In a more recent study, ADCC responses can

induce epitope-specific escape mutations as early as 50 days after T0.[26] Taken together, these studies suggest that the first functional antibody responses to Env appear almost CDK inhibitor concomitantly with binding antibodies, which is approximately 50 days before the emergence of the first detectable neutralizing antibodies against autologous viruses. It goes without saying that antibodies must be present at the time of acquisition to block it and this can only be accomplished by active or passive immunization. In recent years, a good picture of the early events during acquisition after vaginal exposure has emerged (reviewed in refs [21, 22, 36, 37]). Figure 3 summarizes the virological events that occur during the eclipse phase where the ‘window of opportunity’ is key for blocking acquisition. Passive immunization studies in NHPs

using neutralizing antibodies suggest that the window of opportunity is 24 hr at most.[38, 39] Transmission across the mucosal epithelium is thought to occur within hours of exposure and results in infectious virus reaching susceptible CD4+ target cells. Transmission learn more across the mucosal barrier can be passive through epithelial breaks but an active transport mechanism is also known.[40] The nature of the first infected type of CD4+ cell has been debated over the years but recent acute transmission studies strongly suggest that it is a CD4+ CCR5+ memory T cell.[41, 42] Strikingly, most HIV infections are due to a single founder virus,[41, 42] which is also true for model AIDS viruses in NHPs.[41] It takes approximately 24 hr for an infected CD4+ cell to produce infectious virus,[43]

so it is likely that the earliest time that HIV can start to spread to other CD4+ CCR5+ T cells is within the first 24–28 hr, a small number of local infected founder cells 2–3 days after exposure[44, 45] (Fig. 3). Local expansion of the infected founder cells occurs around days 4 to 5 post-exposure,[44, 45] likely aided by an innate response of the mucosal epithelium that attracts additional Doxacurium chloride target cells to the site (ref. [46] and discussed in ref. [36]). Virus or virus-infected cells from the local expansion spread via afferent lymphatics to the draining lymph node, which is rich in additional CD4+ CCR5+ target cells. From there, virus and infected cells spread systemically via the thoracic duct leading to distal and propagating infections in the gut and spleen by haematogenous flow and finally back to lymph nodes. Once the infection spreads from the local focus, it is very likely that the window of opportunity is closed because of the establishment of viral reservoirs and protective niches in distal tissues. The systemic spread of infection ultimately leads to plasma viral loads that cross the 100 copy limit of sensitivity (i.e.

These chains are added very soon after a protein enters the ER, but they undergo extensive remodeling (processing), especially in the Golgi. Processing changes the sensitivity of the N-glycan to enzymes that cleave entire sugar chains or individual monosaccharides, which also changes the find more migration of the protein on SDS gels. These changes can be used to indicate when a protein has passed a particular subcellular

location. This unit details some of the methods used to track a protein as it trafficks from the ER to the Golgi toward its final location. Curr. Protoc. Immunol. 89:8.15.1-8.15.25. © 2010 by John Wiley & Sons, Inc. “
“Calcitonin gene-related peptide (CGRP) is widely distributed and plays important roles in a wide array of biological functions. It is enriched in primary sensory neurons and hence involved in nociception and neurogenic inflammation. Recent studies have shown that CGRP can be produced by immune cells such as monocytes/macrophages following inflammatory stimulation, suggesting a role in innate immunity. However, it is unclear how CGRP is up-regulated in macrophages and if it plays a role in macrophage functions such

as the production of cytokines and chemokines. Using enzyme-linked immunosorbent assay (ELISA) Fluorouracil price and multiplex ELISA, lipopolysaccharide (LPS) was found to induce CGRP in the RAW 264.7 macrophage cell line. LPS-induced inflammatory mediators such as nerve growth factor (NGF), interleukin-1β (IL-1β), IL-6, prostaglandin E2 (PGE2) and nuclear factor-κB (NF-κB) signalling are involved in inducing CGRP, whereas the NGF receptor trkA and CGRP receptor signalling pathways are unexpectedly involved in suppressing LPS-induced CGRP, which leads to the fine-tune regulation of CGRP release. Exogenous CGRP and CGRP receptor antagonists, in a concentration-dependent manner, stimulated, inhibited or had no effect on basal or LPS-induced release of monocyte chemoattractant protein-1, IL-1β, IL-6, tumour necrosis factor-α and IL-10 in RAW macrophages. The ligand-concentration-dependent regulation of the production of inflammatory mediators ALOX15 by CGRP receptor signalling is a novel mechanism underlying

