1,721,065 research outputs found
Modulation of FcεRI-dependent mast cell response by OX40L.
No full textOX40L is expressed by many cell types, including antigen presenting cells (APCs), T cells, vascular endothelial cells, mast cells (MCs), and natural killer cells. The importance of OX40L:OX40 interactions and the OX40L signaling is crucial for the homeostasis and for the modulation of the effector functions of the immune system. However, the lack of non-murine/non-IgG commercially available OX40L-triggering antibodies and the potential signal cross-contamination caused by the binding to the FcγRs co-expressed by several immune cells have limited the study of the OX40L-signaling cascade. We recently characterized the functions and described the molecular events, which follow the engagement of OX40L in MCs, by the use of the soluble OX40 molecule, able to mimic the regulatory T cell-driven engagement of MC-OX40L. This molecule enables signaling studies in MCs with any requirement for OX40-expressing cells. Using this unique reagent, we determined the modality and the extent by which the engagement of OX40L in MCs influences the IgE-dependent MC degranulation. This tool may find a potential application for signaling studies of other OX40L-expressing populations other than MCs, mainly APCs, with similar approaches we reported for the study of OX40L cascade
The overlooked "nonclassical" functions of major histocompatibility complex (MHC) class II antigens in immune and nonimmune cells RID A-5515-2008
No full textBesides their "classical" antigenic peptide-presenting activity, major histocompatibility complex (MHC) class II antigens can activate different cellular functions in immune and nonimmune cells. However, this "nonclassical" role and its functional consequences are still substantially overlooked. In this review, we will focus on these alternative functional properties of MHC class II antigens, to reawaken attention to their present and foreseeable immunobiologic and pathogenetic implications. The main issues that will be addressed concern 1) the role of MHC class II molecules as basic components of exchangeable oligomeric protein complexes with intracellular signaling ability; 2) the nonclassical functions of MHC class II antigens in immune cells; 3) the pathogenetic role of MHC class II antigens in inflammatory/autoimmune and infectious disease; and 4) the functional role of MHC class II antigens in solid malignancies. (C) 1999 Wiley-Liss, Inc
Crossroads between immune responses and physiological regulation: Metabolic control of resistance versus tolerance against disease
No full textIf a threat cannot be avoided, the organism has two defense options: it can try to eliminate the threatening agent or boost physiological mechanisms to tolerate the challenge and its consequences. Both strategies can be (and usually are) used at the same time. Fighting an infection, for instance, requires mounting immune responses to control pathogen burden as well as physiologic adaptations to tolerate stress and damage. Thus, the two strategies are connected and interdependent. We are starting to understand how the regulation of host metabolic physiology during disease impacts both the ability to resist pathogens’ burden and tolerate parenchymal tissue functional damage. Here, we review a number of recent publications that have begun to shed light on the physiological and immunological mechanisms that coordinate host defense and metabolic processes. In particular, we will cover the areas of energetic control, substrates utilization, and the regulatory signals that promote infectious disease tolerance
Exploring a regulatory role for mast cells: 'MCregs'?
No full textRegulatory cells can mould the fate of the immune response by direct suppression of specific subsets of effector cells, or by redirecting effectors against invading pathogens and infected or neoplastic cells. These functions have been classically, although not exclusively, ascribed to different subsets of T cells. Recently, mast cells have been shown to regulate physiological and pathological immune responses, and thus to act at the interface between innate and adaptive immunity assuming different functions and behaviors at discrete stages of the immune response. Here, we focus on these poorly defined, and sometimes apparently conflicting, functions of mast cells
Human MSCs affect the B cell survival and differentiation in CD19 dim and CD19 bright B cell subpopulations
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Triggering of target of an antiproliferative antibody-1 (TAPA-1/CD81) up-regulates the release of tumour necrosis factor-alpha by the EBV-B lymphoblastoid cell line JY
No full textTarget of an antiproliferative antibody-1 (TAPA-1/CD81) has been shown to be non-covalently associated to HLA-DR antigens on the cell surface of B cells. In this study the authors report that triggering of CD81 by MoAb 5A6 or 1D6 significantly (P < 0.05) up-regulates the release of tumour necrosis factor-alpha (TNF-alpha) by the Epstein-Barr virus-positive (EBV)-B lymphoblastoid cell line JY. The accumulation of TNF-alpha in the culture medium of JY cells incubated with either anti-CD81 MoAb was found to be dose-dependent and similar to that obtained following crosslinking of HLA-DR antigens with MoAb L243. The effect of the combination of anti-CD81 and anti-HLA-DR MoAb on the release of TNF-alpha by JY cells was not synergistic or additive. In addition, the combination of anti-CD81 and anti-HLA-DR MoAb did not affect proliferation and homotypic aggregation of JY cells induced by each MoAb used alone. Both anti-CD81 or anti-HLA-DR MoAb induced protein tyrosine phosphorylation. However, different cytoplasmic proteins were phosphorylated following triggering of either molecule. Taken together, the data demonstrate that CD81 and HLA-DR antigens induce similar effector phenomena in the regulation of TNF-alpha release, homotypic aggregation and inhibition of JY cell proliferation
Mast cells enhance B cell activation and proliferation: importance of Mast cell soluble factors and surface molecules
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