It was shown previously to recruit NK cells in an atherosclerotic plaque [11]. Therefore, it is likely that IL-15 plays an important role in the recruitment of activated leucocytes from the blood stream in the infracted myocardial region of persons who died early after MAPK inhibitor an acute coronary event. This hypothesis is supported by the abundant IL-15 expression in the border-necrotic, viable myocardiocytes that surround lymphocytes infiltration in the form of necklace. Although the CD56+bright NK cell subset represents mostly

cytokine-producing, regulatory NK cells in a steady state condition, they are able to become highly cytotoxic under tissue-specific inflammatory Th1 cytokine stimulation, such as the combination of IL-15 with other cytokines [12]. This was confirmed in vitro even with decidual CD56+bright NK cells [27], whose cytotoxicity is normally strongly down-regulated in situ by local immune-endocrine interactions during the first trimester of pregnancy. However, there is no clear evidence for JAK inhibitor the involvement of particular cytotoxic mediator(s) in the

apoptosis of myocardial tissue after infarction. Here, we show for the first time the presence of the pro-apoptotic molecule GNLY in the cytoplasm of CD3+ and CD56+ cells, which take part in lymphocyte infiltration in the centre of MI in the patients who died in the first week after coronary artery thrombosis. GNLY can be easily released from the cells upon pro-inflammatory stimulation [19], what is supported with significantly lower MFI for GNLY in peripheral blood

lymphocytes of MI patients when compared with healthy control. NADPH-cytochrome-c2 reductase In turn, the soluble mature form of GNLY could enhance secretion of Th1 chemokines from macrophages and exhibit chemotactic properties for monocytes, mature dendritic cells, NK cells, and CD4+ and CD8+ T cells with a CD45RO+ phenotype, but not naïve CD45RA+ cells, as was shown previously [19], thus contributing to the accumulation of immune effectors in the myocardium after infarction [2]. On the other side, GNLY could hasten resolution rather than worsen cardiac post-infarction inflammation because of the finding of GNLY+ cells within accumulations of apoptotic leucocytes 1 week after the acute coronary event. K562 killing represents a model for in vitro testing of NK cell-mediated self-aggression, because K562 cells do not express MHC class I protein forms, as is known for damaged tissue cells [30]. Significant spontaneous peripheral blood NK cell- and GNLY-mediated apoptosis of K562 cells, which occurs in the first week after the acute coronary event, disappeared on day 14, with a concomitant decrease in the percentage of GNLY+ cells and the GNLY+ CD56+ bright NK cell subset in the circulation.

19 As expected, IL-17A expression was also ABT-263 purchase largely dependent on Th17-polarizing conditions (i.e. treatment with both TGF-β and IL-6; Fig. 1a), although a small number of IL-17A+ cells was observed in the TGF-β-treated cultures (data not shown), and was enhanced by the addition of IL-23. G-1 treatment resulted in an increase in the percentage of IL-10+ cells within Th 17 cell-polarized cultures (Fig. 1b), including within cultures supplemented with IL-23 (Fig. 1c), which is known to be important in stabilizing the phenotype of Th17 populations.6 This G-1-mediated IL-10 expression was specific as no increase

in the prevalence IL-17A+ cells was observed in either of the Th17-polarizing conditions (Fig. 1b,c). In addition, G-1 treatment had no effect on IFN-γ expression in cultures stimulated with CD3/28 alone (Fig. 1d); however, few IFN-γ+ cells were detected in the other culture conditions tested (see Supplementary material, Fig. S1). To determine whether

the induction of IL-10+ cells translated into a specific increase https://www.selleckchem.com/products/Roscovitine.html in the secretion of IL-10 from G-1-treated cultures, naive T cells were collected and stimulated as above, in the presence of TGF-β and IL-6. After 4 days of differentiation, DMSO-treated and G-1-treated cells were collected, washed with medium to remove any cytokines released over the course of differentiation, and re-plated Tangeritin at 106 cells/ml. Cells were then re-stimulated with anti-CD3ε antibody for 24 hr, after which culture medium was analysed for the presence of newly secreted IL-6, IL-10, IL-17A, TNF-α and IFN-γ by Luminex multiplex assay. Cells differentiated in the presence of G-1 produced approximately threefold more IL-10 than control cultures (Fig. 2a), consistent with our observation that G-1 induced an IL-10-producing population. No difference in the secretion of IL-6, IL-17A, TNF-α or IFN-γ was detected (Fig. 2b–e), again suggesting that G-1 was specifically driving the production of the anti-inflammatory cytokine IL-10, and not pro-inflammatory mediators