the stimulating and suppressing role of CGRP in immune and inflammatory responses. Together, our data suggest that monocytes/macrophages are an important source of CGRP. Inflammation-induced CGRP has a positive or negative reciprocal effect on the production of other pro- and anti-inflammatory mediators. Thereby CGRP plays both facilitating and suppressing roles in immune and inflammatory responses. Calcitonin gene-related peptide (CGRP) is a peptide derived from the alternative splicing of the calcitonin gene.1 It is widely distributed in both central and peripheral nervous systems and exerts a wide array of biological effects.2–4 In peripheral tissues, CGRP is particularly enriched in primary sensory neurons5 and plays an important role in nociception and neurogenic inflammation.

Appropriate regulation of gut immunity thus depends upon a complex three-way interplay between host cells, commensals and pathogens, and can exert a major impact on systemic responses including allergy and autoimmunity. In the gastrointestinal (GI) tract, the immune Saracatinib system is faced with the most demanding of all decision-making, with little room for error. It is imperative at all times to discriminate between, and respond correctly to, beneficial symbionts, harmless food antigens and potential pathogens [1]. There is increasing appreciation that regulatory T cells (Tregs)

play a prominent and essential role in maintaining appropriate responsiveness in the gut [2,3], actively enforcing homeostasis and preventing untoward immune responses occurring. While stimulated by specific antigens, of both self and non-self origin, Tregs can transcend antigen specificity, mediating bystander suppression in a manner likely to modify systemic immune status as suggested by the ‘hygiene hypothesis’. Recent studies have changed our perspective of commensal microbes from benign but inert passengers to active participants in both the postnatal development of mucosal immunity and in its long-term steady-state function. Germ-free mice show extensive deficiencies

in intestinal immune system development, with reduced lymphoid tissue and fewer Tanespimycin lymphocytes [4]. The CD4+ T cell population is diminished, affecting T helper type 1 (Th1) cells disproportionately although, remarkably, Treg frequencies are maintained or increased in germ-free mice. These and other data have established that defined components of the gut flora can play a major role in intestinal homeostasis, including protection against gut injury and mediating oral tolerance against dietary

antigens. MycoClean Mycoplasma Removal Kit In mice which acquire a conventional microbiome, the immune system develops normally while maintaining a continuing dialogue with the commensal population. Here, one of the dominant roles of Tregs is to prevent exuberant responses against gut flora, with which the intestinal tract is in intimate contact. Nevertheless, how commensals communicate with cells to ensure immune homeostasis is still unclear. One critical factor in this interaction at the molecular level is the host Toll-like receptor (TLR) system, as demonstrated by spontaneous colitis in TLR-5-deficient mice [5]. Where colitis is induced experimentally (e.g. by dextran sulphate administration), the absence of TLR signalling then results in greatly aggravated pathology, again indicating that TLR-mediated recognition of commensal molecules contributes to dampening immune reactivity [6]. The requirement for TLR signalling in induction of oral tolerance to dietary antigens [7] also speaks to the bimodal participation of the TLR system in both stimulatory and regulatory arms of the immune response. Recent evidence suggests that TLR signalling can impact Treg homeostasis and that Tregs themselves express TLRs selectively.

Candida albicans is a common pathogenic yeast that normally exists in the human microflora, but that can also cause infections. It is an opportunistic pathogen that usually lives as a commensal in the healthy human host. Alterations in the balance between the commensal and the host, such as those that occur in the immunocompromised patients may trigger infection of the mucosal epithelia, followed by dissemination via the bloodstream and PF-02341066 price colonization of internal organs [6, 7]. Deltamethrin,

a synthetic pyrethroid type II, is highly effective against a broad spectrum of insects. The main sources of general population exposure to this pesticide are contaminated food and water, and it has been reported that deltamethrin is readily absorbed by the oral route [8]. Several studies have shown buy Dabrafenib that pyrethroid insecticide exposure caused alterations in biochemical and haematological profile and reproduction in the exposed animals [9]. While, studies describing the oxidative stress mechanisms in pyrethroid-induced toxicity are limited,

deltamethrin was observed to suppress the immune functions. It is also reported to alter blood parameters and antioxidant defense of mice in previous studies [10, 11]. An investigation therefore was undertaken to assess impact of deltamethrin-induced alteration of host resistance to infection (C. albicans challenge). Animals.  The study was conducted in Swiss albino male mice (30–32 g). Female guinea pigs (250 g) were used for the preparation of complement why for plaque forming cell (PFC) assay. The Central Animal

