The cause of selective IgM deficiency remains unclear, although various mechanisms have been proposed, such as an increase in regulatory T cell functions, defective T helper cell functions and impaired terminal differentiation of B lymphocytes into IgM-secreting cells among others.
Human immunodeficiency virus (HIV) binds CD4 and a chemokine receptor on the surface of a T helper cell to gain entry.
Priming is the first contact that antigen-specific T helper cell precursors have with an antigen.
Others have shown that treatment with PD-L2 Ig led to T helper cell proliferation.
This occurs when a naïve T helper cell recognizes antigen and needs to migrate to the follicle as a T follicular helper cell (TFH cell).
. It presents fragments from it to T cells. The upper, Th0, is a T helper cell. The fragment is presented to it by MHC2.
After the processed antigen (peptide) is complexed to the MHC molecule, they both migrate together to the cell membrane, where they are exhibited (elaborated) as a complex that can be recognized by the CD 4+ (T helper cell) – a type of white blood cell.
Eosinophilic folliculitis associated with HIV infection typically affects individuals with advanced HIV and low T helper cell counts.
Spontaneous regression is common in these tumors, and it is mediated by infiltration of CD8-expressing T cells followed by expression of Type 1 T helper cell cytokines (such as Interferon-gamma) and recruitment of antitumour effector cells.
Immunohistology profile have shown cells consistent with a delayed hypersensitivity with T helper cell infiltrates, dendritic cells and epidermal Langerhans cells.
The first IL-1 receptor-associated kinase (IRAK) was observed in 1994 through experiments with murine T helper cell lines D10N and EL-4.
A high level of secretory IgA results from the interaction of B cells and intestinal antigen presenting dendritic cell (DC) in cooperation with follicular T helper cell (Tfh) in the germinal centers (GCs) of Peyer´s patches.
The APC then travels to a lymph node, where it presents the displayed allergen to a CD4+ T-cell, or T-helper cell.
Increasingly, there is strong evidence from mouse and human-based scientific studies of a broader diversity in CD4+ effector T helper cell subsets.
For example, helminth infections cause potent and highly polarized immune response characterized by increased T-helpercell type 2 (Th2) cytokine and Immunoglobulin E (IgE) production.
It is essentially a T helper cell driven reaction, recruited by dendritic cells.
It has been shown to modulate the expression of Interleukin-6 (IL-6) and affect the balance of T helper cell cytokines.
Mature T helper cells upregulate EBI2 to follow the oxysterol gradient, migrating to the outer edges of the T cell zone to receive signals from antigen-presenting dendritic cells arriving from the tissues.
When stimulated by CD80, T helper cells preferentially differentiate into Th1 cells.
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