomous. Given that previous studies have identified central memory CD4+ T cells as significant producers of IL-2 [34], the increased IL-2 production observed in our system most likely derives from Tcm cells.

A number of surface receptors coupled to ITAM-bearing adaptors ha

A number of surface receptors coupled to ITAM-bearing adaptors have been shown to regulate myeloid cell functions. Among them, CD300e (IREM-2) appeared selectively expressed

by monocytes and mDC and was shown to associate with DAP12 in transfected cells, delivering activating signals 20. In the present study, we provide data supporting that cross-linking of CD300e triggered the intracellular calcium mobilization and ROS secretion in monocytes. Signaling through CD300e activated monocytes and mDC, promoting their survival and leading to the induction of pro-inflammatory cytokine secretion and increased expression of co-stimulatory molecules. Moreover, CD300e-stimulated mDC enhanced the alloreactive response of CbT cells. Altogether, these results

formally support that CD300e functions as an activating Bioactive Compound Library receptor capable of regulating the inflammatory and immune responses. The expression pattern and function of CD300e partially differed from other activating myeloid receptors associated to ITAM-bearing adaptors. Unlike the DAP12-associated TREM-1 31, 32, CD300e was not upregulated upon monocyte activation via TLR4 (data not shown), thus resembling the FcRγ-associated receptor hOSCAR 27. CD300e ligation induced a rapid intracellular calcium mobilization, as well as the production of ROS, supporting that this receptor may regulate the microbicidal activity of monocytes 33. Similarly, and in line with the previous reports on the ability of both hOSCAR and TREM-1 to trigger the respiratory burst in granulocytes 27, 34, we have observed that TREM-1 activates ROS production also in monocytes. Once recruited and activated at inflammatory sites, monocytes upregulate the expression of co-stimulatory molecules (i.e. CD40, CD83, CD80 and CD86) that, together with cytokine secretion, contribute to T-cell activation

and the generation of an optimal adaptive immune response. Herein, we show that CD300e engagement induced an upregulation of CD25, CD83 and CD86, without detectably influencing the expression of CD40 or CD54, in contrast to TREM-1 31 and hOSCAR activation 27. On the contrary, it is Morin Hydrate of note that these two receptors appear capable of triggering the secretion of pro-inflammatory cytokines, including TNF-α and IL-8/CXCL8 in monocytes 27, 31 similarly to CD300e. In our experience, some differences in the functional response patterns were noticed when CD300e was compared with TREM-1 and hOSCAR in monocyte activation assays using specific mAb (Brckalo et al., unpublished data). Yet, it is of note that despite the fact that agonistic mAb are valuable tools to functionally characterize cell surface receptors, data should be cautiously interpreted for comparative analysis between different molecules, unless validated with their natural ligands.

The authors thank Dr G Brennan, Queen’s University of Belfast,

The authors thank Dr. G. Brennan, Queen’s University of Belfast, for his help in proof reading and language corrections. None of the authors has any conflicts of interest associated with this study. “
“Cry1Ac protoxin from Bacillus thuringiensis is a potent mucosal immunogen and adjuvant. When delivered selleck compound intranasally (i.n.) Cry1Ac elicits significant antibody response and is able to improve vaccination against Naegleria

fowleri infection, but the functional effects occurring in nasal lymphocytes when this protein is administered alone have not been determined. Here, we investigated the effects of i.n. immunization with Cry1Ac on antibody production, lymphocyte activation and cytokine production in lymphocytes from nasal-associated lymphoid tissue (NALT) and nasal passages (NP). Our results show that i.n. immunization with Cry1Ac induced significant specific IgA and IgG cell responses, especially in NP. Besides, it increased the proportion of lymphocytes expressing the activation markers CD25 and CD69 in both nasal tissues, selleck inhibitor but differently. CD25 was increased in B cells along with CD4 and CD8 T cells from NALT and