House Facility of the University provided the animals. The study was approved by the Institutional Animal Ethics Committee. The animals were given mild anesthesia using di-ethylether. The animals were bred and maintained under standard conditions: temperature 25 ± 2 °C and photoperiod of 12 h. Commercial pellet diet and water were given ad libitum. Animals were divided in five different groups.  Group I:  Control animals, treated with corn oil orally, and normal saline intraperitoneally (i.p.) for 10 days. After taking the blood from orbital plexus of mice for haemagglutination titre (HT) assay, animals were sacrificed by cervical dislocation under mild anesthesia and their liver and spleen were aseptically removed. The spleens of few animals (n = 5–6) were used for PFC assay, whereas spleen from rest of the animals (n = 5–6) were homogenized with a tissue homogenizer (Potter-Elvehjem homogenizer) using 5 ml of saline and used for infection investigation. Colony forming unit (CFU) was counted in liver and spleen by the method of Srivastava et al., [12]. Chemicals.  Antibiotic antimycotic solution (100X), fetal bovine serum (FBS), yeast extract, peptone, dextrose, agar, Hank’s balanced salt solution (HBSS), Histopaque-1077, phosphate buffer saline (PBS) and RPMI-1640 medium were purchased from Sigma-Aldrich Co. (St Louis, MO, USA). Deltamethrin.

aeruginosa and those isolated from chronic Inhibitor Library order skin wounds with respect to the production of virulence determinants such as pyocyanin and extracellular protease. The six strains fell into three categories:

the first included the two type strains as well as one of the clinical isolates (PAO1, NCTC 6750 and 15159), the second contained the clinical isolates 23:1 and 27:1 and, finally, strain 14:2 (also a clinical isolate) formed a group on its own. In the first group, all strains expressed pyocyanin, elastase and alkaline proteinase, and two of the three produced the quorum-sensing molecule C4-HSL, while the second group showed no expression of C4-HSL or elastase. Interestingly, strain 14:2 was negative for the expression of C4-HSL, pyocyanin and the proteases. A similar spread in the expression of virulence factors and quorum-sensing molecules among P. aeruginosa strains has been described by others, for instance, Luzar & Montie (1985) and Lee et al. (2005), who investigated chronically

infected cystic fibrosis patients. Both studies showed not only variations between strains isolated from different patients but also changes associated with disease progression. Isolates from patients with more advanced disease showed lower pyocyanin and protease production, suggesting that the evolution of P. aeruginosa strains towards a less virulent phenotype may confer a survival advantage during chronic infection. Thus, in our study, the clinical isolate 14:2, which had Acalabrutinib manufacturer the greatest inhibitory effect on biofilm formation by S. epidermidis and lacked the production of C4-HSL, pyocyanin and proteases, may represent a less virulent strain that has become adapted to enhance its persistence

in the chronic sore environment (Lee et al., 2005). In a recent study by Qin et al. (2009), extracellular products from P. aeruginosa were shown to disrupt S. epidermidis biofilms and it was suggested that extracellular polysaccharide could be responsible for the effect. Thus, the authors proposed that extracellular polysaccharides from P. aeruginosa may represent a novel target for the development of agents to control S. epidermidis biofilms at sites of infection. Mannose- and galactose-containing extracellular polysaccharides were detected in biofilms of all the strains of P. aeruginosa tested here, and thus the inhibition of S. epidermidis Exoribonuclease biofilm formation seen in our study may occur through a mechanism similar to that proposed by Qin and colleagues for biofilm dispersal. Expression of the two extracellular polysaccharides, Pel and Psl, is known to vary according to the strain and environmental conditions (Branda et al., 2005). Although 14:2 did not appear to produce higher levels of these polysaccharides than the other strains, which could account for its enhanced effect on S. epidermidis biofilms, it is possible that, for instance, differences in their relative expression may play an important role.

