Compare and Contrast the Development of B and T Cells

Compare and Contrast the maturation of B and T CellsThe epithelial surfaces of the body serve as an trenchant barrier against most microorganisms, and they are rapidly repaired if wounded. Adaptive immunity is initiated when an unlettered resistant response fails to eliminate a new infection, whereby an worked up antigen set outing kiosks (APCs) boot pathogens antigens are delivered to the draining lymphoid tissues. An adaptive resistive response differs from the immanent immunity in its ability to target structures that are specific to feature strains and variants of pathogen.T stalls are unwrapd in the hit the books marrow. They are transported still, as pro-thymocytes to the thymus where they sustain the run of maturation and selection. The regulation of T stall maturation in the thymus is termed central tolerance. During gestation, most T booths fixd bear the da Gamma/deta T cadre receptor (TcR) on their surface. In the adult, most T carrells bear the alpha/ beta TcR. The newly tracked TcR then, has to be time-tested for recognition of self-MHC/peptide. The T kioskular telephones are tested at a face of development known as double positive degree, meaning that they bear two CD4 and CD8 receptors on their surface. Cells with TcRs that recognize self-MHC/peptide with very lower-ranking phylogenetic relation exit die. This process is known as death by neglect. Cells with TcRs with medium similitude for MHC arrive survival tapers and undergo a process known as positive selection. Finally, electric cadreular phones which receive a high affinity signal via their TcR die by apoptosis, a process known as negative selection. Cells that interact with MHC trend I conk out CD8 positive T cell, and those that interact with MHC class II construct CD4 positive T cells, before migrating out into the peripheral lymphoid system (Wood P, 2006).Mature B cells, like T cell, are as well as develop form pluripotent stem cells. However unlik e T cells lymphocytes, B cell maturation occurs in the bone marrow. There are 4 different stages of B cell development pro-B, pre-B, immature B, and mature B cells. During its development, B cells acquire B cell surface marker verbiage such as B220, CD19, CD20, etc. as well as antigen receptors. The stromal cells facing the bone marrow provide essential growth signals to developing B cells, including cytokines such as IL7 and cell to cell contact, via VLA4/VCAM and Kit/SCF. During B cell development, gene segment rearrangements take place, just like in T cells where TcR rearrangements (central tolerance) in like manner occur. However, for B cells, the immunoglobulin to a great extent chain gene venue (variable-V, joining-J and diversity-D segments), situated on chromosome 14, rearranges. In haematopoietic stem cells, the Ig heavy chain genes are in germline configuration (Kurosaki T et al., 2009). As B cells develop to pro-B cells, a D-J recombination is the first gene rearran gement to take place. The intervening deoxyribonucleic acid is normally deleted from the chromosome as a circle. Gene rearrangements are mediated by recombinase activitng genes, RAG proteins. As the developing B cell proceeds from pro- to pre-B cell stage, a V-DJ gene arrangement takes place to form the VDJ coding bar that encodes the variable domain on the antibody heavy chain. Gene rearrangement takes place on both copies of chromosome 14 in a developing B cell, just once a productive VDJ block has been assembled on one chromosome 14, rearrangement ceases on the other chromosome, ensuring only one type of Ig is produced by any single B cell. This process is known as allelic exclusion. If a developing B cell fails to make a productive VDJ block, it pass on fail to produce antibody heavy chain and die in the bone marrow (Murphy K et al, 2008).T and B cell activatingT cell activation takes place in draining lymph nodes (also spleen) close to web site of infection. T cell recog nizes antigen on MHC (Major Histocompatibility Complex) molecules becomes activated and differentiates to effector cells. Effector T cells migrate to site of infection and carry out effector functions. The T lymphocytes arrive through venules, and cross through the endothelial to the lymph nodes. Antigen presenting cells such (APC) such as dendritic cells, and macrophages presented antigens to T cells. On recognition of the antigen, a low affinity interaction is formed. These T cells then leave lymph node though the lymphatic system. Those T cells that recognize the antigens wall with high affinity will be retained and the process of proliferation and specialization occurs. However, initial B cell activation takes place in T cell zone of lowly lymphatic tissues (i.e. in lyhmph nodes). Mostly IgM producing plasma cells are produced at this state. B cells, unlike T cells, are activated by the ineraction with antigen-specific T cell, by linked recognition. Antigen-activated B cell m igrates to B cell celestial sphere of lymph nodes to