TY - JOUR. T1 - Expression of the costimulatory receptor CD30 is regulated by both CD28 and cytokines. AU - Gilffillan, Molly C.. AU - Noel, Patricia J.. AU - Podack, Eckhard R.. AU - Reiner, Steven L.. AU - Thompson, Craig B.. PY - 1998/3/1. Y1 - 1998/3/1. N2 - Costimulation was originally defined and characterized during primary T cell activation. The signaling events that regulate subsequent antigen encounters by T cells are less well defined. In this study we examined the role of CD30 in T cell activation and defined factors that regulate expression of CD30 on T cells. We demonstrate that CD30 expression is restricted to activated T cells and regulated by CD28 signal transduction. In contrast to CD28-expressing TCR Tg cells, CD28-deficient TCR Tg cells did not express CD30 when cultured with peptide and APCs. However, rIL-4 reconstituted CD30 expression on CD28-deficient TCR Tg cells. Blockade of CD28 interactions or depletion of IL-4 inhibited the induction of CD30, suggesting that both ...
During evolutionary adaptation in the immune system, host defense is traded off against autoreactivity. Signals through the costimulatory receptor CD28 enable T cells to respond specifically to pathogens, whereas those through the related costimulatory receptor, ICOS, which arose by gene duplication, are critical for affinity maturation and memory antibody responses. ICOS ligand, unlike the pathogen-inducible CD28 ligands, is widely and constitutively expressed in the immune system. Here, we show that crosstalk between these two pathways provides a mechanism for obviating the normal T cell dependence on CD28. Several CD28-mediated responses-generation of follicular helper T cells, germinal center formation, T helper 1 cell-dependent extrafollicular antibody responses to Salmonella and bacterial clearance, and regulatory T cell homeostasis-became independent of CD28 and dependent on ICOS when the E3 ubiquitin ligase Roquin was mutated. Mechanisms to functionally compartmentalize ICOS and CD28 signals are
Signaling mediated through the IL-2R, in conjunction with signals mediated through the T cell Ag receptor, promotes the proliferation and effector function of T cells (32). Some of the signals, such as up-regulation of the IL-2R α-chain, result from cooperative signals mediated both through the T cell Ag receptor as well as through the IL-2R itself; however, the relative role of signals delivered through these pathways has not been fully elucidated. Human tumor-reactive effector T cells have been shown to proliferate extensively in vitro in the presence of high-dose IL-2 alone (33). In addition, between 15 and 20% of melanoma and renal cancer patients treated with high-dose IL-2 alone respond to therapy (6), which may reflect the ability of IL-2 to maintain the proliferation of T cells that were activated by prior exposure to tumor Ags.. Interactions between the costimulatory receptor CD27 and its ligand, CD70, have also been found to play a key role in T lymphocyte activation, proliferation, ...
In addition to activation via the TCR complex, resting purified T cells can be activated to proliferate by mAb directed against the two surface molecules, CD2 and CD28. We demonstrate here that only the CD2 plus CD28 combined activation induces the expression and secretion of IL-1 alpha, a cytokine classically considered as a monokine. In contrast, neither IL-1 beta nor IL-6 were produced. A second monokine, TNF-alpha was transiently expressed by T cells activated with either CD2 or CD28 mAb, but was expressed to higher levels and with a prolonged kinetics in cells activated by the CD2 plus CD28 combination. The prolonged expression of the IL-1 alpha gene could account, at least in part, for the monocyte-independent and long lasting T cell proliferation induced by the CD2 plus CD28 co-stimulation. Secretion of monokines, such as IL-1 alpha, by activated T cells, could play a regulatory role in immune responses, as well as contribute to autoimmune processes. ...
