Acutely Infected Langerhans Cells Are More Efficient than T Cells in Disseminating HIV Type 1 to Activated T Cells Following a Short Cell-Cell Contact

1995 ◽  
Vol 11 (8) ◽  
pp. 877-884 ◽  
Author(s):  
SEYOUM AYEHUNIE ◽  
RICHARD W. GROVES ◽  
ANN-MARIE BRUZZESE ◽  
RUTH M. RUPRECHT ◽  
THOMAS S. KUPPER ◽  
...  
Keyword(s):  
T Cells ◽  
Langerhans Cells ◽  
Cell Contact ◽  
Activated T Cells ◽  
Short Cell ◽  
Hiv Type 1 ◽  
Cell Cell

A monocytic cell line is triggered to produce IL-1β by cell-cell contact with activated T cells

Cytokine ◽  
1991 ◽  
Vol 3 (5) ◽  
pp. 454
Author(s):  
P. Isler ◽  
J.-H. Zhang ◽  
E. Roosnek ◽  
J.-M. Dayer
Keyword(s):  
T Cells ◽  
Cell Line ◽  
Cell Contact ◽  
Activated T Cells ◽  
Monocytic Cell ◽  
Monocytic Cell Line ◽  
Cell Cell

scholarly journals Mesenchymal Stromal Cells Rapidly Suppress TCR Signaling-Mediated Cytokine Transcription in Activated T Cells Through the ICAM-1/CD43 Interaction

2021 ◽  
Vol 12 ◽  
Author(s):  
Shuwei Zheng ◽  
Ke Huang ◽  
Wenjie Xia ◽  
Jiahao Shi ◽  
Qiuli Liu ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
T Cell Activation ◽  
Cell Activation ◽  
Inflammatory Diseases ◽  
Cell Contact ◽  
Dependent Manner ◽  
Tcr Signaling ◽  
Activated T Cells ◽  
Cell Cell

Cell-cell contact participates in the process of mesenchymal stromal cell (MSC)-mediated T cell modulation and thus contributes to MSC-based therapies for various inflammatory diseases, especially T cell-mediated diseases. However, the mechanisms underlying the adhesion interactions between MSCs and T cells are still poorly understood. In this study, we explored the interaction between MSCs and T cells and found that activated T cells could rapidly adhere to MSCs, leading to significant reduction of TNF-α and IFN-γ mRNA expression. Furthermore, TCR-proximal signaling in activated T cells was also dramatically suppressed in the MSC co-culture, resulting in weakened Ca2+ signaling. MSCs rapidly suppressed TCR signaling and its downstream signaling in a cell-cell contact-dependent manner, partially through the ICAM-1/CD43 adhesion interaction. Blockade of either ICAM-1 on MSCs or CD43 on T cells significantly reversed this rapid suppression of proinflammatory cytokine expression in T cells. Mechanistically, MSC-derived ICAM-1 likely disrupts CD43-mediated TCR microcluster formation to limit T cell activation. Taken together, our results reveal a fast mechanism of activated T cell inhibition by MSCs, which provides new clues to unravel the MSC-mediated immunoregulatory mechanism for aGVHD and other severe acute T cell-related diseases.

scholarly journals Activated T cells induce expression of B7/BB1 on normal or leukemic B cells through a CD40-dependent signal.

1993 ◽  
Vol 177 (4) ◽  
pp. 925-935 ◽  
Author(s):  
E A Ranheim ◽  
T J Kipps
Keyword(s):  
Cell Proliferation ◽  
T Cells ◽  
B Cells ◽  
B Cell ◽  
Cd4 T Cells ◽  
Cell Phenotype ◽  
Cell Contact ◽  
Activated T Cells ◽  
Antigen Presenting ◽  
Cell Cell

