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PubMed1987

Ion channels activated by specific Ti or T3 antibodies in plasma membranes of human T cells.

T lymphocytes are activated to proliferate via a surface membrane receptor recognizing the antigen/major histocompatibility complex. This membrane component is comprised of at least five polypeptide subunits, collectively termed the Ti-T3 receptor complex. A transient increase in cytosolic free calcium occurs as an early event in the T-cell activation process and is necessary for induction of the endogenous IL-2 and certain other genes. Monoclonal antibodies specific to epitopes of either the Ti or the T3 components were shown to be effective agonists, also leading to such transient rises in cytosolic free calcium and activating the lymphocytes. Here we show, using micropipette-supported bilayers formed from membranes of the human T-cell line REX, that Ti- or T3-specific antibodies cause opening of ligand gated ion channels. Both types of specific antibodies yielded similar histograms of conductance amplitudes which show a channel with a conductance of 2-3 pS in symmetrical 100 mM CaCl2 solutions. These channels allow the passage of calcium and barium ions and are blocked by lanthanum ions, suggesting that they are specific for calcium. We propose that these channels, by allowing the entry of external calcium, may account for a large fraction of the rise in intracellular calcium observed upon triggering of the Ti-T3 receptor.

Antibodies, Monoclonal↗

PubMed1993

Characterization of thymic nurse-cell lymphocytes, using an improved procedure for nurse-cell isolation.

Thymic nurse cells (TNC), multicellular complexes consisting of lymphoid cells enclosed within cortical epithelial cells, were isolated from mouse thymus by a modified procedure allowing immunofluorescent labeling and flow cytometric analysis of their lymphoid contents (TNC-L). Collagenase was the only protease used for tissue digestion, to ensure that surface antigen markers remained intact. Zonal unit-gravity elutriation was used to enrich the TNC on the basis of their high sedimentation rate, followed by immunomagnetic bead depletion to remove residual mononuclear cell contaminants and a density separation to remove debris. The TNC-L were then released from inside TNC by a short period of culture. The measured contamination of TNC-L with exogenous thymocytes was around 0.5%. Three-color immunofluorescent labeling revealed that TNC-L included, as well as a majority of immature CD4+8+3low thymocytes, about 12% of apparently mature CD4+8-3high and CD4-8+3high thymocytes. TNC are located in the cortex, where mature cells are rare; the occurrence of mature phenotype cells within these structures suggests that they represent a microenvironment for the selection and generation of mature T cells.

Animals↗

PubMed1992

The development of functionally responsive T cells.

The work reviewed in this article separates T cell development into four phases. First is an expansion phase prior to TCR rearrangement, which appears to be correlated with programming of at least some response genes for inducibility. This phase can occur to some extent outside of the thymus. However, the profound T cell deficit of nude mice indicates that the thymus is by far the most potent site for inducing the expansion per se, even if other sites can induce some response acquisition. Second is a controlled phase of TCR gene rearrangement. The details of the regulatory mechanism that selects particular loci for rearrangement are still not known. It seems that the rearrangement of the TCR gamma loci in the gamma delta lineage may not always take place at a developmental stage strictly equivalent to the rearrangement of TCR beta in the alpha beta lineage, and it is not clear just how early the two lineages diverge. In the TCR alpha beta lineage, however, the final gene rearrangement events are accompanied by rapid proliferation and an interruption in cellular response gene inducibility. The loss of conventional responsiveness is probably caused by alterations at the level of signaling, and may be a manifestation of the physiological state that is a precondition for selection. Third is the complex process of selection. Whereas peripheral T cells can undergo forms of positive selection (by antigen-driven clonal expansion) and negative selection (by abortive stimulation leading to anergy or death), neither is exactly the same phenomenon that occurs in the thymic cortex. Negative selection in the cortex appears to be a suicidal inversion of antigen responsiveness: instead of turning on IL-2 expression, the activated cell destroys its own chromatin. The genes that need to be induced for this response are not yet identified, but it is unquestionably a form of activation. It is interesting that in humans and rats, cortical thymocytes undergoing negative selection can still induce IL-2R alpha expression and even be rescued in vitro, if exogenous IL-2 is provided. Perhaps murine thymocytes are denied this form of rescue because they shut off IL-2R beta chain expression at an earlier stage or because they may be uncommonly Bcl-2 deficient (cf. Sentman et al., 1991; Strasser et al., 1991). Even so, medullary thymocytes remain at least partially susceptible to negative selection even as they continue to mature.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1989

Antigen-specific recognition of autologous leukemia cells and allogeneic class-I MHC antigens by IL-2-activated cytotoxic T cells from a patient with acute T-cell leukemia.

