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Inhibition of Cdk Activity

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...

Inhibition of CDK Activity

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Inhibitors of Viral Protein Synthesis

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Related Experiment Video

Updated: Jul 7, 2026

Generation of Multivirus-specific T Cells to Prevent/treat Viral Infections after Allogeneic Hematopoietic Stem Cell Transplant

Generation of Multivirus-specific T Cells to Prevent/treat Viral Infections after Allogeneic Hematopoietic Stem Cell Transplant

Published on: May 27, 2011

CD4+ T-cell effectors inhibit Epstein-Barr virus-induced B-cell proliferation.

S Nikiforow¹, K Bottomly, G Miller

¹Department of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06520, USA.

Journal of Virology

|March 27, 2001

Summary

CD4+ T cells prevent rapid proliferation of Epstein-Barr virus (EBV)-infected B cells. This immune surveillance is crucial for controlling early-stage EBV-driven B-cell growth, unlike later stages controlled by CD8+ T cells.

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Last Updated: Jul 7, 2026

Generation of Multivirus-specific T Cells to Prevent/treat Viral Infections after Allogeneic Hematopoietic Stem Cell Transplant

Generation of Multivirus-specific T Cells to Prevent/treat Viral Infections after Allogeneic Hematopoietic Stem Cell Transplant

Published on: May 27, 2011

Establishment of Epstein-Barr Virus Growth-transformed Lymphoblastoid Cell Lines

Establishment of Epstein-Barr Virus Growth-transformed Lymphoblastoid Cell Lines

Published on: November 8, 2011

An Efficient and Simple Method to Establish NK and T Cell Lines from Patients with Chronic Active Epstein-Barr Virus Infection

An Efficient and Simple Method to Establish NK and T Cell Lines from Patients with Chronic Active Epstein-Barr Virus Infection

Published on: March 30, 2018

Area of Science:

Immunology
Virology
Cell Biology

Background:

Epstein-Barr virus (EBV) can cause B-cell lymphoproliferative disease and lymphoma in immunodeficient individuals.
Immortalized B-cell lines readily form in vitro without immune surveillance.
Memory T cells inhibit EBV-transformed B-cell foci in regression assays.

Purpose of the Study:

To identify the specific T-cell subset responsible for regulating the early proliferative phase of EBV-infected B cells.
To analyze T-cell surveillance mechanisms governing EBV-mediated B-cell proliferation using quantitative methods.

Main Methods:

Quantitative analysis of T-cell surveillance on EBV-infected B cells.
In vitro infection of B cells with EBV and assessment of proliferation.
Manipulation of T-cell populations (CD4+ and CD8+) to determine their role in immune control.

Main Results:

CD4+ T cells significantly limit the proliferation of newly infected, activated CD23+ B cells.
In the absence of T cells, EBV-infected CD23+ B cells exhibit rapid division within the first three weeks post-infection.
Removal of CD4+ T cells, but not CD8+ T cells, abrogated immune control over early B-cell proliferation.
Purified CD4+ T cells effectively inhibited the outgrowth of EBV-infected B cells in vitro.

Conclusions:

CD4+ effector T cells are essential for preventing the early proliferative phase of EBV-induced B-cell growth.
This contrasts with the role of CD8+ cytolytic T cells in eliminating established EBV-infected lymphoblastoid cell lines.