Cognate interactions between antigen-presenting B and T cells play crucial roles in immunologic responses. T cells that have been activated via the crosslinking of CD3 are able to induce B cell proliferation and immunoglobulin secretion in a major histocompatibility complex-unrestricted and contact-dependent manner. We find that such activated human CD4+ T cells, but not control Ig-treated T cells, may induce normal or leukemic B cells to express B7/BB1 and significantly higher levels of CD54 intercellular adhesion molecule 1 via a process that also requires direct cell-cell contact. To discern what cell surface molecule(s) may be responsible for signalling B cells to express B7/BB1, we added various monoclonal antibodies (mAbs) specific for T or B cell accessory molecules or control mAbs to cocultures of alpha-CD3-activated T cells and resting B cells. We find that only alpha-CD40 mAbs can significantly inhibit the increased expression of B7/BB1, suggesting that the ligand for CD40 expressed on activated T cells may be an important inducer of B7/BB1 expression. Subsequent experiments in fact demonstrate that alpha-CD40 mAbs, but not control mAbs, induce changes in B cell phenotype similar to those induced by activated T cells when the mAbs are presented on Fc gamma RII (CDw32)-expressing L cells. These phenotypic changes have significant effects on B cell function. Whereas chronic lymphocytic leukemia (CLL) B cells normally are very poor stimulators in allogeneic mixed lymphocyte reactions (MLRs), CLL-B cells preactivated via CD40 crosslinking are significantly better presenters of alloantigen, affecting up to 30-fold-greater stimulation of T cell proliferation than that induced by control treated or nontreated CLL-B cells. Similarly, the MLR of T cells stimulated by allogeneic nonleukemic B cells can be enhanced significantly if the stimulator B cells are preactivated via CD40 crosslinking. The enhanced MLR generated by such preactivated B cells may be inhibited by blocking B7/BB1-CD28 interaction with CTLA4Ig. These studies demonstrate a novel, CD40-dependent pathway for inducing B cell expression of B7/BB1 and enhancing B cell antigen-presenting cell activity that can be initiated via cell-cell contact with alpha-CD3-stimulated CD4+ T cells.

scholarly journals αII-spectrin in T cells is involved in the regulation of cell-cell contact leading to immunological synapse formation?

PLoS ONE ◽  
2017 ◽  
Vol 12 (12) ◽  
pp. e0189545 ◽  
Author(s):  
Justyna M. Meissner ◽  
Aleksander F. Sikorski ◽  
Tomasz Nawara ◽  
Jakub Grzesiak ◽  
Krzysztof Marycz ◽  
...  
Keyword(s):  
T Cells ◽  
Synapse Formation ◽  
Immunological Synapse ◽  
Cell Contact ◽  
Cell Cell

Proliferation of highly purified T cells in response to signaling via surface receptors requires cell-cell contact

1989 ◽  
Vol 9 (2) ◽  
pp. 151-158 ◽  
Author(s):  
David Schwartz ◽  
Richard C. K. Wong ◽  
Talal Chatila ◽  
Amin Arnaout ◽  
Richard Miller ◽  
...  
Keyword(s):  
T Cells ◽  
Cell Contact ◽  
Surface Receptors ◽  
Cell Cell

Allogeneic Dendritic Cell Induction of HIV-Specific Cytotoxic T Lymphocyte Responses from T Cells of HIV Type 1-Infected and Uninfected Individuals

1997 ◽  
Vol 13 (1) ◽  
pp. 33-39 ◽  
Author(s):  
MARC DUPUIS ◽  
MADHUSUDAN V. PESHWA ◽  
CLAUDIA BENIKE ◽  
SMRITI K. KUNDU ◽  
EDGAR G. ENGLEMAN ◽  
...  
Keyword(s):  
T Cells ◽  
Dendritic Cell ◽  
T Lymphocyte ◽  
Cytotoxic T Lymphocyte ◽  
Cell Induction ◽  
Hiv Type 1 ◽  
Lymphocyte Responses

scholarly journals Requirement for an Intact T-Cell Actin and Tubulin Cytoskeleton for Efficient Assembly and Spread of Human Immunodeficiency Virus Type 1

