The virus destroys a type of white blood cell in the immune system called a
T-helper cell, and makes copies of itself inside these cells.
Th17 cells have recently been identified as a unique CD4+
T-helper cell subset, characterized by IL-17 production that promotes tissue inflammation.[31],[32] In this study, similar to Th1 and Th2 cells, circulatory Th17 cell counts also decreased.
Interestingly, our results reveal that despite decreased
T-helper cell response ([IL-2.sup.+] [CD4.sup.+]), the cytotoxic effector activity ([IL-2.sup.+] [CD8.sup.+]) was higher than that observed in healthy volunteers.
It attenuates the
T-helper cell Type 1 response causing suppression of cytokines such as IL-1, IL-6, interferon-[gamma] (INF), and tumor necrosis factor-[alpha] (TNF).
Peripheral T-cell lymphomas of follicular
T-helper cell derivation with Hodgkin/Reed-Sternberg cells of B-cell lineage: both EBV-positive and EBV-negative variants exist.
Venkataraman et al., "Peripheral T-cell lymphomas of follicular
T-helper cell derivation with Hodgkin/reed-sternberg cells of B-cell lineage: both EBV-positive and EBV-negative variants exist," American Journal of Surgical Pathology, vol.
Transcription factor IRF4 determines germinal center formation through follicular
T-helper cell differentiation.
They discovered that naive, activated, and effector T-killer and
T-helper cell populations occurred in similar percentages in the virus-infected patients and RA patients but not in the healthy controls.
(93) What this means is that too many regulatory T-cells form while
T-helper cell counts drop, resulting in there being more regulatory T-cells than T-helpers.
The reactions included: (1) Reaction with T-lymphocyte (CD-3); (2) reaction with
T-helper cell (CD-4); (3) reaction with T-suppressing cell (CD-8); (4) reaction with B-lymphocyte (CD-20).
Modulation of the lineage-specific differentiation of
T-helper cell subsets represents one of the major contributions of Treg cells to peripheral tolerance [15].