Culturing of leukemic blood lymphocytes from a patient with acute T-cell lymphoblastic leukemia (T-ALL) with interleukin-2 (IL-2) yielded T-cell line AK-1 with a remarkable cytotoxic specificity. This line mediated strong lysis of tumor target lines expressing major histocompatibility complex (MHC) class I antigens, such as Raji, CEM, and Molt-4 cells, but no killing of K562 and Daudi cells, which are deficient in MHC class I. In contrast, lymphokine-activated killer (LAK) cells from normal donors destroyed all these tumor targets, without MHC restriction. Line AK-1, originating from residual normal T cells present in the leukemic blood, lysed autologous leukemic blasts and peripheral blood lymphocytes (PBL) from many but not all allogeneic individuals but failed to kill autologous remission lymphocytes. Destruction of the autologous leukemic targets by AK-1 could be inhibited by unlabeled competitor target cells that were lysed by AK-1, but not by target cells that were not lysed. This suggests that AK-1 specifically recognized an alien determinant on the autologous ALL cells, crossreactive with allogeneic MHC class I antigens. This reactivity with some degree of tumor specificity may be a leukemic equivalent to responses reported for populations of tumor infiltrating lymphocytes (TIL) seen in some solid tumors.

Adult↗

PubMed1993

Regulation of apoptosis in thymocytes.

Programmed cell death, or apoptosis, is tightly regulated during the development of T lymphocytes. Several studies have indicated that in normal mice, thymocyte are sensitive to apoptosis primarily during a brief period relatively late in the CD4+8+ maturation stage, when both positive and negative selection are thought to occur. One factor regulating sensitivity to apoptosis may be the expression and signalling capacity of the TcR/CD3 complex on developing thymocytes. In the present study, we report that sensitivity to apoptosis in immature thymocytes may also be regulated by a mechanism that can prevent induction of apoptosis in many thymocytes. This protective mechanism is induced by TcR/CD3 engagement and cross-linking, as well as by agents that mimic TcR/CD3-dependent phosphoinositol bisphosphate hydrolysis and activate Ca++ fluxes and Protein Kinase C. Cyclosporin A (CsA) inhibits the protective mechanism, permitting the induction of apoptosis by TcR/CD3 or TcR/CD3-mimicking stimuli in otherwise resistant thymocytes. In contrast, mature naive T cells do not undergo apoptosis following stimulation by these agents, even in the presence of CsA, suggesting that in mature naive T-cells the apoptotic machinery itself is normally no longer inducible. We discuss the possible implications of these results for regulation of T-cell development. In this study we also demonstrate that CsA can inhibit the ability of accessory cells to trigger thymocyte apoptosis in accessory cell-dependent assays, which may explain previous reports that CsA can inhibit the induction of thymic clonal deletion in vivo.

Animals↗

PubMedDate not supplied

Swainsonine, a glycosylation inhibitor, enhances both lymphocyte efficacy and tumour susceptibility in LAK and NK cytotoxicity.

Swainsonine (SW) inhibits the formation of N-linked complex oligosaccharides and has previously been shown to inhibit experimental metastasis in nude mice models. The present studies with human effector cells have shown that SW enhanced both lymphokine activated killer cell (LAK) and natural killer (NK) cytotoxicity in standard 51Cr-release assays. SW also increased the susceptibility of human K562 and Colo 320 target cells to NK and LAK cytotoxicity. The peak response of both LAK effectors and targets to SW occurred at 1-2 micrograms/ml SW. A novel finding was that SW enhanced the interleukin 2 (IL-2) beta chain receptor subunit expression on both LAK and NK cells to a greater extent than its enhancement of the IL-2R alpha (CD25 or TAC) receptor expression on LAK effectors. In addition, increases in both these receptors occurred at the doses of SW which augmented LAK cytotoxicity. We conclude that the anti-metastatic effects of SW have an immunological component which is maximal at 1-2 micrograms/ml SW. This suggests that dosage may be an important consideration to obtain optimal potential of SW in any future human cancer therapy.

Antigens, CD↗

PubMed1997

Reconstituted killer cell inhibitory receptors for major histocompatibility complex class I molecules control mast cell activation induced via immunoreceptor tyrosine-based activation motifs.

