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These factors are usually produced by the newly activated T helper cell.
"We did not know at that time whether the T helper cells would be functional," explains Walker.
CD4 continues to be expressed in most neoplasms derived from T helper cells.
A subsequent study furthermore showed that extensive T helper cell plasticity is also prominent in man.
This results in the dysregulation of the immune system, and eventually to other further anti-self reactions, including against the T helper cell population.
It appears to be essential for the normal function of T helper cells type 2 (Th2 cells).
Important lymphokines secreted by the T helper cell include:
Of note, recent evidence suggest that functional plasticity is an intrinsic capacity of T helper cells.
CD4+ T helper cells are white blood cells that are an essential part of the human immune system.
All of the latter CD4 T cell groups are not considered T helper cells.
The theory is based on the fact that the body produces T helper cells, white blood cells that are at the core of the immune response.
Once the two-signal activation is complete the T helper cell (T) then allows itself to proliferate.
T helper cells also directly interact with macrophages, cells that engulf foreign matter and display antigens on its surface.
Some T cells, called T helper cells, produce cytokines that direct the immune response.
HIV directly infects a small number of T helper cells, and also impairs other immune system responses indirectly.
The same interactions that stimulate the T helper cell also stimulate the B cell, hence the term "costimulation".
One theory of how allergies arise is that an imbalance in T helper cell subtypes tips the body's immune response towards overreacting to a particular antigen.
Mature dendritic cells activate T helper cells and cytotoxic T cells.
Monocytes, one type of leukocyte, detect the antigen and relay the recognition to T helper cells, creating antinuclear antibodies leading to an immune response.
Thus, IL-21 may contribute to the mechanism by which CD4+ T helper cells orchestrate the immune system response to viral infections.
It has been shown to modulate the expression of Interleukin-6 (IL-6) and affect the balance of T helper cell cytokines.
The T helper cells then activate B cells, which are also in the presence of these antigens, causing the production of autoantibodies.
This cytokine is responsible for inducing T helper cells to become type 2 helper T cells.
RANKL is expressed by T helper cells, and is thought to be involved in dendritic cell maturation.
Knockout studies in mice suggested that this gene plays a role in T helper cell activation, and may be involved in inflammation and immune regulation.