The induction of survival versus apoptosis is a central issue during T cell development and activation. The differential regulation of thymocyte survival versus death through TCR-mediated selection signals plays a key role in establishing a functional mature T cell repertoire (1). In mature T cells, several studies have demonstrated that signals from MHC molecules are required for the survival of resting T cells (2)(3)(4). In addition, the induction of apoptosis is strictly regulated after antigenic triggering (5). However, during T cell activation, the T cell costimulatory molecule CD28 is believed to contribute to survival signals (6)(7)(8).. Several molecules have been identified that play key roles in regulating apoptosis in T cells (9). Important advances in understanding T cell apoptosis have come through the study of Bcl-2 family members. Bcl-2-related proteins function to promote either cell survival (such as Bcl-2 and Bcl-XL) or cell death (such as Bax and BAD). Several studies have ...
A population of individual T cells expressing an invariant V24JQ T cell antigen receptor (TCR) chain and high levels of CD161 (NKR-P1A) appears to play an immunoregulatory role through production of both T helper (Th) type 1 and Th2 cytokines. and cytokine secretion in response to CD1d+ target cells, demonstrating a physiological accessory molecule function for CD161. However, CD1d-restricted target cell lysis by activated V24invt T cells, which involved a granule-mediated exocytotic mechanism, was CD161-impartial. In further contrast to the mouse, the signaling pathway involved in V24invt T cell costimulation through CD161 did not appear to involve stable association with tyrosine kinase p56Lck. These results demonstrate a role for CD161 as a novel costimulatory molecule for TCR-mediated acknowledgement of CD1d by human V24invt T cells. (Camarillo, CA). Functional Analysis of T Cells. For activation of T cells (105/ well), anti-CD3 mAb OKT3 was bound overnight in PBS (50 l/well) to 96-well ...
The CD28 antibody is specific for the mouse CD28 costimulatory molecule, expressed on most thymocytes, CD4+ and CD8+ T cells, and natural killer (NK) cells. Ligation of CD28 with CD80 (B7-1) and CD86 (B7-2) provides a costimulatory signal for T cell activation. Clone 37.51 has been shown to activate T cells in combination with CD3. Activation and proliferation of T cells can be induced by interaction of the T cell receptor with peptide-MHC complexes. The T cell receives a signal transduced through the CD3 complex. Cytokines or other costimulatory signals from accessory cells are required in addition. Activated T cells can be used for any downstream processes, such as cytokine analysis or immunoprecipitation. Cells can also be transfected with high efficiency. - Italia
The CD28 antibody is specific for the mouse CD28 costimulatory molecule, expressed on most thymocytes, CD4+ and CD8+ T cells, and natural killer (NK) cells. Ligation of CD28 with CD80 (B7-1) and CD86 (B7-2) provides a costimulatory signal for T cell activation. Clone 37.51 has been shown to activate T cells in combination with CD3. Activation and proliferation of T cells can be induced by interaction of the T cell receptor with peptide-MHC complexes. The T cell receives a signal transduced through the CD3 complex. Cytokines or other costimulatory signals from accessory cells are required in addition. Activated T cells can be used for any downstream processes, such as cytokine analysis or immunoprecipitation. Cells can also be transfected with high efficiency. - España
B7-DC costimulates PD1−/− CD4+ T cells. (a) Purified CD4+ T cells from wt (open bars) or PD-1 KO mice (filled bars) were stimulated with 30 ng/well of preco
Costimulation is a fundamental principle of T-cell activation. In addition to T-cell receptor engagement, the interaction between CD80 and/or CD86 with CD28 and/or cytotoxic T-lymphocyte antigen 4 (CTLA-4) receptors is required to regulate T-cell activation and tolerance. While the importance of costimulation is clearly established, the exact molecular mechanism is unknown. We demonstrate that T-cell proliferation and the ability of CD8(+) T-effector cells to kill were enhanced slightly by CD80 but dramatically by CD86 costimulation. To further analyse the cellular process of costimulation, we developed a single-cell assay to analyse Ca(2+) signals following costimulation with bi-specific antibodies. We found that this stimulation method worked in every human T-cell that was analysed, making it one of the most efficient T-cell activation methods to date for primary human T cells. The enhanced proliferation and killing by costimulation was paralleled by an increase of Ca(2+) influx following CD86 ...
