Cd4 T Cell Infection
Cd4 T Cell Infection - Related Videos
02:40
Effect of an Immunomodulatory Pharmacological Agent on the Interaction Between Dendritic Cells and CD4+ T Cells
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2025
This video demonstrates a method of converting dendritic cells (DCs) to tolerogenic DCs (TolDCs) using an immunomodulatory pharmacological agent. This conversion is confirmed by evaluating the TolDC function through their immunosuppressive effect on CD4+ T cells.
08:20
In Vitro Differentiation of Human CD4+FOXP3+ Induced Regulatory T Cells (iTregs) from Naïve CD4+ T Cells Using a TGF-β-containing Protocol
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Cited by 24 •
2016
This protocol describes the reproducible generation and phenotyping of human induced regulatory T cells (iTregs) from naïve CD4+ T cells in vitro. Different protocols for FOXP3 induction allow for the study of specific iTreg phenotypes obtained with respective protocols.
12:07
Preparation and Use of HIV-1 Infected Primary CD4+ T-Cells as Target Cells in Natural Killer Cell Cytotoxic Assays
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Cited by 12 •
2011
Cytotoxicity assays to measure natural killer cell lytic responses to HIV-infected cells is limited by the purity of the target cells. We demonstrate here the isolation of a highly purified population of HIV-1 infected primary T-cell blasts by taking advantage of HIV-1 s ability to down-modulate CD4.
08:11
Assessing the Innate Sensing of HIV-1 Infected CD4+ T Cells by Plasmacytoid Dendritic Cells Using an Ex vivo Co-culture System.
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Cited by 1 •
2015
Unlike cell-free HIV-1 particles, infected CD4+ T cells are effectively sensed by plasmacytoid dendritic cells (pDCs). This manuscript describes a method where peripheral blood mononuclear cells (PBMCs) or isolated pDCs are co-cultured with HIV-1 infected T cells to evaluate innate sensing by pDCs as assessed by release of type-I IFN.
11:28
Imaging CD4 T Cell Interstitial Migration in the Inflamed Dermis
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Cited by 11 •
2016
The mechanisms that govern the interstitial motility of CD4 effector T cells at sites of inflammation are relatively unknown. We present a non-invasive approach to visualize and manipulate in vitro-primed CD4 T cells in the inflamed ear dermis, allowing for study of the dynamic behavior of these cells in situ.
FAQs
The chemokine coreceptor works with the CD4 receptor during the earliest stage of HIV entry. Binding to both receptors enables the viral and cellular membranes to fuse, allowing the viral material to enter the lymphocyte. Studying this receptor-dependent step helps explain how infection begins and identifies a critical point for investigating interventions that could limit viral entry.
After membrane fusion, HIV uses reverse transcription to convert its genetic material into a form that can be incorporated into the host cell. Integration then places viral genetic material within the host genome, enabling the infected cell to produce new virions. Examining this sequence connects the initial entry event with sustained replication and pathogen production.
Productive infection can reduce the population or function of CD4-positive T lymphocytes, cells that coordinate adaptive immune responses. As these cells are progressively lost or dysregulated, the immune system becomes less able to organize effective responses. This relationship makes CD4 T cell infection central to studies of HIV pathogenesis and the development of immune dysfunction.
HIV provides a well-defined example in which receptor binding, membrane fusion, reverse transcription, genome integration, and virion production are linked to progressive loss of immune function. Following these connected stages allows researchers to relate molecular events inside infected lymphocytes to broader disease mechanisms, including viral pathogenesis, immune dysregulation, and transmission.
Experimental models reproduce or examine the cellular and viral events associated with infection, including entry, replication, genome integration, and production of new virions. They help investigators connect mechanisms observed in CD4-positive lymphocytes with changes in immune function. These models also provide a foundation for evaluating approaches relevant to therapies, vaccines, and infection control.
Studies can clarify how HIV causes disease, disrupts immune regulation, and spreads between hosts. The resulting knowledge supports several applied areas named in the source material: antiretroviral therapy development, vaccine research, diagnostic assay development, and experimental models for controlling infection. Together, these outputs connect cellular immunology with strategies for detecting and managing HIV.