such as TNF-α and IFN-γ. Taken together, these data show that G-1 can specifically drive IL-10 expression within, and secretion from, CD4+ T-cell populations. As G-1-induced IL-10 expression was dependent on Th17-polarizing conditions, we sought to determine the relationship between G-1-induced IL-10+ cells and those expressing the characteristic Th17 cytokine IL-17A. Hence, naive T cells were again collected by FACS and polyclonally stimulated in the presence of TGF-β and IL-6. Cells were cultured with increasing doses of G-1 (1–500 nm) and analysed for IL-17A and IL-10 by intracellular cytokine staining (Fig. 3a). Our data reveal a dose-dependent increase in IL-10+ IL-17A− (Fig. 3a,b) and IL-10+ IL-17A+ cells (Fig.

Recurrent pregnancy loss (RPL), commonly defined as three or more spontaneous pregnancy losses before 20 weeks of gestation, is as frequent as in 1–2% of reproductive couples.[2] The expected prevalence of pregnancy loss following three or more episodes is one in 300 pregnancies, 0.3%.[3] The etiology of RPL is multifactorial, STA-9090 solubility dmso and sometimes women with RPL showed multiple causative factors following thorough evaluation.[4] In general, more than half of women

with RPL have autoimmune or alloimmune abnormalities. Antiphospholipid syndrome is a well-known autoimmune factor, which causes thrombosis in the uterine vessels and decrease in blood supply to the fetomaternal interface. Alloimmune abnormalities seem to significantly contribute to the pathogenesis of RPL, even though the exact extent of these abnormalities remains to be defined. Natural killer cells have been extensively studied in RPL. High proportion and high cytotoxicity of NK cells have been reported as poor prognostic factors.[5-7] In addition, an increased population of CD4+ Th1 cells is also thought to be harmful in early pregnancy.[8-10] Recent advances in immunologic studies have widened our knowledge of how the immune response is regulated.

Regulatory T cells are considered the most important immune regulator, especially in the peripheral immune system.[11, learn more 12] Recently, a new T-cell subset was introduced as another key effector T cell. These Th17 cells, which secrete IL-17, are thought to play a role in chronic inflammation and protection from fungal infection.[13, 14] There is growing evidence that regulatory T and Th17 cells are involved in establishment and maintenance of pregnancy as regulator and effector cells, respectively.

Many researchers suggest that an immune imbalance between effectors Terminal deoxynucleotidyl transferase and regulatory cells may lead implantation failure and many other pregnancy disorders. This review will discuss recent and review recent studies concerning regulatory T and Th17 cells in RPL and infertility. For immune homeostasis, the balance between effector cells and regulator cells is necessary. Some conditions such as microbial infection trigger immune activation to defend against microorganisms or repair tissue damage. However, this activated immune response should be downregulated and return to the same normal state as prior to activation. The idea of immune regulation by thymic lymphocytes was introduced by Gershon and Kondo in 1970,[15] and T lymphocytes that were capable of suppressing an immune response were named as suppressor T cells.[16] Even though there were many efforts to identify these cells, the search for the elusive suppressor T cells was not successful for a few decades. In 1995, CD4+ CD25+ T cells were reported as a particular T-cell subset with regulatory function in mice.

A variation in reactivity levels was found, with the same effector cells (effector A) showing higher

reactivity, as in the previous experiment. The results given are for the ADCC activity with NK values (reactivity without antibodies) subtracted. CD8+ Veliparib cells were also tested as effector cells and, as expected, the activity without antibodies was overall at a negligible level, although with low, yet detectable ADCC activity for effector A cells and anti-HERV-H/F Gag antibodies. The results for both types of effector cells are shown in Fig. 5 both as increments where results with preimmune sera are subtracted from the results with immune sera and also as the value in folds (immune sera/preimmune sera). We find that increments are the most accurate and instructive values, as artificially increased values may result from calculating folds, when the denominator is below 1·0. The causative agent(s) initiating MS continues to evade exposure of their nature. The processes leading to cell death are also incompletely understood, although parts of the process are known, thus offering possibilities for different types of intervention in the course or the symptoms of the disease. Cytotoxicity reactions are not investigated greatly, either for the types of possible effector cells or for the antibodies/epitopes involved, although these reactions