Dr. Allisons pioneer work has transformed the fields of basic and tumour immunology. Early in his career, he identified and characterized key molecules involved in T-cell activation, including the T-cell receptor (TCR), the prototypical costimulatory receptor CD28 and coinhibitory receptor CTLA-4, providing evidence that T-cell responses are determined by a complex process involving antigen driven TCR signalling plus integration of costimulatory and coinhbitory signals. His landmark translation studies showing antibody-mediated blockade of CTLA-4 co-inhibitory function could enhance antitumor immunity and result in tumour rejection in mice prompted clinical development of ipilimumab, a CTLA-4 blocking monoclonal antibody. Ipilimumab is the first drug of its kind to show survival benefit in melanoma patients and was approved by the FDA in 2011 as a standard-of-care therapy for late-stage melanoma patients. Dr. Allisons concept of antibody-mediated blockade of immunologic checkpoints as cancer ...
Therapeutic tumor immunity requires the presence and appropriate activation of tumor antigen specific CD8+ T cells and migration of activated tumor-antigen specific CD8+ T cells into a tumor microenvironment where immunosuppressive barriers have been eliminated. Antibody mediated blockade of CTLA-4 and PD-1 is a clinically effective strategy to dampen tumor mediated immunosuppression in a minority of patients with advanced cancer, and this approach may be potentiated through vaccination to prime additional CTL clones and through direct stimulation of T cell costimulatory molecules of the TNF superfamily. Here we provide a systematic comparison of anti-tumor vaccination with either heat shock protein gp96-Ig or traditional peptide/adjuvant vaccines given alone or in combination with CTLA-4 or PD-1 blockade and direct T cell costimulation via OX40, 4-1BB and TNFRSF25. Through the tracking of tumor-antigen specific CD4+ and CD8+ T cell responses, these studies demonstrate that both TNFRSF4 and ...
T cell activation through the TCR can result in either cell proliferation or cell death. The role of costimulatory receptors in regulating T cell survival has not been defined. Here, we present data demonstrating that CD28 costimulation enhances the in vitro survival of activated T cells. One mechan …
The 2 signal model provides the framework for our understanding of T cell responses. Using high throughput microarray analysis we have uncovered several novel TCR-induced genes and pathways that play critical roles in dictating the outcome of antigen recognition. We identified Egr-2 and Egr-3 as playing an important role in determining the fate of TCR recognition (Signal 1). Egr-2 and Egr-3 null T cells induce more aggressive autoimmune disease but are more effective in mounting anti-tumor responses. A second gene that was revealed by our screen is the adenosine A2aR. Activating the receptor can promote tolerance and inhibit autoimmune disease. Alternatively employing A2aR null mice and specific antagonists promotes anti-tumor immunity and enhances vaccine responses. In addition to Signal 1, we are also interested in understanding mechanisms of costimulation. Along these lines we have identified the mammalian Target of Rapamycin (mTOR) as playing a central role in dictating the outcome of ...
We have shown that a "KIR-CAR" can be simply constructed by swapping the two immunoglobulin-like domains of the KIR2DS2 ectodomain with an scFv capable of binding a desired target antigen. When delivered to T cells together with DAP12, this KIR-based CAR triggers antigen-specific cytotoxicity, cytokine production, and proliferation that is comparable with second-generation CD3ζ-based CARs in vitro without the need for additional domains from costimulatory receptors. The ability of a KIR-based CAR to activate T cells in the absence of added costimulation is interesting in light of the critical importance of costimulation for full T-cell activation and acquisition of effector function. KIR2DS2, the natural KIR upon which the presented KIR-CAR is based, has previously been reported to deliver a costimulation-like signal to T cells. In these studies, engagement of the KIR in T-cell clones lacking DAP12 expression augmented anti-CD3-induced IFNγ production (16). The mechanism of this costimulatory ...