2007 ◽  
Vol 81 (11) ◽  
pp. 5547-5560 ◽  
Author(s):  
Clare Jolly ◽  
Ivonne Mitar ◽  
Quentin J. Sattentau
Keyword(s):  
Human Immunodeficiency Virus ◽  
T Cells ◽  
Plasma Membrane ◽  
T Cell ◽  
Immunodeficiency Virus ◽  
Fixed Cell ◽  
Cell Spread ◽  
Hiv 1 ◽  
Cell Cell

ABSTRACT Human immunodeficiency virus type 1 (HIV-1) infection of CD4+ T cells leads to the production of new virions that assemble at the plasma membrane. Gag and Env accumulate in the context of lipid rafts at the inner and outer leaflets of the plasma membrane, respectively, forming polarized domains from which HIV-1 buds. HIV-1 budding can result in either release of cell-free virions or direct cell-cell spread via a virological synapse (VS). The recruitment of Gag and Env to these plasma membrane caps in T cells is poorly understood but may require elements of the T-cell secretory apparatus coordinated by the cytoskeleton. Using fixed-cell immunofluorescence labeling and confocal microscopy, we observed a high percentage of HIV-1-infected T cells with polarized Env and Gag in capped, lipid raft-like assembly domains. Treatment of infected T cells with inhibitors of actin or tubulin remodeling disrupted Gag and Env compartmentalization within the polarized raft-like domains. Depolymerization of the actin cytoskeleton reduced Gag release and viral infectivity, and actin and tubulin inhibitors reduced Env incorporation into virions. Live- and fixed-cell confocal imaging and assay of de novo DNA synthesis by real-time PCR allowed quantification of HIV-1 cell-cell transfer. Inhibition of actin and tubulin remodeling in infected cells interfered with cell-cell spread across a VS and reduced new viral DNA synthesis. Based on these data, we propose that HIV-1 requires both actin and tubulin components of the T-cell cytoskeleton to direct its assembly and budding and to elaborate a functional VS.

scholarly journals The Activated Type 1–Polarized Cd8+ T Cell Population Isolated from an Effector Site Contains Cells with Flexible Cytokine Profiles

1999 ◽  
Vol 190 (8) ◽  
pp. 1081-1092 ◽  
Author(s):  
Anthony G. Doyle ◽  
Kathy Buttigieg ◽  
Penny Groves ◽  
Barbara J. Johnson ◽  
Anne Kelso
Keyword(s):  
T Cells ◽  
T Cell ◽  
Cell Population ◽  
Expression Profiles ◽  
Lung Parenchyma ◽  
Activated T Cells ◽  
Cytokine Genes ◽  
Effector Site

The capacity of activated T cells to alter their cytokine expression profiles after migration into an effector site has not previously been defined. We addressed this issue by paired daughter analysis of a type 1–polarized CD8+ effector T cell population freshly isolated from lung parenchyma of influenza virus–infected mice. Single T cells were activated to divide in vitro; individual daughter cells were then micromanipulated into secondary cultures with and without added IL-4 to assess their potential to express type 2 cytokine genes. The resultant subclones were analyzed for type 1 and 2 cytokine mRNAs at day 6–7. When the most activated (CD44highCD11ahigh) CD8+ subpopulation from infected lung was compared with naive or resting (CD44lowCD11alow) CD8+ cells from infected lung and from normal lymph nodes (LNs), both clonogenicity and plasticity of the cytokine response were highest in the LN population and lowest in the activated lung population, correlating inversely with effector function. Multipotential cells were nevertheless detected among clonogenic CD44highCD11ahigh lung cells at 30–50% of the frequency in normal LNs. The data indicate that activated CD8+ T cells can retain the ability to proliferate and express new cytokine genes in response to local stimuli after recruitment to an effector site.

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