2d,e).63 Mechanisms that operate where these maternal immune cells directly encounter placental antigens may dampen their effector activities by creating a local immunosuppressive environment. This strategy seems advantageous in that the systemic maternal responses can remain largely intact to defend against pathogens. Work by multiple groups has demonstrated trophoblast-produced soluble factors that may create such an environment by modulating the proliferation and blastogenesis of maternal

lymphocytes. Extracts from day 80 placenta have been shown to inhibit the proliferation of maternal lymphocytes,64 and co-culture of chorionic girdle trophoblasts with maternal lymphocytes caused a decrease in proliferation and a reduction in cytokine production.65,66 Also, a >100,000 kDa molecule isolated from culture supernatants of day 20 conceptuses, termed horse conceptus-derived Torin 1 immunosuppressive factor, was found to inhibit lymphocyte proliferation by inhibiting IL-2R expression.67 Further investigation into trophoblast-produced immunomodulatory factors is warranted, based upon the important role they play in other species. In

humans and mice, trophoblast molecules such as Fas ligand and indoleamine 2,3 dioxygenase have been identified as providing protection from T-cell cytotoxicity,68,69 and the molecules Crry (mouse) and decay-accelerating factor (human) confer protection from the complement cascade.70,71 hCG has been implicated as immunoregulatory molecule Mannose-binding protein-associated serine protease in human

pregnancy;72 however, a study measuring in vitro inhibition of MAPK inhibitor equine lymphocyte proliferation did not support such a role for eCG.64 Evidence also exists that the endometrium of the pregnant mare may be a primary source of local immunosuppressive factors. Prostaglandins in culture supernatant from endometrium of pregnant mares were shown to reduce lymphocyte blastogenesis.73,74 Recently, local populations of regulatory T cells (Tregs) have been identified at the equine materno–fetal interface. The Treg marker FOXP3 has been demonstrated at both the gene and protein levels in the CD4+ cells that surround the endometrial cups.49 Endometrial cup lymphocytes isolated from day 43 to 46 of pregnancy showed a threefold increase in the number of CD4+FOXP3+ cells compared to peripheral lymphocytes. This is consistent with an increase in Tregs observed during pregnancy in multiple other species.75–79 Local regulatory activity by Tregs at the placental interface may be a mechanism by which the early MHC class I+ trophoblast populations are able to resist destruction by the large accumulation of maternal lymphocytes with which they are in contact. In the same day 43–46 endometrial cup lymphocyte samples, an increase in the number of interferon gamma (IFNG)+ lymphocytes was also observed. This observation initially appears to be in conflict with the traditional dogma of a TH2 bias during successful pregnancy.

The successful treatment of 13 sheep affected by ringworm due to Trichophyton mentagrophytes with a mixture consisting of essential oils (EOs) of Thymus serpillum 2%, Origanum vulgare

5% and Rosmarinus officinalis 5% in sweet almond (Prunus dulcis) oil. The effectiveness of EOs and of the major components of the mixture (thymol, carvacrol, 1,8 cineole, α-pinene, p-cymene, γ-terpinene) against the fungal clinical isolate was evaluated by a microdilution test. Thirteen animals were topically administered with the mixture twice daily for 15 days. The other sheep were administered with a conventional PXD101 cell line treatment (seven animals) or left untreated (two animals). Minimum inhibitory concentration (MIC) values were 0.1% for T. serpillum, 0.5% for O. vulgare, 2.5% for I. verum and 5% for both R. officinalis and C. limon. Thymol and carvacrol showed MICs of 0.125% and 0.0625%. A clinical and aetiological cure was obtained at the end of each treatment regimen in only the treated animals. Specific antimycotic drugs licenced for food-producing sheep are not available within the European Community. The mixture tested here appeared to be a versatile tool for limiting fungal growth. “
“Non-steroidal anti-inflammatory Talazoparib in vivo drugs (NSAIDs) are one of the most common pharmacological agents. They have three primary therapeutic properties including anti-inflammatory, anti-pyretic and analgesic effects.

Seven NSAIDs were tested against two species of dermatophytes. Percentage inhibition was determined for effective agents. Diclofenac, aspirin and naproxen showed more potential to inhibit Protein Tyrosine Kinase inhibitor the growth of dermatophytes. Epidermophyton floccosum revealed susceptibility to more number of the tested agents than Trichophyton mentagrophytes. In conclusion, many NSAIDs may have a high potential to inhibit the growth of dermatophytes, while some of the agents belonging

