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In immunology, a naive T cell (T h 0 cell) is a T cell that has differentiated in the thymus, and successfully undergone the positive and negative processes of central selection in the thymus. Among these are the naive forms of helper T cells ( CD4 + ) and cytotoxic T cells ( CD8 + ).
V(D)J recombination (variable–diversity–joining rearrangement) is the mechanism of somatic recombination that occurs only in developing lymphocytes during the early stages of T and B cell maturation. It results in the highly diverse repertoire of antibodies/immunoglobulins and T cell receptors (TCRs) found in B cells and T cells, respectively.
The VDR is widely distributed in tissues, and is not restricted to those tissues considered the classic targets of vitamin D. The VDR upon binding to 1,25(OH) 2 D heterodimerizes with other nuclear hormone receptors, in particular the family of retinoid X receptors. This VDR/RXR heterodimer complex binds to the specific VDRE in the promoters of ...
Thus it may be possible, to take a large sample of cells from someones immune system, and look quickly at the range of sub-types present in the sample. The ability to obtain data quickly from tens or hundreds of thousands of cells, one cell at a time, should provide a good idea, of the size of the person's immune repertoire.
CD2 was shown to prime naive T cells (T N) even without CD28 or TCR. [2] Also, CD27 is a receptor constitutively expressed on T N (its expression is downregulated upon TCR stimulation) and enhances T cell proliferation. [9] The differentiation of T helper cells (T H) into different subsets also partially depends on their co-stimulatory molecules.
The vitamin D receptor (VDR also known as the calcitriol receptor) is a member of the nuclear receptor family of transcription factors. [5] Calcitriol (the active form of vitamin D , 1,25-(OH) 2 vitamin D 3 ) binds to VDR, which then forms a heterodimer with the retinoid-X receptor .
The remaining cells exit the thymus as mature naive T cells, also known as recent thymic emigrants. [13] This process is an important component of central tolerance and serves to prevent the formation of self-reactive T cells that are capable of inducing autoimmune diseases in the host.
T-cell anergy can arise when the T-cell does not receive appropriate co-stimulation in the presence of specific antigen recognition. [2] B-cell anergy can be induced by exposure to soluble circulating antigen, and is often marked by a downregulation of surface IgM expression and partial blockade of intracellular signaling pathways.