Natural killer and T cells express at their surface, members of a multigenic family of killer cell inhibitory receptors (KIR) for major histocompatibility complex Class I molecules. KIR engagement leads to the inhibition of natural killer and T cell activation programs. We investigated here the functional reconstitution of KIR in a non-lymphoid cell type. Using stable transfection in the RBL-2H3 mast cell line, we demonstrated that (i) KIR can inhibit signals induced by FcepsilonRIgamma or CD3zeta polypeptides that bear immunoreceptor tyrosine-based activation motifs; (ii) two distinct immunoreceptor tyrosine-based inhibition motifs-bearing receptors, i.e. KIR and FcgammaRIIB, use distinct inhibitory pathways since KIR engagement inhibits the intracellular Ca2+ release from endoplasmic reticulum stores, in contrast to FcgammaRIIB, which only inhibits extracellular Ca2+ entry; (iii) KIR require co-ligation with an immunoreceptor tyrosine-based activation motif-dependent receptor to mediate their inhibitory function. This latter finding is central to the mechanism by which KIR selectively inhibit only the activatory receptors in close vicinity. Taken together our observations also contribute to define and extend the family of immunoreceptor tyrosine-based inhibition motif-bearing receptors involved in the negative control of cell activation.

Animals↗

PubMed2001

The immunological synapse.

The adaptive immune response is initiated by the interaction of T cell antigen receptors with major histocompatibility complex molecule-peptide complexes in the nanometer scale gap between a T cell and an antigen-presenting cell, referred to as an immunological synapse. In this review we focus on the concept of immunological synapse formation as it relates to membrane structure, T cell polarity, signaling pathways, and the antigen-presenting cell. Membrane domains provide an organizational principle for compartmentalization within the immunological synapse. T cell polarization by chemokines increases T cell sensitivity to antigen. The current model is that signaling and formation of the immunological synapse are tightly interwoven in mature T cells. We also extend this model to natural killer cell activation, where the inhibitory NK synapse provides a striking example in which inhibition of signaling leaves the synapse in its nascent, inverted state. The APC may also play an active role in immunological synapse formation, particularly for activation of naïve T cells.

Animals↗

PubMed2004

CD28 signals in the immature immunological synapse.

T cell recognition of peptide-MHC complexes on APCs results in the aggregation of TCRs at a central supramolecular activation complex (c-SMAC) within a mature immunological synapse. T cells require a second "costimulatory" signal for activation, the most important of which, for naive T cells, is from CD28. However the time at which CD28-derived signals are induced relative to c-SMAC formation is not well understood. In this study, we have assessed the kinetics of CD28 localization and function relative to well-established aspects of c-SMAC formation. CD28 accumulates at the immature synapse alongside the TCR and is likewise enriched at the synapse at the onset of the calcium signal. In addition, using CD28 deficient or reconstituted murine cells in a single-cell recording approach shows that CD28 regulates this signal within seconds of a TCR-mediated rise in intracellular calcium levels. Finally, CD28 exerts effects on both the initiation and stabilization of the synapse in parallel with its effects on the downstream proliferation of T cells. Together, the data show that CD28 functions in the immunological synapse before the formation of the c-SMAC.

Adjuvants, Immunologic↗

PubMed2002

HIV-1 gp120 modulates the immunological function and expression of accessory and co-stimulatory molecules of monocyte-derived dendritic cells.

Initiation of a primary immune response requires antigen specific CD4(+) T helper (T(h)) cells to assist in priming of CD8(+) cytotoxic T cell (CTL) activity. This is optimal when T(h) cells and CTL recognize antigen when presented to them by a dendritic cell (DC) in the context of major histocompatibility complex (MHC) class I and class II complexes. We have hypothesized that human DC exposed to HIV-1 gp120 IIIB envelope glycoprotein may activate or alter the immunological activation of DCs. Our findings have led us to conclude that HIV-1 gp120 LAV/IIIB activates monocyte-derived DC when they are in their immature state while HIV-1 gp120 exhibits highly selective effects on mature DC. We have observed that following maturation of DCs with lipopolysaccharide (LPS) that they are less susceptible to the modulatory effects of gp120. Although HIV-1 gp120 activates immature DC, it does so in a manner that abrogates their normal function in host immune responses and consequently disturbs the homeostatic balance of host immune response to infection. We suggest that HIV-1 gp120 may support sustained productive infection and transinfection of activated T cells that cluster with gp120-activated DC. We believe that these are promoted by mechanisms that are dependent, at least in part, on altered cytokine responses, enhanced expression of cellular adhesion molecules and augmented DC-mediated activation of T cells in nonspecific and antigen-specific immune reactivities. Consequently, HIV-1 gp120 may actively contribute to the immunopathogenesis of AIDS.