to this pharmaceutical group used in this study showed a potential activity on tested fungi. “
“The occurrence of resistance or side effects in patients receiving antifungal agents leads to failure in the treatment of mycosis. The aim of this experimental study was to investigate the in vitro effects of IB-367 alone and in combination with three standard antifungal drugs, fluconazole (FLU), itraconazole (ITRA) and terbinafine (TERB), against 20 clinical isolates of dermatophytes belonging to three species. Minimum inhibitory concentrations (MICs), minimal fungicidal concentrations (MFCs), synergy test, time-kill curves, fungal biomass (FB) and hyphal damage using 2,3-bis-(2-methoxy-4-nitro-5-sulfenylamino carbonil)-2H-tetrazolium hydroxide assay (XTT) were performed to study the efficacy of IB-367. In this study, we observed that TERB and ITRA had MICs lower values for all the strains compared to IB-367 and FLU. Synergy was found in 35%, 30% and 25% of IB-367/FLU, IB-367/ITRA and IB-367/TERB interactions respectively.

9 ng/mL for IL-2 and 31.25 ng/mL for IL-10. NO2− determination was carried out by the Griess assay as described 40 with some modifications. Briefly, 100 μL of each sample was added to each well of a 96-well plate

in duplicate, 50 μL of 1% sulfanilamide (Sigma) in 2.5% H3PO4 was added and incubated for 5 min, 50 μL of 0.1% naphtylenediamine dihydrochloride (Sigma) was added and incubated for 10 min (room temperature, in the dark); absorbance was read at 540 nm. Standard curves were prepared with sodium nitrite and the detection limit was 1.56 μM. Statistical differences between groups were determined by the unpaired two-tailed Student t-test or One-Way ANOVA with Dunnett’s or Bonferroni’s Multiple Comparison tests using the PRISM software (GraphPad). This work was supported by grants IN-200608 and IN-209111 from PAPIIT (DGAPA, UNAM, Mexico) and by grants 79775, DNA Damage inhibitor 102399 and 102984 from CONACYT (Mexico). The authors are grateful to M. V. Z. Georgina Díaz and M. V. Z. Jorge Omar García for their expert advice and help in the care of the animals and Katharine A. Muirhead for helpful advices on cell tracking dyes. E. P. T.

Selleck Luminespib is recipient of a PhD fellowship from CONACYT (Registro 199991). This work was performed in partial fulfillment of the requirements for the PhD Program of Doctorado en Ciencias Biomédicas of E. P. T. at the Universidad Nacional Autónoma de México. Conflict of interest: The authors have declared no financial or commercial conflict of interest. “
“IgG4 and IgE are immunoglobulin isotypes which are mediated by the same Th2-mediated mechanism. The postulated pathogenic

and protective function of IgE or IgG4, respectively, in allergic disease is opposite in parasitic infection. The possible role of IgG4 against recombinant major allergens on the appearance of different forms of Anisakis simplex-associated Isotretinoin allergic disease was studied. Gastro-allergic anisakiasis (GAA) and Anisakis-sensitization-associated chronic urticaria (CU+) were compared for specific IgE, IgG4 and the respective recognition of Ani s 1 and Ani s 7. Gastro-allergic anisakiasis showed higher IgE and IgG4 levels against crude extract and both recombinant allergens. Whereas IgE recognition of Ani s 7 did not differ and supports both clinical entities to be associated with previous acute parasitism, the IgE recognition rates of Ani s 1 and IgG4 recognition of both Ani s 1 and Ani s 7 were higher in GAA. IgG4 levels were associated with IgE, but also with age, time to last parasitic episode and frequency of fish intake. Logistic regression analysis showed that the presence of specific IgG4 against Ani s 7 was an independent marker associated with GAA. In the diagnosis of Anisakis-associated allergic disease phenotypes (GAA versus CU+), measurement of specific IgG4 against recombinant allergens could be useful. Further, evaluation of specific IgE and IgG4 facilitates more insight into the protective versus pathogenic potential of IgE and IgG4.

