Compare and contrast T-cell development with B-cell development

Introduction The pathways of development of these cells are very complicated and unique, but there are similarities. B cells produce antibodies that bind foreign matter invading the host organism; this allows cells such as cytotoxic T cells to destroy infected cells / structures. T cells, on the other hand, are T helper cells that secrete cytokines to regulate immune responses, and cytotoxic T cells that destroy pathogenic cells and structures. B cell B cells originate from pluripotent hematopoietic stem cells that produce lymphoid progenitor cells in the bone marrow.

Mature B cells such as T cells are also pluripotent stem cells. However, unlike T cell lymphocytes, B cell maturation occurs in the bone marrow. B cell development has four different stages: pro B cells, pre B cells, immature B cells, and mature B cells. During its development, B cells acquire expression of B cell surface markers such as B220, CD19, CD20, etc., as well as antigen receptors. Stromal cells in the bone marrow provide the proliferation signals necessary for the generation of B cells via VLA4 / VCAM and Kit / SCF, including cytokines such as IL7 and cell-cell contact. During B cell development, rearrangement of the gene fragments occurs as well as TcR rearrangement (central tolerance) in T cells. However, for B cells, the immunoglobulin heavy chain loci located on chromosome 14 (variable V, ligation J and diversity D segments) were rearranged. In hematopoietic stem cells, the Ig heavy chain gene is in a germline configuration (Kurosaki T et al., 2009).

What we remember now is the fact that T cells are a type of lymphocyte. Immature T cells (and B cells, another major lymphocyte) require the Rag 1, 2 gene to mature / differentiate at the next developmental stage. Immature T cells can enter CD4 + (helper T cells) or CD8 + (cytotoxic T cells) cells. CD4 and CD8 are specific receptors on the surface or T cells. Antigen presenting cells (APCs) express MHC-I or MHC-II molecules that help to present several pathogens to lymphocytes. CD4 + T cells interact with MHC-II molecules on APC and then differentiate further into Th1 or Th2 cells, depending on which signaling molecule is secreted by APC and act on CD4 + T cells. In the case of interleukin (IL) 12, CD4 + T cells differentiate into Th1 cells. If it is IL-4, it will differentiate into Th2 cells. Th1 cells secrete more IL-12 (which helps other CD4 + cells to differentiate into Th1 cells) and IFN-γ, which activates macrophages and CD8 + T cells.

Amino acids have been shown to affect B cell and T cell development, maturation and function in the gut. The absence of arginine has been shown to impair early B cell maturation in F / A-2 + / + transgenic mice, resulting in a sharp decrease in B cell numbers and a decrease in serum IgM levels in the small intestine. Studies with amino acid transporter ASCT2 deficient mice (Slc1a5 - / - mice) showed that ASCT2 plays an important role in the development of T helper 1 (Th1) and Th17 responses and regulation of CD4 T helper cell function. Due to the reduction in glutamine input, it was found that mTORC1 signaling was decreased in T cells and the proinflammatory CD4 + T cell response was attenuated. Cobbold et al found that depletion of essential amino acids inhibits T cell activation and proliferation and mTOR signaling in dendritic cells. Glutamine is known to be necessary for T cell activation