Acquired Immunodeficiency Syndrome↗

PubMed1996

Functional and molecular characterization of tumour-infiltrating lymphocytes and clones thereof from a major-histocompatibility-complex-negative human tumour: neuroblastoma.

Neuroblastoma (NB) is a major-histocompatibility-complex(MHC)-negative neuroectodermal tumour that is often infiltrated with lymphocytes. A detailed characterization of NB-associated tumour-infiltrating lymphocytes (TIL) has never been carried out. Here we have investigated the immunophenotype and the cytotoxic activities of TIL from nine and seven NB patients respectively. Furthermore, the T cell receptor (TcR) variability and the patterns of cytokine gene expression of fresh versus recombinant (r) interleukin (IL)-2-cultured TIL were studied in four NB cases. The results obtained showed the following: (1) freshly isolated TIL were comprised of a mixture of CD4+ and CD8+ T cells partially expressing HLA-DR and/or CD25. The CD4/CD8 ratio ranged from 0.5 to 5 in the different cases. Upon culture of TIL with rIL-2, an increased proportion of CD56+ and CD8+ lymphocytes was consistently observed; (2) IL-2-expanded TIL lysed natural-killer(NK)sensitive and lymphokine-activated-killer(LAK)-sensitive target cell lines; (3) reverse-transcriptase/polymerase-chain-reaction (RT-PCR) experiments showed that most TcR V beta genes were expressed both in fresh and in cultured TIL, suggesting that such cell populations were polyclonal; (4) interferon gamma, IL-4, IL-5, tumour necrosis factor (TNF) alpha, IL-8, IL-10 mRNA and, to a lesser extent, IL-2 mRNA were expressed by cultured TIL, as assessed by RT-PCR; the corresponding tumour samples consistently contained TNF alpha, IL-8 and IL-10 mRNA, whereas IL-2 and IFN gamma mRNA were faintly expressed in some NB tumours and IL-4 and IL-5 mRNA were never detected. A total of 90 clones were subsequently raised from IL-2-expanded TIL from six NB patients; 87/90 clones were of T cell lineage with a CD4+ or CD8+ immunophenotype, whereas the 3 remaining clones were of NK cell origin. Upon triggering of the CD3-TcR complex, 64% CD4+ and 77% CD8+ T cell clones killed the murine P815 mastocytoma cell line. Virtually no T cell clone lysed a LAK-sensitive NB cell line whereas 15% CD4+ and 17% CD8+ clones mediated NK-like activity against the K562 cell line. Finally, the patterns of cytokine production by CD4+ clones were roughly consistent with those of a T helper (TH) 1 profile and similar to those observed in CD8+ clones.

Base Sequence↗

PubMed1996

Hypoproliferative human lamina propria T cells retain the capacity to secrete lymphokines when stimulated via CD2/CD28 pathways.

Human lamina propria (LP) T cells exhibit a reduced proliferative capacity in response to antigen-specific stimulation. To investigate the functional state of such hypoproliferative T cells, we determined the capacity of LP T cells to produce lymphokines when stimulated by monoclonal antibodies that crosslink either the TCR/CD3 complex or accessory pathway molecules (CD2,CD28). We found that TCR/CD3-mediated proliferative responses of LP T cells were greatly diminished when compared to peripheral blood (PB) T cells, but were largely restored when cells were preincubated in IL-2. Despite their proliferative hyporesponsiveness, LP T cells (as compared to PB T cells) secreted equal amounts of IL-2 and increased amounts of IFN-gamma, IL-4 and IL-5; these increased cytokine responses were most evident when cells were stimulated via the accessory pathways. In further studies, purified CD4+ LP T cells were compared with purified CD4+/CD45RO+ PB T cells (i.e., the PB T cell subset they most resemble). LP T cells produced significantly more IFN-gamma and IL-5 but less IL-4 than their CD45RO+ PB counterparts. Overall, LP T cells are unresponsive T cells following stimulation via the TCR/CD3 pathway but nevertheless retain the capacity to produce increased levels of TH1 and TH2-type lymphokines following stimulation via the CD2/CD28 accessory pathway; thus, they are best classified as modified "anergic" T cells.