form organized original centres, where additional B cell specialization processes take place. It is important to note that T cells recognize the peptide, while B cells recognize the coat protein.For T and B lymphocyte activation 2 signals are hypothesized to be required. Firstly, the antigen stimulus signal and secondly, the co-stimulatory stimulus. The absence of the second signal results in anergy or apoptosis. CD28/B7 interaction is the co-stimulatory signals for T cells while CD40/CD40 ligand, on the activated T cells, interaction is for B cells. For both T and B lymphocytes, in it resting G0 cell cycle, the cell appear to have a large nucleus, with forgetful cytoplasm and show little evidence of organelles. However, when these cells enter G1/S/G2 cell cycle, cell shows an increase in cell size, chromatin de-condensation is seen. Cell department occurs rapidly, generating effector cells of either T or B lymphocytes. Effect or T cells involve Th1, Th2 and T regulatory, as well as T cytotoxic cell and memory T cells. On the other hand, effector B cells include plasma cell and memory B cell.T and B cell effector functionsB cell response to T-dependent protein antigen results in germinal centres formation in B cell areas of lymph nodes, and specialized processes such as Ig class-switching, somatic mutation and affinity maturation, memory B cell and plasma cell generation take place there. Emerging form germinal centres are somatically mutated and class-switched B cells, which no longer just produce IgM. Memory B cells are long-lived, resting and re-circulating cells, responsible for immunization part which helpto generate rapid and vigorous immune response on second find for that specific antigen. Plamablast cells migrate to other sites such as bone marrow, and become plasma cells, producing large amounts of secreted antibody. Some of which can live for long periods. The effector functions of B cells re fer to what antibodies do after their contact with the antigen. The antibody effector functions include neutralization, complement fixation (IgM, IgG1/2/3), oposonization and antibody dependent cell-mediated cytotoxicity.In contrast, T cell effector functions differ significantly from B cell effector functions. Antigen presenting cells present peptide via MHC which can either interact with CD4+ or CD8+ T cells. Helper T cells are defined by the cytokines they produce. Nave CD4+ T cells (Th0), on interaction with APC, can differentiate to Th1 or Th2 cells, depending on the cytokine environment. Th1 cells co-ordinate inflammatory immune responses to intracellular pathogens while Th2 cells help B cells to make antibodies required for immune responses to extracellular pathogens, this is known as humoral immunity. Th1 and Th2 cells both act to bring forward the generation of more leukocytes. Besides Th0/Th1/Th2, other CD4+ T cell subsets dwell (Zhu J et al., 2010). Resting T cells can differentiate into activated helper T cell, as well as activated cytotoxic T cell (CD8+ T cell). Initially, CD8+ T cells interact with potential target cells via low affinity/non-specific interactions between adhesion molecules on the T cell (LFA-1 and CD2) and the target cell (ICAM1, ICAM2). This interaction has no effect on the cytoskeleton of the T cell and is a transient interaction unless recognition of specific peptideMHC complexes occurs. If peptideMHC I complex is present, the affinity of the adhesion molecule interaction increases and there is clustering of T cell receptor and associated molecules at the point of contact with the target cell forming the immunologic synapse. This also signals for cytoskeletal rearrangements organized by the microtubule organizing complex which focuses the cytotoxic granules of the T cell at the point of contact with the target. Notice here, that T cells, unlike B cells do not produce antibodies against antigens. Granules containing perforin and other enzymes including granzymes are released and induce the activation of the cathepsin pathways in the target cell leading to apoptosis. CD8+ T cells can also kill target cells via the Fas/FasL pathway which also induces apoptosis (Peter EJ 2007).In conclusion, adaptive immune responses occur when individual lymphocytes capable of responding to antigen proliferate and differentiate to become an antigen-specific effector cells and memory cells. The process of lymphocyte cell cycle progression, proliferation and differentiation in response to antigen and stimuli is known as lymphocyte activation. B cell activation is initiated by the ligation of the B cell receptor (BCR) with antigen and ultimately results in the production of protective antibodies against potentially pathogenic invaders. While naive or memory T cells encounter foreign antigen along with proper co-stimulation they undergo rapid and extensive clonal expansion. In human, this type of proliferation is fairly lau ghable to cells of the adaptive immune system and requires a considerable expenditure of might and cellular resources.