may play a significant role in MS pathogenesis by killing CNS cells expressing the epitopes. The type of effector cells gaining most attention recently have been CD8+ T cells FK506 research buy rather than CD4+ T cells [14, 15], which for several years were regarded as the main participants

in the disease processes [16], due in part to extensive investigations based on the animal model of brain inflammation, experimental autoimmune encephalomyelitis (EAE). This model has some similarities but also significant differences from MS, illustrated markedly by the lack of efficacy of clinical MS trials targeting CD4+ T cells [17]. Different types of cytotoxic activities of possible significance are due to NK [18] or ADCC, both executed mainly by CD56+ cells. In particular, the latter type of Lonafarnib concentration cytotoxicity may be worthwhile studying, as increased production of oligoclonal antibodies against both known and unknown epitopes (including HERV and herpesvirus epitopes) is one of the characteristic and puzzling findings in MS [19-21]. For several years we have grown blood lymphocytes from MS patients in our laboratory [9]. Some of these lymphocytes, particularly when sourced from MS patients in relapse, have changed the growth pattern into continuously growing B lymphoblastoid cell cultures expressing and producing endogenous retroviruses, predominantly HERV-H/F, and also HERV-W, together with low amounts of Epstein–Barr virus proteins.

Analogous to our findings with CXCR3−/− mice, CCR2−/− and CCR5−/− mice remain susceptible to EAE [40, 41]. Whether this is due to the adoption of compensatory trafficking pathways by the single knockout mice will only be determined by future experiments with double or triple knockouts. The redundancy of chemokines in the EAE model is further illustrated

by a previous publication showing that simultaneous blockade of CXCR3 and CXCR4 was therapeutically efficacious in adoptively transferred EAE in comparison to targeting CXCR3 alone [42]. In conclusion, the strategy of antagonizing individual chemokine/chemokine receptor interactions in individuals with MS, including those patients with this website a skewed

effector population, might be undermined by inherent redundancies in chemokine networks. The ideal therapeutic target would be a molecule that is exclusively expressed on autoimmune effector cells and that is critical for pathogenicity. Until such a Sotrastaurin mw molecule is identified, the treatment of autoimmune disease will have to balance therapeutic effectiveness against the untoward consequences of immunosuppression. About 8- to 12-week-old C57BL/6 and CD45.1 congenic B6 Ly5.2/Cr mice were obtained from NCI Frederick (Frederick, MD, USA). Cxcr3−/− mice were provided by C. Gerard, the generation and characterization of which were described previously [43]. CXCL10−/− mice were obtained from The Jackson Laboratory (Bar Harbor, ME, USA). Mice were housed in micro-isolator cages under specific pathogen-free, barrier facility conditions. All procedures were conducted in strict accordance with protocols approved by the University of Michigan Committee on Use and Care of Animals. Active induction

of EAE involved s.c. injection of 100 μg MOG35–55 MEVGWYRSP-FSRVVHLYRNGK (Biosynthesis, Lewisville, TX, USA) in CFA (Difco, Detroit, MI, USA) containing 4 mg/mL heat-killed Mycobacterium tuberculosis H37Ra (Difco). Each mouse also received 300 ng of Bordetella PT(List Biological Laboratories) Fluorometholone Acetate i.p. on day 0 and 2 postimmunization. For passive induction, mice were immunized as above, but without administration of PT. Ten days postimmunization, a single-cell suspension was prepared from pooled draining inguinal, axillary, and brachial LNs and passed through a 70 μm cell strainer (BD Falcon, Franklin Lakes, NJ, USA). LN cells were cultured in vitro for 4 days with MOG35–55 under conditions favorable to the generation of Th1 cells (rmIL-12, 6 ng/mL; rmIFN-γ, 2 ng/mL; anti-IL-4 (clone 11B11), 10 μg/mL) or Th17 cells (rmIL-1α, 10 ng/mL; rmIL-23, 8 ng/mL; anti-IL-4 (clone 11B11), 10 μg/mL; anti-IFN-γ (clone XMG1.2) 10 μg/mL). After 4 days culture, LN cells were collected and 2 × 106 CD4+ T cells injected i.p. in sterile PBS.