CD2 Antigens↗

PubMed2005

Chemical inhibitors when timing is critical: a pharmacological concept for the maturation of T cell contacts.

Cellular signal transduction proceeds through a complex network of molecular interactions and enzymatic activities. The timing of these molecular events is critical for the propagation of a signal and the generation of a specific cellular response. To define the timing of signalling events, we introduce the combination of high-resolution confocal microscopy with the application of small-molecule inhibitors at various stages of signal transduction in T cells. Inhibitors of Src-family tyrosine kinases and actin dynamics were employed to dissect the role of the lymphocyte-specific tyrosine kinase Lck in the formation and maintenance of T cell receptor/CD3-dependent contacts. Anti-CD3epsilon-coated coverslips served as a highly defined stimulus. The kinetics of the recruitment of the yellow fluorescent protein-tagged signalling protein ZAP-70 were detected by high-resolution confocal microscopy. The analysis revealed that at 5 min after receptor engagement, Lck activity was required for maintenance of contacts. In contrast, after 20 min of receptor engagement, the contacts were Lck-independent. The relevance of the timing of inhibitor application provides a pharmacological concept for the maturation of T cell-substrate contacts.

Animals↗

PubMed1993

Human intestinal mucosa alters T-cell reactivities.

BACKGROUND: Compared with T cells in peripheral blood, lamina propria T lymphocytes have a low proliferative response to stimulation via the T-cell antigen receptor/CD3 complex or by protein kinase C activators yet largely preserve or even show an enhanced reactivity to CD2 and CD28 triggering. Coculture of peripheral blood T lymphocytes with intestinal mucosa supernatant leads to a similar functional behavior as found in freshly recovered lamina propria T lymphocytes. The aim of this study is to characterize the nature of substances in the mucosal supernatant responsible for downregulation of T-cell receptor-dependent signals. METHODS: Mucosal supernatant was produced, dialyzed, digested with proteinase K, reduced by 2-mercaptoethanol or dithiothreitol, and tested for its activity on peripheral blood T lymphocytes. RESULTS: Supernatant lost its activity after dialysis through a membrane (pore size 12,000-14,000). Digestion with proteinase K does not abolish its activity suggesting that the substances are neither proteins nor peptides. However, its effects on T lymphocyte proliferation can be reversed by reducing agents like 2-mercaptoethanol or dithiothreitol, suggesting that oxidative substances are contained in mucosal supernatants. CONCLUSIONS: Our data support the view that mucosal substances that down-regulate antigen receptor-induced T lymphocyte proliferation are small, nonprotein, nonpeptide molecules with oxidative properties.

Antigens, Differentiation, T-Lymphocyte↗

PubMed2004

Automatic generation of lymphocyte heterogeneity: Division-dependent changes in the expression of CD27, CCR7 and CD45 by activated human naive CD4+ T cells are independently regulated.

Lymphocyte differentiation is a complex process regulated by the integration of signals received through a variety of cell surface receptors that results in populations of differentiated cells that have acquired novel characteristics and effector functions. Differentiation of T and B lymphocytes into effector cells, such as cytokine-secreting CD4+ T cells, cytotoxic CD8+ T cells and Ig-secreting B cells, as well as alterations in cell surface phenotype, have been reported to be associated with cell division. Nevertheless, the genesis of heterogeneity in effector cell type is unknown. A strictly deterministic view holds that heterogeneity arises from distinct signalling histories for each functionally or phenotypically different cell type. In contrast, a probabilistic interpretation proposes that internal stochastic regulation of gene expression gives rise to lymphocytes of mixed phenotypes. To help distinguish between these explanations, we examined the expression of CD27, CCR7, CD45RA and CD45RO by human naive CD4+ T cells in the context of the division history of the lymphocyte. Our results show that each marker independently changes with progressive divisions, strongly supporting the proposal that phenotypic heterogeneity in lymphocytes can arise as the result of independent stochastic processes controlling the expression of individual molecules.

Antibodies, Monoclonal↗

PubMed2001

Calmodulin-dependent kinase II mediates T cell receptor/CD3- and phorbol ester-induced activation of IkappaB kinase.