NP, while CD69 was increased in B cells from both tissues but only in CD4 T cells from NP. Finally, we found that Cry1Ac augmented especially a Th2 profile of cytokines, as the proportion of T cells that spontaneously

produced IL-4, IL-5 and IL-10 was increased and this effect was higher in NP than in NALT. Buspirone HCl These data contribute to explain the potent immunogenicity of Cry1Ac via i.n. route. The nasal mucosa is an important site for host defence against invading pathogens as it is the first site of contact with inhaled antigens [1]. In addition to its role in the defence of the upper and lower respiratory tracts, the nasal lymphoid system cooperates with the systemic immune system and affects immune reactions at distant mucosal sites, such as the urogenital tract and the gut [2, 3]. Consequently, new vaccination strategies based on nasal application have been designed and have proven to be effective procedures for the induction of antigen-specific immunity in respiratory and reproductive tissues [4]. There is much evidence to suggest that nasal-associated lymphoid tissue (NALT) may have an important role in the induction of mucosal immune responses after nasal immunization [5], while nasal passages (NP) and their associated lymphocytes are considered effector sites. However, only a few studies have systematically analysed the distinctive phenotypic and functional features existing in the lymphocyte populations residing at the different nasal compartments [5–8].

The pathways are tightly controlled, with transcription often det

The pathways are tightly controlled, with transcription often determined by specific LY2109761 research buy transcription factors, and post-translational modifications that include phosphorylation, methylation, acetylation, ubiquitination and O-GlcNAylation to regulate outcomes. Several of

these genes, which are regulated by oxidative stress and may act in the development of CKD, are reviewed in the following paragraph. The Forkhead (FoxO) proteins are a family of transcription factors that play a critical role in the regulation of genes in ageing. They comprise FoxO1 to FoxO4 and FoxO6; however, FoxO1 has most association with CKD. FoxO1 has increased levels of phosphorylation in the kidneys of elderly overweight people with type 2 diabetes and CKD21 and old hypertensive rats with CKD.1 FoxOs induce apoptosis mainly by upregulation of pro-apoptotic genes such as Bax,22 yet they can also detoxify harmful cellular oxidants like

O2- and H2O2 and protect cells.23 Their exact role in oxidative stress-induced CKD needs further investigation. Nuclear factor-kappa B (NF-κB) comprises a family of rapid-acting nuclear transcription factors that transcriptionally regulate a wide variety of genes involved in inflammation, immunity, apoptosis, cell proliferation and differentiation. In oxidative stress-induced kidney disease, NF-κB is activated by ROS and initiates signalling pathways involved in renal fibrosis.24 It has been implicated in the transcriptional activation of the cell cycle inhibitor p21,25 linking this transcriptional regulator with renal cell

senescence. The adapter protein p66shc is a mediator PD0325901 concentration of mitochondrial dysfunction.26 An isoform of the ShcA protein, p66shc antagonizes the cell proliferative actions of two other isoforms, p46shc almost and p52shc. Oxidative stress induces the phosphorylation of serine 36 of p66shc before its translocation into the mitochondria. Here, it translates oxidative stress into Ca2+-mediated mitochondrial damage and subsequent apoptosis.27 Although the role of p66shc has been noted in glomerulopathies and diabetes,28 and its differential expression has been demonstrated in ageing kidneys,1 the functional significance of p66shc in the pathogenesis of CKD needs further investigation. Uremic toxins may also be a source of oxidative stress in CKD patients. Uric acid is the hepatic end-product of purine metabolism in humans. It is synthesized by xanthine oxidoreductase, which catalyses the oxidation of hypoxanthine to xanthine and xanthine to uric acid. Resulting hyperuricaemia is associated with an increased risk for developing CKD and enhances its progression.29 In addition, retention of uremic toxins promotes inflammation, and therefore oxidative stress, by priming polymorphonuclear lymphocytes, activating IL-1β and IL-830 and stimulating the innate immune response through CD8+ cells.

In addition, the present guideline does not provide recommendatio

In addition, the present guideline does not provide recommendations regarding the management of individuals with established CKD, with respect to the prevention of other (non-renal) adverse outcomes, including retinopathy, hypoglycaemia, bone disease and cardiovascular Selleckchem CH5424802 disease. It is important to note however, that in an individual with type 2 diabetes, the prevention of these complications may be a more important determinant for

their clinical care. Consequently, the recommendations made must be balanced against the overall management needs of each individual patient. Screening for CKD aims to identify abnormal urine albumin excretion and declining GFR, so that interventions can be given to slow progression of kidney disease, to prevent ESKD and to reduce the risk of CVD. Assessment of kidney function in people with find more type 2 diabetes includes measurement of urinary albumin excretion and estimation