Changes of CD8/HLADR+ T cells during a period of seven years HAART ( ± SD,/ μL). Patient numbers: Effective group (A) (n = 25), Ineffective group (B) (n = 18)
Signaling through CD27 plays a role in T cell activation and memory. However, it is currently unknown how this costimulatory receptor influences CD4 effector T (Teff) cells in inflamed tissues. In the current study, we used a murine model of inducible self-antigen expression in the epidermis to elucidate the functional role of CD27 on autoreactive Teff cells. Expression of CD27 on Ag-specific Teff cells resulted in enhanced skin inflammation when compared with CD27-deficient Teff cells. CD27 signaling promoted the accumulation of IFN-γ and IL-2-producing T cells in skin draining lymph nodes in a cell-intrinsic fashion. Surprisingly, this costimulatory pathway had minimal effect on early T cell activation and proliferation. Instead, signaling through CD27 resulted in the progressive survival of Teff cells during the autoimmune response. Using BH3 profiling to assess mitochondrial cell priming, we found that CD27-deficient cells were equally as sensitive as CD27-sufficient cells to mitochondrial ...
Altor is building on our IL-15 technology to create a next-generation targeted IL-15 scaffold platform to recognize and target specific antigens found in various cancers and viral infections. We have adapted the IL-15 superagonist complex to create a functional scaffold for the design of multi-specific fusion protein complexes. Using an antibody or single-chain T cell receptors (STARTM) as recognition domains linked to the IL-15 scaffold, we have generated both bivalent and bispecific product candidates (TxM).. Extensive characterization of these product candidates consisting of therapeutic antibodies and this scaffold indicates that such a targeted immunotherapeutic can potentiate the anti-tumor activities of the therapeutic antibody as well as potently facilitate immune responses. Thus, we are utilizing this IL-15 scaffold platform to generate multiple targeted IL-15 product candidates that can simultaneously promote killing of target cells and retain immunostimulatory functions of ...
We next determined the function of the CD4+CD25+ T cells. For these experiments we used the CD4+CD25- and CD4+CD25+ peripheral blood T cells whose FoxP3 expression levels were shown in Figure 1 (a and b). These T cell subsets were assessed for their ability to respond to T cell receptor (TCR) stimulation, and for the ability of the CD25+ cells to suppress the in vitro activation of the CD25- cells. When cultured in the presence of feeder cells along with soluble anti-CD3 and anti-CD28, the CD4+CD25- cells responded with robust proliferation, whereas the CD4+CD25+ cells did not (Figure 1c). When the two populations were cocultured, the level of proliferation, as measured by 3H-thymidine incorporation, was dramatically reduced (Figure 1c). The level of suppression seen was correlated with the ratio of CD4+CD25-:CD4+CD25+ cells in the culture, with more CD25+ cells resulting in more suppression of CD25- cell proliferation. These results are not due to exhaustion of the resources within the culture ...
The modulation of co-stimulatory pathways represents a novel therapeutic strategy to regulate autoimmune diseases. Auto-reactive CD4+ T cells play a critical role in initiating the immune response leading to inflammation and autoimmune diseases. Blocking co-stimulatory signals prevents T-cell activation, thus diminishing autoimmune responses and possibly preventing the progression of autoimmune disease. Blockade of several co-stimulatory pathways has been investigated in animal models and has led to clinical trials testing specific blocking agents in humans. In this review we will describe the role of co-stimulatory pathways, primarily the CD28-B7 pathway, in autoimmune diseases, and we will present in vivo and in vitro studies supporting the efficacy of co-stimulation blockade in animal models of autoimmune disease. Finally, we will discuss the clinical therapeutic efficacy of blocking monoclonal antibodies in preventing or reducing auto-antigen driven T-cell activation in humans with ...