Numerous fundamental biological processes involve the NFkappaB family of transcription factors. The mechanisms by which this family of proteins is regulated are therefore of widespread importance. In most cells, NFkappaB is bound to inhibitory IkappaB proteins and sequestered in the cytoplasm. NFkappaB-inducing signals result in activation of a large multisubunit kinase complex, IKK, which phosphorylates IkappaB. IkappaB is subsequently degraded, releasing NFkappaB, which translocates to the nucleus. We previously reported that inhibitors of the calcium-binding protein calmodulin (CaM) prevent phorbol ester-induced phosphorylation of IkappaB. Here we show that KN93, an inhibitor of CaM-dependent kinases (CaMKs), also inhibits the phosphorylation of IkappaB. The effect of both CaM and CaMK inhibitors on IkappaB phosphorylation is due to the inhibition of the activity of CaMK II because neither drug has any effect when a derivative of CaMK II that is insensitive to these inhibitors is expressed. When CaMK II is inhibited, phorbol ester is no longer able to activate IKK, placing CaMK II in the signaling pathway that leads to IKK activation. CaM and CaMK inhibitors also block T cell receptor/CD3-induced activation but have no effect on the ability of the cytokine tumor necrosis factor alpha or the phosphatase inhibitor calyculin A to induce degradation of IkappaB. Finally we show that expression of a constitutively active CaMK II results in the activation of NFkappaB. The results identify CaMK II as a mediator of IKK activation specifically in response to T cell receptor/CD3 and phorbol ester stimulation.

CD3 Complex↗

PubMed1991

Biochemical identification of a direct physical interaction between the CD4:p56lck and Ti(TcR)/CD3 complexes.

The CD4 and CD8 antigens function in synergy with the TcR/CD3 complex in the generation of intracellular signals leading to T cell proliferation. The association of the protein-tyrosine kinase p56lck with CD4 and CD8 provides a potential mechanism in the generation of intracellular signals. Several studies have shown that CD4 can co-modulate with TcR/CD3 suggesting that these receptor complexes may associated on the surface of the T cell. Nevertheless, it has proven difficult to formally demonstrate a direct physical interaction between the CD4 and TcR/CD3 complexes using biochemical techniques. In this study, we have used the sensitivity of the in vitro kinase assay to show a direct physical linkage between the CD4:p56lck complex and various CD3 subunits. Immunoprecipitation of CD4 from cell lysates derived from the T lymphoblastoid line HPB-ALL results in the co-purification of p56lck with an additional polypeptide at 20 kDa. Re-precipitation analysis and isoelectric focusing demonstrated that this band corresponds to the CD3 epsilon chain. An alternative approach which involves the labeling of microsomal membranes with [gamma-32P]ATP revealed the presence of CD3 epsilon and zeta chains in anti-CD4 immunoprecipitates. By contrast, we were unable to demonstrate the association of the CD4:p56lck and TcR/CD3 complex in resting peripheral blood lymphocytes. These data indicate that the CD4:p56lck and TcR/CD3 complexes have the ability to form stable complexes on the surface of certain T cell lines.

Animals↗

PubMed1999

Human decidualized endometrial T lymphocytes do not substantially down-regulate CD3zeta.

PROBLEM: The T-cell antigen receptor (TCR) has been reported to be down-regulated on T-cells in the decidualized endometrium in early pregnancy. METHOD OF STUDY: The expression of CD3zeta, a component of the TCR complex, has been investigated in human first-trimester decidual T-cells using flow cytometric analysis of permeabilized cells. RESULTS: Levels of CD3zeta expression were significantly lower in decidual than in peripheral T-cells from non-pregnant women, as assessed by mean fluorescence intensity (4.2 vs. 5.5, logarithmic scale, P < 0.05). However, when decidual and peripheral T-cells from the same subjects were analyzed (n = 10), mean levels of CD3zeta were slightly, but not significantly, lower in decidual than in peripheral T-cells (P > 0.1). CD3zeta was not substantially down-regulated systemically as mean cytoplasmic CD3zeta levels did not differ significantly between peripheral blood T-cells from pregnant women and non-pregnant controls (P > 0.2). CD8+ cells outnumber CD4+ cells in decidua, but neither the proportions of these two T-cell subsets positive for cytoplasmic CD3zeta nor the mean levels of CD3zeta were significantly different. CONCLUSIONS: These results indicate that human decidual T-cells do not greatly down-regulate CD3zeta, but it is unclear if a small decrease in mean levels may be sufficient to compromise their capacity for activation.

CD3 Complex↗