Associations with other components were generally weak or null, except for the association of nocturia CT99021 in vivo with increased odds of hypertension (adjusted OR 2.00, 95% CI 1.27–3.14) and increased triglycerides (adjusted OR 1.64, 95% CI 1.07–2.51), and mild LUTS (AUASI 2–7) and mild incomplete emptying with a waist circumference greater than 102 cm. Kupelian et al.24 hypothesized that possible pathophysiological mechanisms to explain the relationship of voiding rather than storage symptoms with MS of BACH survey

data the influence of hyperglycemia on the parasympathetic neurons in the pelvic ganglion. Chronic hyperinsulinemia induced peripheral neuropathy resulting in increased bladder neck obstruction and reduced bladder contractility.7,25 Increased glucose levels are likely to be accompanied by hyperinsulinemia which results in an increase in insulin-like growth factor (IGF). IGF is involved in prostate growth.26 In the Baltimore Longitudinal Study on Aging (BLSA) cohort, men with elevated fasting glucose were three times more likely to have BPH than men with normal glucose levels.27 Increased fasting glucose and diabetes were also associated with the presence of LUTS in this cohort study. Other studies including

the NHANES III cohort (Rohrmann et al.28), Flint Men’s Health Study,29 and a case-control study by Neuhouser et al. (LUTS-MS30) also demonstrated the association of IGF with the risk of LUTS in men. C-reactive protein (CRP), a well-known inflammatory Obeticholic Acid order marker, is known to have an association

Digestive enzyme with cardiovascular diseases. Kupelian et al.31 assessed the relationship between CRP level and LUTS, and found a statistical significant association between CRP levels and overall LUTS among both men and women. There was a dose-response relationship between CRP levels and associated LUTS. However, Hong et al.32 studied the relationship between CRP and overactive bladder (OAB) in women without MS and found no significant correlation between CRP level and OAB symptoms. Many studies support the association of CRP and LUTS, but further research should be conducted to differentiate the significance of inflammatory process with or without MS in the development of LUTS. The prevalence of MS is increasing all over the world and Korea is not an exception. Most of the studies of MS and LUTS in Korea are risk analyses of BPH. Jang et al.33 analyzed the association of MS and BPH in 1412 men. They found that there was a significant correlation between each MS factor and prostate volume. Koo et al.34 also reported that MS is associated with prostate volume-related factors, but not with voiding dysfunction in Korean men aged 60 years or older. Among the subcategories of MS, they reported that obesity is the factor most strongly related to prostate volume. Yim et al.35 studied the correlation of prostate volume with MS and its related parameters.

The role of siglec-H as an endocytic receptor has been characterized by Zhang et al.,31 who targeted pDCs using anti-siglec-H IgG coupled to ovalbumin. Siglec-H-dependent uptake led to cross-presentation of ovalbumin antigens to CD8+ T cells via MHC class I molecules on pDCs, resulting in antigen-specific CD8+ T-cell expansion.31 Mouse CD33 differs from PS 341 human CD33 because it also encodes a charged transmembrane containing a lysine residue. To date, it has not been shown whether this feature enables murine CD33 to associate with adaptor molecules such

as DAP12. However, a preliminary analysis of CD33-deficient mice revealed no clear-cut differences in regulation of inflammatory responses.34 Negative regulatory functions of different CD33rSiglecs have been observed in studies of cell expansion, cytokine production, Crizotinib order cellular activation and induction of apoptosis

(reviewed in ref. 1). It is likely, although not directly demonstrated in most cases, that the cytoplasmic ITIM and ITIM-like motif are important in these functions via recruitment of downstream targets such as SHP-1 and SHP-2 tyrosine phosphatases as well as other SH2-domain-containing effector molecules.1,35 Below we summarize recent data supporting a role of CD33rSiglecs in the regulation of inflammatory and immune responses. Using over-expression in mouse RAW and human THP-1 macrophage-like cell lines, siglec-9 expression was shown to suppress the Toll-like receptor (TLR) -dependent production of pro-inflammatory cytokines, tumour necrosis factor-α (TNF-α)