To our knowledge, expression of B7-H1 within RCC tumors of the kidney has not been previously demonstrated. We also believe that B7-H1 is the first T cell costimulatory molecule that has been reported to exhibit a strong association with the aggressiveness of a solid (nonhematologic) tumor and patient cancer-specific survival. Finally, our study provides previously undescribed evidence that B7-H1 may function at the clinical level to promote cancer progression, perhaps through impairment of host T cell-mediated immunity, as has recently been reported in the basic scientific literature (2, 6).. B7-H1 represents a recently identified cell-surface glycoprotein belonging to the B7 family of costimulatory molecules (1). Constitutive B7-H1 protein expression is normally restricted to macrophage-lineage cells, where it may participate in the costimulatory activation of naïve T cells or deletion of activated T cells (1, 23). Several human cancers, however, have also been reported to aberrantly express ...
Treatment of advanced, poorly immunogenic tumors in animal models, considered the closest simulation available thus far for conditions observed in cancer patients, remains a major challenge for cancer immunotherapy. We reported previously that established tumors in mice receiving an agonistic mAb to the T cell costimulatory molecule 4-1BB (CD137) regress due to enhanced tumor antigen-specific cytotoxic T lymphocyte responses. In this study, we demonstrate that several poorly immunogenic tumors, including C3 tumor, TC-1 lung carcinoma, and B16-F10 melanoma, once established as solid tumors or metastases, are refractory to treatment by anti-4-1BB mAb. We provide evidence that immunological ignorance, rather than anergy or deletion, of tumor antigen-specific CTLs during the progressive growth of tumors prevents costimulation by anti-4-1BB mAb. Breaking CTL ignorance by immunization with a tumor antigen-derived peptide, although insufficient to stimulate a curative CTL response, is necessary for ...
CD26, also known as dipeptidyl peptidase IV (DPP-IV), is a homodimeric cell surface serine peptidase that degradates IFN-gamma-induced cytokines, acts as a T cell costimulatory molecule, and participates in multiple immunopathological roles in leukocyte homing and inflammation. Alterations in its peptidase activity are characteristic of malignant transformation. The enzymatic activity increases dramatically with tumour grade and severity. CD26 is expressed in various blood cell types, but also e.g. in cells that are histogenetically related to activated fibroblasts. Alterations in CD26 density have been reported on circulating monocytes and CD4+ T cells during rheumatoid arthritis and systemic lupus erythematosus ...
Interleukin-2 (IL-2) stimulates both activated CD4+ and CD8+ T cells to proliferate. IL-2 signals through an identical receptor complex and promotes the same dose-dependent phosphorylation of the canonical transcription factor STAT5 in both cell types. Despite this, CD8+ T cells enter the S phase earlier and proliferate to a greater extent than do CD4+ T cells in response to IL-2. We identified distinct IL-2 signaling dynamics in CD4+ and CD8+ T cells. In IL-2-stimulated CD8+ T cells, STAT5 phosphorylation increased rapidly and was sustained for 6 hours. In contrast, CD4+ T cells had a biphasic response, with maxima at 15 min and 2 to 4 hours after stimulation. Both cell types required vesicular trafficking, but only CD4+ T cells required new protein synthesis to maintain high phosphorylation of STAT5. Two subunits of the IL-2 receptor, IL-2Rβ and IL-2Rγ, were twice as abundant in CD8+ T cells than in CD4+ T cells. Reduction of IL-2Rβ abundance by 50% was sufficient to convert CD8+ T cells to ...
Protein Kinase C Theta Type (nPKC Theta or PRKCQ or EC 2.7.11.13) - Pipeline Review, H1 2017 Size and Share Published in 2017-05-30 Available for US$ 3500 at Researchmoz.us
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Un metodo per espandere γδ cellule T dalle cellule mononucleate del sangue periferico (PBMC) è descritta. PBMC cellule derivate γδ T...
The present results verify the previously suggested, but not definitively proven, mechanism that α-GalCer-activated iNKT-cells at least partly protect NOD mice from type 1 diabetes by driving the maturation of tolerogenic DCs. In contrast, iNKT-conditioned DCs in B6.H2g7 mice mature to an alternative immunogenic state that supports rather than inhibits AI4 T-cell-induced type 1 diabetes. The downstream maturation of iNKT-conditioned DCs in NOD and B6.H2g7 mice to a tolerogenic versus an immunogenic state is due to the induction of quantitatively different expression levels of T-cell costimulatory and inhibitory molecules.. A series of T-cell costimulatory molecules were upregulated to a much greater extent on iNKT-conditioned DCs from B6.H2g7 than NOD mice. In particular, CD70 and OX40L expression levels were unchanged or strongly upregulated on iNKT-conditioned DCs from NOD and B6.H2g7 mice, respectively. This could be significant given a report that iNKT-cells promote CD8+ cytotoxic T-cell ...