There has been ample this website recognition that many urologists worldwide operate on patients with no urodynamic studies at all, solely basing their operative intent on clinical complaints and imaging examinations believing that enlarged prostate gland is directly related to obstruction and urinary symptoms.[2, 3] We believe that the main reason this is done is due to the lack of recognition of the importance and experience of the urodynamic examination in helping to decide the best option in a particular clinical situation, or difficulties in the availability of the exam

due to regional differences. Although it is expected that a regular residency program should provide sufficient training, the amount to accomplish that was not established and therefore some centers may not instruct urodynamicists with

am appropriate volume of exams. This prospective study evaluated 64 junior urologists after an intensive 4-month period at the urodynamic lab and 110 urologists attending voiding dysfunction courses and their modification in attitude after experiencing Crizotinib the exam. Moreover, we looked at how urologists modified their clinical practice after being exposed to intense urodynamic practice as well as how it impacted their rank scale on auxiliary exams and other decisive parameters to decide who should have operations and when. Sixty-four consecutive junior urologists (median age: 29 ± 2.7) admitted to a fellowship program in voiding dysfunction in a 4-month period were prospectively studied with paired questionnaires before and after the mentioned period of training. All enrolled Adenosine triphosphate junior-urologists finished the regular 4-year training period (2 years on general surgery followed by 2–3 years on urology – median 2.7) before the intensive fellowship and all of them were board eligible, although only 37.5% were board-certified.

The certified urologists performed more than 50 transurethral resections of the prostate (TURP) during their training program as a minimum requirement to apply to the national Board of Certification. The median time of urological practice before applying to the fellowship was 2.8 ± 0.21 years. The fellowship program allowed the junior urologist to do more than 400 full-urodynamic exams with free-flow rate, followed by cystometry phase and EMG-P/Q or video-urodynamic depending on the case, under supervision allowing deep and interactive discussion on all exams in a tertiary urodynamic center – 1200 urodynamics per year with a board certified urologist specialized in urodynamics and voiding dysfunctions. Junior urologists were asked to complete questionnaires before and after the 4-month period to measure the impact of formal urodynamic training on the perception of the value of the exam, as well as the scale of different parameters on the appropriate BPH management.

gingivalis can also interact with TLR4 by means of LPS, although in a rather unusual way. The organism can

enzymatically modify the lipid A moiety of its LPS to either evade or antagonize TLR4 activation (Fig. 3), in contrast to the classical enterobacterial find more LPS that is a potent TLR4 agonist [55]. These modifications involve the generation of atypical LPS molecules with 5-acyl monophosphate lipid A structure (weak TLR4 agonist) or with 4-acyl monophosphate lipid A structure (potent TLR4 antagonist) [12, 55]. The atypical nature of P. gingivalis LPS molecules not only explains the failure of TLR4 to contribute to the host response against P. gingivalis in vivo [69] but additionally protect the organism against cationic antimicrobial peptides [84, 85]. Porphyromonas gingivalis possesses a plethora of other mechanisms to manipulate innate immunity, possibly reflecting its ability to cope with diverse

challenges or in different settings. For instance, through RAD001 the use of distinct virulence factors, P. gingivalis is thought to exploit interactions with erythrocytes, DC, and aortic endothelial cells, which not only promote its fitness but also contribute to the pathogenesis of atherosclerosis [86-88]. Additional in vitro and animal model studies suggest that, through enzymatic modification of host proteins, P. gingivalis can breach immune tolerance in susceptible individuals and exacerbate rheumatoid arthritis [89]. The reader is referred to specialized reviews for additional information on systemic effects associated with P. gingivalis [62, 90-92]. Recent studies indicate that P. gingivalis can potentially also manipulate adaptive immunity by acting on APC and GECs. Indeed, the interaction of P. gingivalis with DC induces a cytokine

pattern that favors CD4+ T helper 17 (Th17) polarization at the expense of the Th1 lineage [93]. Specifically, P. gingivalis induces IL-1β, IL-6, and IL-23, but not IL-12, which moreover is particularly susceptible to proteolysis by the P. gingivalis gingipains [93]. GECs stimulated with P. gingivalis produce a potent admixture of pro- and anti-inflammatory cytokines and chemokines [17, 94]. For example, P. gingivalis infected GECs overexpress pro-IL-1β, although secretion ASK1 requires an additional stimulus such as extracellular ATP to activate the processing enzyme caspase-1 through the NLRP3 inflammasome [29, 95]. One major function of IL-1β is to enhance the antigen-driven proliferation of CD4+ T cells; however, P. gingivalis additionally inhibits GEC production of CXCL10 (IP-10) and other Th1 chemoattractants (CXCL9 and CXCL11) through downregulation of IRF-1 and Stat1 expression (Fig. 1) [96]. The inhibitory effect on CXCL10 is “dominant” in that GECs exposed to P. gingivalis cannot express this chemokine in response to other oral bacteria that otherwise can readily induce CXCL10 [96]. In a related context, the ability of P.