PubMed Health⌕ Search

PubMed · 8178050

[Cell cooperation in immune responses].

Abstract

All immune responses are assisted by different subpopulations of cells with complementary properties. Beside T and B lymphocytes specialized into effector killers, pro-inflammatory or antibody-producing cells, there are accessory and helper cells which exert various functions, such as antigen degradation and presentation, activating signal amplification and support of antigen-activated lymphocytic clones expansion and their functional differentiation. These cells, whose role is to co-operate with effector lymphocytes, are either lymphocytes, such as antigen-presenting B cells and helper T cells, or cells of haematopoietic origin belonging to the monocytic lineage, such as macrophages, monocytes and dendritic cells. Co-operation between subpopulations of the immune system takes place either by cell-to-cell interactions, or by indirect interactions via soluble mediators. Direct interactions postulate the involvement of receptor molecules and ligand-molecules expressed at cell surface. Indirect interactions are mediated by cytokines secreted by accessory or helper cells and acting at short distance to the point of secretion. Surface molecules and cytokines are well characterized both biochemically and functionally, and we are now in a position to manipulate the essential stages of cellular or hormonal immune response by using either cytokines and their inhibitors, or agonists or antagonists of surface receptors. Co-operation between cells participates in the autoregulation of the immune system. Through modulation of surface molecules and synthesis of cytokines the immune system can amplify discreet signals or repress untimely responses.(ABSTRACT TRUNCATED AT 250 WORDS)

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

C Carnaud. 1994-01-01. [Cell cooperation in immune responses].. https://pubmed.ncbi.nlm.nih.gov/8178050/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Differential cell signaling testing for cell-cell communication inference from single-cell data by dominoSignal.

MOTIVATION: Algorithms for ligand-receptor network inference have emerged as commonly used tools to estimate cell-cell communication from reference single-cell data. Many studies employ these algorithms to compare signaling between conditions and lack methods to statistically identify signals that are significantly different. We previously developed the cell communication inference algorithm Domino, which considers ligand and receptor gene expression in association with downstream transcription factor activity scoring. We developed the dominoSignal software to innovate upon Domino and extend its functionality to test statistically differential cellular signaling. RESULTS: This new functionality includes the compilation of active signals as linkages from multiple subjects in a single-cell data set and testing condition-dependent signaling linkage. The software is applicable for analysis of single-cell data sets with multiple subjects as biological replicates as well as with bootstrapped replicates from data sets with few or pooled subjects. We use simulation studies to benchmark the number of subjects in compared groups and cells within an annotated cell type sufficient to accurately identify differential linkages. We demonstrate the application of the Differential Cell Signaling Test (DCST) in the dominoSignal software to investigate consequences of cancer cell phenotypes and immunotherapy on cell-cell communication in tumor microenvironments. These applications in cancer studies demonstrate the ability of differential cell signaling analysis to infer changes to cell communication networks from therapeutic or experimental perturbations, which is broadly applicable across biological systems. AVAILABILITY: dominoSignal is available through Bioconductor at https://www.bioconductor.org/packages/release/bioc/html/dominoSignal.html.

Cell Communication↗

ZAP-70 kinase regulates HIV cell-to-cell spread and virological synapse formation.

HIV efficiently spreads in lymphocytes, likely through virological synapses (VSs). These cell-cell junctions share some characteristics with immunological synapses, but cellular proteins required for their constitution remain poorly characterized. We have examined here the role of ZAP-70, a key kinase regulating T-cell activation and immunological synapse formation, in HIV replication. In lymphocytes deficient for ZAP-70, or expressing a kinase-dead mutant of the protein, HIV replication was strikingly delayed. We have characterized further this replication defect. ZAP-70 was dispensable for the early steps of viral cycle, from entry to expression of viral proteins. However, in the absence of ZAP-70, intracellular Gag localization was impaired. ZAP-70 was required in infected donor cells for efficient cell-to-cell HIV transmission to recipients and for formation of VSs. These results bring novel insights into the links that exist between T-cell activation and HIV spread, and suggest that HIV usurps components of the immunological synapse machinery to ensure its own spread through cell-to-cell contacts.

Cell Communication↗

Gap junctional intercellular communication capacity by gap-FRAP technique: a comparative study.

Gap junctions play an important role in vital functions, including the regulation of cell growth and cell differentiation. Connexins 43 (Cx43) are the most widely expressed gap junction proteins. Cellular localization of phosphorylated Cx43 has been implicated in the capacity of gap junctional intercellular communication (GJIC). To follow the functionality of GJIC of different cell types, in monolayer cultures, characterized by different patterns of phosphorylated Cx43, we used a fluorescence recovery after photobleaching (FRAP) technique, and compared two tracers, 5(6)-carboxyfluorescein diacetate (CFDA) and calcein acetoxymethylester (AM). The GJIC capacity was quantified by estimating fluorescence redistribution parameters. The functionality of GJIC was in relation with the staining localization of phosphorylated Cx43 to the cell-cell contact areas, corresponding to gap junctions between contacting cells. GJIC involvement in fluorescence restitution after photobleaching was checked by a gap junction channel inhibition assay. We demonstrated that the choice of the dye did not significantly influence the fluorescence recovery percentages despite a cell line-dependent CFDA release, whereas it had an important impact on fluorescence kinetic profiles. This study reinforces the interest of the gap-FRAP approach to quantify modifications in the functionality of gap junctions and, above all, argues about the limits of CFDA for 3-D future approaches.

Cell Communication↗