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Del Guercio. 1905[1904]. Sulle differenze esistenti fra la Schizoneura Reaumuri Kalt. ed il Pachypappa vesicalis Koch e sulla convenienza di escludere la prima dal genere per essa indicate. Redia 2(2):306 ...
Given the opposing negative effect of CTLA-4 on T cell activation (4, 5), we next assessed whether CTLA-4 coligation could alter the surface expression of rafts. Coligation of CTLA-4 with either TcR, or the combination of TcR and CD28 potently inhibited GM1 expression (Fig. 1 A). On average, CTLA-4 inhibited the percentage of GM1-positive cells by 70-90% so that the level of expression at 48-96 h exceeded that of the resting population by only 5-10%. CTLA-4 also inhibited the expression level on cells that had been induced to express GM1 as a result of anti-CD3 or anti-CD3/CD28 ligation (i.e., MIF of positively gated cells), albeit to a much lesser extent (i.e., MFI: 48 h: anti-CD3 versus anti-CD3/CTLA-4: 12.1 [61%] to 11.0 [55%]; anti-CD3/CD28 versus anti-CD3/CD28/CTLA-4: 13.6 [69%] to 11.9 [60%]). Inhibition of GM1 expression correlated with the anti-CTLA-4 blockage of proliferation (Fig. 1 B), and CD25 expression (Fig. 1 C). Our findings therefore show that CD28 and CTLA-4 have striking ...
CD4+CD28null T cells are a population of lymphocytes rarely found in healthy individuals.1,3 Although cell numbers increase with age, disease-associated expansions, in addition to ACS, have also been reported in inflammatory disorders such as rheumatoid vasculitis.18 The present study has addressed a critical point concerning antigen specificity and found that hHSP60 was recognized by CD4+CD28null cells via the MHC class II presentation pathway in ,50% of our patients with ACS. This finding is of significance because of the frequency and damaging potential of CD4+CD28null cells and the almost ubiquitous expression of HSPs.. The association between HSPs and atherosclerosis has been a subject of recent interest.7 The elevated expression of these proteins in atheromatous lesions, correlating with the severity of atherosclerosis, is consistent with a focal role that HSPs may play in the pathogenesis of the disease.19,20 This, combined with a growing body of evidence that suggests that risk factors ...
Adoptive transfer of CD4+CD25+ T cells inhibits HSV-1-specific CD8+ T cell responses. Purified CD4+CD25+ and CD4+CD25− T cells (2 × 106/mouse) were adoptively transferred into WT B6 mice 24 h before HSV infection, and the immune response was measured on days 7 and 28 p.i. (A) On days 7 and 28 p.i., spleen cells were incubated with gB498-505, and CD8/IFN-γ production was measured by intracellular staining. The number shown in each plot is the mean percentage of IFN-γ-producing CD8+ T cells obtained from four mice per group. (B) The resulting decrease in IFN-γ-secreting CD8+ T cells in B6 mice after adoptive transfer of CD4+CD25+ T cells were also measured by a standard ELISPOT assay. On days 7 and 28 post HSV infection, spleen cells were analyzed for the number of IFN-γ-secreting CD8+ T cells in response to SSIEFARL peptide. The error bars represent the mean ± SD of four different mice in the same group. *P , 0.05 compared with HSV-infected B6 mice receiving no adoptive transfer. Without ...