of GFR for the purposes of screening, diagnosis and monitoring response to management. In a significant proportion of people with type 2 diabetes, CKD may progress (i.e. declining GFR) in the absence of increasing albuminuria. Thus both GFR and albuminuria are important in screening, diagnosis and monitoring. Albuminuria may be assessed by measurement of the AER or the ACR with AER being regarded as the gold standard. The GFR is most commonly estimated rather than measured. Albumin excretion typically increases in a continuous manner over several years,

rather than showing an abrupt transition from normal to abnormal values. The average increase in AER ranges from 10 to 30% per year until overt nephropathy develops. However, in some people, the rate of increase in AER slows after the stage of microalbuminuria.1 Regression from microalbuminuria to normoalbuminuria may occur in people with newly diagnosed type 2 diabetes due to interventions or for unknown reasons,2,3 while in others regression does not occur.4 Regular monitoring of albuminuria in people with type 2 diabetes is warranted on the basis of the rate of progression of albuminuria in type 2 diabetes and ESKD associated with increasing MycoClean Mycoplasma Removal Kit albuminuria and the increased risk of CVD.5 There is a high intra-individual variability in 24 h albumin excretion with a coefficient of variation of 40–50%, therefore a diagnosis of persistent microalbuminuria should be based on repeated measurements, especially if long-term treatment of normotensive individuals are being considered. While increasing albuminuria is a risk factor for both CVD and ESKD, cross sectional studies have also shown a high degree of heterogeneity in people with type 2 diabetes compared with type 1 diabetes with respect to CKD. As such a significant proportion of people with type 2 diabetes may have CKD and be normoalbuminuric.

Surprisingly, we found that Tregs produce high amounts of CXCL8 (

Surprisingly, we found that Tregs produce high amounts of CXCL8 (IL-8), a potent neutrophil chemoattractant. Tregs also produced other CC and CXC family chemokines, including CCL2-5, CCL7, and CXCL10. Whereas ectopic expression of FOXP3 suppressed cytokine production, it

significantly induced CXCL8. Moreover, supernatants from Tregs attracted neutrophils via a CXCL8-dependent mechanism. These data provide the first evidence that Napabucasin although classical Tregs are defined by their lack of proinflammatory cytokine production, they secrete significant quantities of chemokines and thus may have an unappreciated role in directing the recruitment of immune cells. A notable characteristic of classically defined FOXP3+ Tregs is their inability to secrete T-cell-derived inflammatory cytokines such as IFN-γ and TNF-α 1. Although it is generally accepted that Tregs express a variety of chemokine receptors 2–5, very little is known about their capacity to produce chemokines and thereby direct trafficking of immune cells. Tregs reside in both lymphoid and non-lymphoid tissues 4, 6, and are present during the initiation of inflammatory responses. We speculated that, in addition to their known capacity to suppress immune cells upon arrival into inflammatory tissues, Tregs might regulate the recruitment of additional

immune cells by directly secreting chemokines themselves. We therefore investigated Rucaparib purchase the chemokine expression profile of human FOXP3+ Tregs and surprisingly found that they produce substantial amounts of CXCL8 in addition to other chemokines. Evidence that Tregs also stimulated the migration of neutrophils

suggests that these immunoregulatory cells may have an unappreciated role in recruitment of innate immune cells. As Tregs (-)-p-Bromotetramisole Oxalate are present in the early stages of an immune response, we investigated whether they may have the capacity to influence the recruitment of innate immune cells such as neutrophils via production of chemokines. We initially focused on CXCL8, which is made by a variety of leukocytes and signals through CXCR1 and CXCR2, since this is a strong chemoattractant for neutrophils 7, 8. CD4+CD25− and CD4+CD25+ T cells were isolated using magnetic separation, stimulated with αCD3/αCD28-coated beads and levels of secreted CXCL8 in supernatants were determined. As shown in Fig. 1A, CD4+CD25+ T cells produced similar levels of CXCL8 compared to CD4+CD25− T cells, with an average of 2.3±2.1 ng/mL of CXCL8 and 0.7±0.8 ng/mL of CXCL8, respectively. Recent studies have demonstrated that a significant proportion of Tregs have the capacity to produce IL-17 9–12 and Th17 cells are known to produce CXCL8 13, 14.