and IL-6, in macrophages following lipopolysaccharide (LPS) or peptidoglycan stimulation.35 In contrast, production of the anti-inflammatory cytokine IL-10 Adenosine triphosphate was enhanced. These effects were abolished when the critical tyrosine residues in ITIM and ITIM-like motifs of siglec-9 were mutated.35 These observations are consistent with earlier studies of human monocytes in which siRNA-mediated knockdown of CD33 led to spontaneous secretion of pro-inflammatory cytokines36 and collectively they indicate that ITIM-bearing CD33rSiglecs may restrain the pro-inflammatory functions of macrophages. Cross-talk between CD33rSiglecs and TLR signalling pathways was also demonstrated for siglec-H.32,33 Following cross-linking of siglec-H expressed in pDCs with antibodies, type-I interferon production in response to TLR-9 ligation with CpG was strongly inhibited. This paradoxical inhibition of cytokine production via DAP12-coupled ‘activating’ receptors has been observed with several pDC-expressed receptors and may be the result of a signalling pathway in pDCs shared with B cells that suppresses type 1 interferon production.37 Siglec-E is a typical inhibitory murine siglec expressed on myeloid cells.38,39 Boyd et al.40 have recently demonstrated a TLR- and MyD88-dependent up-regulation of siglec-E on murine bone-marrow-derived macrophages.

In B cells, IRF4 is instead recruited to high-affinity ETS–IRF composite motifs (EICE) through its interaction with PU.1 or the closely related transcription factor Ixazomib supplier SPI-B [11, 13]. This cooperative DNA binding relies on two protein–protein

contacts, one between the phosphorylated PEST region of PU.1 and the RD of IRF4, and the other depending on an association of the DBD of PU.1 with that of IRF4 [11, 13]. As T cells express only low amounts of PU.1 and SPI-B, IRF4 instead interacts with a heterodimer of the activator protein 1 (AP-1) family member JUN and basic leucine zipper transcription factor ATF-like (BATF) in these cells. The resulting IRF4–JUN–BATF heterotrimeric complex then binds to AP-1–IRF4 composite elements (AICEs) [14-17]. Consistent with the functional

cooperation of these transcription factors, the binding of BATF to AICE was diminished in Irf4–/– T cells and conversely, IRF4 binding was diminished in Batf–/– cells [14, 16]. In T cells, two types of AICEs have been described that differ in the distance between the IRF4- and AP-1-binding sites. selleck inhibitor In one type of AICE, the AP-1 and IRF-binding motifs are adjacent, whereas in the other type of AICE, these motifs are separated by four nucleotides [16]. The cooperative assembly of BATF–JUN with IRF4 involves both DNA binding to the respective AP-1 and IRF consensus elements and physical BATF–IRF4 interactions that require the presence of the amino acid residues His55, Lys63, and Glu77 at the BATF leucine zipper motif [15, 16]. IRF4 has been shown to bind together with BATF–JUN heterodimers P-type ATPase to AICE in T cells, B cells, and DCs. Thus, in B cells and DCs, IRF4 cooperates with both ETS factors and BATF–JUN heterodimers to bind to EICEs and AICEs, respectively. In contrast, in T cells, IRF4 binds almost entirely to AICEs due to limited expression of ETS factors [14-16]. In addition, IRF4 cooperates with other transcription factors, including members of the NFAT, STAT, or homeobox protein families [4] as well as with B-cell lymphoma 6 (BCL-6) [18], FOXP3 [19], retinoic acid related

orphan receptor gamma t (ROR-γt) [20], and the SMAD2–SMAD3 complex [21]. Depending on the respective interaction with transcriptional cofactors expressed in a specific cellular context, IRF4 can operate as transcriptional activator or repressor [4]. In contrast to IRF1 and IRF2, which are upregulated by IFN signaling, IRF4 expression is primarily not induced by type I or II IFNs, but by other stimuli, including antigen receptor engagement, stimulation with LPS, or signaling induced by CD40- or interleukin-4 (IL-4) [3, 18]. In T cells, IRF4 is strongly induced within a few hours upon T-cell receptor (TCR) stimulation and its expression declines when the cells return to a resting state. As TCR signaling is the major pathway to induce IRF4 in T cells, IRF4 is expressed across all known T-cell subsets [12, 22-24].

18,19 In humans, CR1 is mostly restricted to erythrocytes and podocytes18 but like MCP, rodents only have limited expression of CR1 that is generated by alternative splicing from the Cr1/2 gene.21 In place of MCP, the rodent-specific complement regulator Crry is expressed ubiquitously in mice (e.g. endothelium, mesangium, tubules)18,19 and is considered a functional homolog of human MCP.13,22 Clinically, strong connections between complement and kidney diseases have been provided by cases of deficiency or dysfunction of the fluid-phase complement regulators fH