Asthma affects approximately 300 million people worldwide and is the most common chronic lung disease, which usually is associated with bronchial inflammation. Most research has focused upon the role of CD4+ T cells and relatively few studies have addressed the phenotypic and functional roles of CD8+ T cell types and subtypes.Human NK-like CD8+ T cells may involve cells that have been described as CD8+CD28-, CD8+CD28-CD57+, CD8+CD27-, or CD8+ effector-memory (TEM) cells, among other. However, most of the data which is available regarding these various cell types were obtained in murine models, did not thoroughly characterize these cells with phenotypically or functionally or did not involve asthma-related settings.Nevertheless, one may conceptualize three principal roles for human NK-like CD8+ T cells in asthma: disease-promoting, regulatory and/or tissue repair. Although evidence for some of these roles is scarce, it is possible to extrapolate some data from overlapping or related CD8+ T cell
TLR ligands act directly upon T cells to restore proliferation in the absence of protein kinase C-theta signaling and promote autoimmune ...
OBJECTIVE: The nonsynonymous polymorphism rs763361 of the CD226 gene, which encodes DNAX accessory molecule 1, which is involved in T cell costimulation pathways, has recently been identified as a genetic risk factor for autoimmunity. The purpose of this study was to test for association of the CD226 rs763361 polymorphism with systemic sclerosis (SSc) in European Caucasian populations. METHODS: CD226 rs763361 was genotyped in 3,632 individuals, consisting of a discovery sample (991 SSc patients and 1,008 controls) and a replication sample (999 SSc patients and 634 controls). All study subjects were of European Caucasian origin. Expression of CD226 was assessed on peripheral blood mononuclear cells obtained from 21 healthy donors genotyped for CD226 rs763361. RESULTS: The CD226 rs763361 T allele was found to be associated with SSc in both the discovery and the replication samples, showing the following results in the combined populations: odds ratio (OR) 1.22 (95% confidence interval [95% CI] ...
Human mucosal associated invariant T (MAIT) CD8 + and Tc17 cells are important tissue-homing cell populations, characterized by high expression of CD161 ( ++) and type-17 differentiation, but their origins and relationships remain poorly defined. By transcriptional and functional analyses, we demonstrate that a pool of polyclonal, precommitted type-17CD161 ++CD8αβ + T cells exist in cord blood, from which a prominent MAIT cell(TCR Vα7.2 +) population emerges postnatally. During this expansion, CD8αα T cells appear exclusively within aCD161 ++CD8 +/MAIT subset, sharing cytokine production, chemokine-receptor expression, TCR-usage, and transcriptional profiles with their CD161 ++CD8αβ + counterparts. Our data demonstrate the origin and differentiation pathway of MAIT-cells from a naive type-17 precommitted CD161 ++CD8 +T-cell pool and the distinct phenotype and function of CD8αα cells in man. © 2012 by The American Society of Hematology.
In the Research Article "A rationally designed NRP1-independent superagonist SEMA3A mutant is an effective anticancer agent," the right panel graph of Fig. 5D (siNRP1) was erroneously duplicated in the left panel (siCtl). However, correct experimental values were reported in table S4 (provided as an Excel file) that contains raw data relating to both siCtl and siNRP1 panels of Fig. 5D. The left panel of Fig. 5D has been replaced so that it now contains a graph plotted with correct siCtl values, as originally displayed in table S4. This error does not change the findings or conclusions of the study. The PDFs and HTML (full text) have been corrected.. ...
Interleukin (IL)-4 is considered to be essential for T helper (Th)2 cell development, yet in areas of primary T cell activation, CD4+ cells are its only source. This implies that other signals must drive the initial expression of IL-4 production. The role of CD28 co-stimulation in Th2 subset development has been described. However, in mice deficient for CD28, Th2 responses are diminished, but not abrogated. Cytokines produced within the lymphoid tissue, e.g. IL-7, may be important in the primary activation of naive CD4+ cells. We have found that human naive CD4+ cells purified from umbilical cord blood express the IL-7 receptor and respond vigorously to IL-7 during primary stimulation. Naive CD4+ cells grown in IL-4, in the presence or absence of IL-2, fail to produce Th2 cytokines upon restimulation. In contrast, IL-7 induces development of a population of T cells that produce large amounts of IL-4. Growth in IL-7 also increases IL-2-induced production of interferon (IFN)-gamma and IL-10 production. IL
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CD4+ T cells play a major role in adaptive immune responses to intracellular and extracellular microbes by regulating the functions of B cells, CD8+ T cells, an...
