How T cells and B cells involve in specific immune response?

 

The T and B lymphocytes (T and B Cells) are involved in the acquired or antigen-specific immune response given that they are the only cells in the organism able to recognize and respond specifically to each antigenic epitope. The B Cells have the ability to transform into plasmocytes and are responsible for producing antibodies (Abs). Thus, humoral immunity depends on the B Cells while cell immunity depends on the T Cells.

T cells are activated to produce armed effector T cells the first time they encounter their specific antigen in the form of a peptide:MHC complex on the surface of an activated antigen-presenting cell (APC). The most important antigen-presenting cells are the highly specialized dendritic cells, whose only known function is to ingest and present antigen. Tissue dendritic cells ingest antigen at sites of infection and are activated as part of the innate immune response. This induces their migration to local lymphoid tissue and their maturation into cells that are highly effective at presenting antigen to recirculating T cells. These mature dendritic cells are distinguished by surface molecules, known as co-stimulatory molecules, that synergize with antigen in the activation of naive T cells.

. B cells are at the centre of the adaptive humoral immune system and are responsible for mediating the production of antigen-specific immunoglobulin (Ig) directed against invasive pathogens (typically known as antibodies). B cells migrate to the spleen where they differentiate through distinct transitional B cell stages termed T1 and T2, before differentiating into long-lived mature follicular (FO) or marginal zone (MZ) B cells. Thus, B cells experience both antigen-dependent and -independent phases of selection, tightly regulated through signalling events. T3 B cells do not give rise to mature B cells, but instead represent a subset of anergic B cells which have been selected away from the B cell developmental pathway.Mature FO B cells recirculate between secondary lymphoid organs in search of antigen. Following cognate Ag encounter, B cells receiving T cell help can enter a couple of different developmental possibilities. Firstly the cells can undergo plasmacytic differentiation, form extrafollicular plasmablasts and form IgM secreting plasma cells. These cells do not have somatically mutated Ig genes and are short lived, but provide a rapid initial response to antigen. The second developmental possibility is the establishement of a germinal centre, a specialised structure within which B cells undergo rounds of proliferation accompanied by affinity maturation: an iterative process of Ig gene mutation and selection resulting in a B cell pool which can bind to Ag with the highest affinity. The cells also undergo class switch recombination. Memory B cells and plasma cells expressing somatically mutated and generally high affinity BCRs of switched isotypes exit the GC.

Step-by-step explanation

Peptides from intracellular pathogens that multiply in the cytoplasm are carried to the cell surface by MHC class I molecules and presented to CD8 T cells. These differentiate into cytotoxic T cells that kill infected target cells. Peptide antigens from pathogens multiplying in intracellular vesicles, and those derived from ingested extracellular bacteria and toxins, are carried to the cell surface by MHC class II molecules and presented to CD4 T cells. These can differentiate into two types of effector T cell, called TH1 and TH2. Pathogens that accumulate in large numbers inside macrophage and dendritic cell vesicles tend to stimulate the differentiation of TH1 cells, whereas extracellular antigens tend to stimulate the production of TH2 cells. TH1 cells activate the microbicidal properties of macrophages, and induce B cells to make IgG antibodies that are very effective at opsonizing extracellular pathogens for uptake by phagocytic cells. TH2 cells initiate the humoral immune response by activating naive antigen-specific B cells to produce IgM antibodies. These TH2 cells can subsequently stimulate the production of different isotypes, including IgA and IgE, as well as neutralizing and/or weakly opsonizing subtypes of IgG.