and fI.23–27 Unlike the membrane-bound inhibitors, the fluid-phase inhibitors circulate in the plasma and are largely produced outside the kidney in the liver.15,16,28 However, there is evidence that fH can be synthesized by some phagocytic cells and by murine platelets selleck chemicals llc and podocytes.16,18,29,30 These observations notwithstanding, the current view of fH function, supported by both clinical NVP-BGJ398 in vivo and animal modelling studies, is that it works principally as a fluid-phase protein to prevent AP complement activation in the plasma as well as on the cell

surface (Fig. 3). The latter activity of fH is dependent on its C-terminal domains that bind to surface deposited C3b in the context of host cell-specific polyanionic constituents (Fig. 3).31,32 The identity of the host cell components with which fH interacts has not been positively identified, although heparin has been used frequently as a model ligand in in vitro experiments and several studies have shown that fH can bind to glycosaminoglycans expressed on the cell surface.33,34 Whatever the binding partner(s) may be, it is clear that fH attachment to renal endothelial cells is essential to kidney health, particularly under pathological conditions.32,35 Many of the kidney disorders that have been linked to complement can be attributed to insufficient complement regulation, either as a result of regulator deficiency or dysfunction, or due to exuberant AP complement amplification that overwhelms the normal regulatory mechanisms.36–39 A few of these conditions are highlighted and discussed below.

Ischaemia-reperfusion injury (IRI) is one of the most frequent causes of acute renal failure (ARF) and can have devastating effects on kidney function. Not only does IRI contribute G protein-coupled receptor kinase to 50% of intrinsic cases of ARF, but systemic illnesses such as congestive heart failure or sepsis can also reduce renal blood flow and cause ischaemic injury.40 Transplant surgery also involves IRI and can cause ARF from depressed blood flow during anaesthesia on top of the inflammation from the ischaemic tissue being transplanted. When hypoxic conditions exist (i.e. reduced blood flow), cell metabolism is impaired, which generates reactive oxygen species and apoptotic signals.41 While ischaemia causes initial injury, the following reperfusion is far more damaging.

They are not only involved in tissue development and homeostasis but also perform various immune regulatory functions 1–4. They are efficient effector cells of the innate immune system as they have the capacity to respond to parasite, viral or bacterial infections. In addition, eosinophils have an important role in bridging innate and adaptive immunity. In particular, activated eosinophils are crucial in promoting TH2 responses by secreting TH-cell polarizing cytokines such as IL-4 and IL-13, and this release of IL-4 also promotes rapid differentiation of B cells into IgM plasma cells 5, 6. Thus, in T-cell-dependent immune responses eosinophils are required for the early protective IgM response

7, 8. In contrast, the generation of an antigen-specific IgG response seems not to be affected as in eosinophil-deficient ΔdblGATA-1 this website mice B-cell maturation in germinal centers and their differentiation into memory B cells and plasma cells were shown to be normal 9. Eosinophils, however, are crucial for the long-term survival of plasma cells in the BM as in their absence the plasma cells quickly die by apoptosis. Thus, as a major source of the plasma cell survival factors APRIL and IL-6, eosinophils CHIR-99021 mouse have an essential function in the

long-term maintenance of humoral immunity 9. Eosinophils produce and store a wide range of cytokines whose release is dependent on the nature of the activating stimulus 10–12. Eosinophils respond by piecemeal degranulation leading to a highly controlled secretion of specific mediators 13. Full activation of eosinophils may induce de-granulation and thus a rapid release of tissue-destructive cationic proteins. Activated eosinophils may also respond by the ejection of extracellular traps consisting of mitochondrial DNA and granule-derived mediators 14. Human eosinophils

have been shown to express constitutively not only the TH2-related cytokines IL-4, IL-13 and IL-10 but also IL-12 and IFN-γ, see more which are characteristic of TH1 responses 11, 15. Upon immunization, IL-4 production by eosinophils is up-regulated, although similar effects were seen when animals were injected with aluminum potassium sulfate (alum) alone, an adjuvant commonly used in antigen priming 7, 8. To further investigate the activation of eosinophils and their expression of cytokines, BALB/c mice were immunized with the T-cell-dependent antigen 2-phenyl-oxazolone (phOx) precipitated in alum or emulsified with CFA. Eosinophil activation was monitored in the primary response and also after secondary challenge with soluble antigen. We found that only in the presence of antigen was a stable activation of eosinophils and continuous expression of plasma cell survival factors achieved. By contrast, injection of adjuvant alone only transiently enhanced cytokine production. Together, these data suggest that in immune responses, eosinophils are primed to become effector cells that prevent plasma cells from undergoing apoptosis.