In this study we show that CPS and nordihydrocapsiate (CPT) inhibit early and late events in T cell activation, including CD69, CD25 and ICAM-1 cell surface expression, progression to the S phase of the cell cycle and proliferation in response to TCR and CD28 co-engagement ...
CD3 epsilon兔单克隆抗体[E272](ab32186)可与人样本反应并经IP, IHC, ICC实验严格验证,被3篇文献引用。所有产品均提供质保服务,中国75%以上现货。
CD40山羊多克隆抗体(ab10959)可与小鼠样本反应并经WB, ELISA实验严格验证,被4篇文献引用。所有产品均提供质保服务,中国75%以上现货。
TY - JOUR. T1 - CD161 (NKR-P1A) costimulation of CD1d-dependent activation of human T cells expressing invariant Vα24JαQT cell receptor α chains. AU - Exley, Mark. AU - Porcelli, Steven. AU - Furman, Margo. AU - Garcia, Jorge. AU - Balk, Steven. PY - 1998/9/7. Y1 - 1998/9/7. N2 - A population of human T cells expressing an invariant Vα24JαQ T cell antigen receptor (TCR) α chain and high levels of CD161 (NKR-P1A) appears to play an immunoregulatory role through production of both T helper (Th) type 1 and Th2 cytokines. Unlike other CD161+ T cells, the major histocompatibility complex-like nonpolymorphic CD1d molecule is the target for the TCR expressed by these T cells (Vα24(invt) T cells) and by the homologous murine NK1 (NKR- P1C)+ T cell population. In this report, CD161 was shown to act as a specific costimulatory molecule for TCR-mediated proliferation and cytokine secretion by Mα24(invt) T cells. However, in contrast to results in the mouse, ligation of CD161 in the absence of TCR ...
The CD2 receptor on T lymphocytes is essential for T cell adhesion and stimulation by antigen presenting cells (APCs). Blockade of CD2 function is immunosuppressive in both model systems and humans, indicating the importance of CD2 for the cellular immune response. Although the affinity of the molecular interaction between CD2 and its counter-receptor, CD58, is relatively low when measured in solution, this interaction mediates tight adhesion within the 2D cell-cell interface. To understand the mechanisms responsible for regulating the avidity of the CD2-CD58 interaction, we measured the number, affinity, and lateral mobility of CD2 molecules on resting and activated T cells. Cell activation caused a 1.5-fold increase in the number of CD2 sites on the cell surface, and the 2D affinity of CD2 for CD58 increased by 2.5-fold. The combination of T cell activation and CD2 ligation to CD58 decreased the laterally mobile fraction of the ligated CD2. Together, these changes would substantially enhance CD2
The CD8 antigen is a disulfide-linked dimer, which exists either as a CD8α homodimer or as a CD8α/β heterodimer. CD8α is required for surface expression of CD8β. The molecular weight of each monomer of α or β is approximately 32-34 kDa. CD8 binds to a non-polymorphic domain (α3 domain) of MHC Class I molecules. CD8 is expressed on a subset of human peripheral blood T lymphocytes. A subset of NK cells possess the CD8 antigen but show low to medium density of expression. CD8α homodimer is expressed by NK cells and γ/δ+ T cells. CD8 is also present on most thymocytes where it is frequently co-expressed with CD4, and on a subpopulation of bone marrow cells. The CD8 molecule acts with the T Cell Receptor (TCR) as a coreceptor for MHC class I restricted antigen recognition. CD8 is widely used as a marker of cytotoxic T lymphocytes. *Alexa Fluor and Pacific Blue are registered trademarks of Molecular Probes, Inc ...