According to CSR, postgerminative B cells and related plasma cells mount and produce immunoglobulins characterized by a new constant region. The second mechanism, also carried out in the germinal center, is called isotype-switching or class-switch recombination (CSR). Such editing, which takes place in the germinal center, is followed by the positive selection of the cells which display an improved antigen recognition. The first mechanism is called somatic hyper mutation process (SHM) and consists in a modulation of the antigen receptor affinity by inserting random point mutations in the sequences coding for the variable regions of the receptorial immunoglobulin. Compared to T lymphocytes, B lymphocytes are characterized by the presence of further mechanisms aimed at improving the efficacy of the response.

After the first encounter with the antigen, B lymphocytes proliferate as well, giving rise to expanded populations of cells sharing the same antigen receptor. Gene rearrangement and the establishment of a memory cell population are features which are shared by B lymphocytes, whose antigen receptor (BCR) consists in membrane-bound immunoglobulins. The receptor that plays a key role in the activation of the transcriptional program of naive T cells towards the formation of memory T cells is the T cell receptor or TCR, whose rearrangement during the maturation in the thymus allows recognition of any virtually possible antigenic determinant.

Only a few cells survive and enter the third stage, called вЂњmemory,вЂќ during which they tend to persist and self-renew, ready to encounter the same antigen to which they had been previously exposed. Initially there is a phase of вЂњexpansionвЂќ during which clones of naive T cells expand and differentiate into effector T cells following exposure to foreign antigens in the framework of the major histocompatibility system (MHC) this is followed by a phase called вЂњcontraction,вЂќ during which most effector T cells undergo apoptosis. In T cells the process of memory formation can be divided into 3 distinct phases. The first consists of an antigen-dependent clonal proliferation, and the second of a capability to maintain for a very long time (sometimes throughout life) a population of derived cells able to proliferate again on the occasion of a further encounter with the same antigen. The two mechanisms underlying this last function, which is called immunologic memory, are basically the same in both populations. They feature both the need to recognize the antigen and the ability to arouse a faster and stronger response when they encounter their cognate antigen for a second time. The lymphoid cells which are traditionally considered as the effectors of adaptive immunity are T and B lymphocytes. They recognize their ligands in a non-MHC restricted way and, as part of the innate immunity, are generally considered unable to remember antigens and to increase the magnitude of their response over time. The lymphoid cells which are traditionally considered as the effectors of innate immunity are NKT cells and the so-called ILC (innate lymphoid cells), among which NK cells are one of the most important populations. This difficulty is also caused by the fact that, from a phylogenetic point of view, the adaptive immunity can be considered an evolution and an improvement of the innate immunity, and the coexistence of partially similar and mutually intertwined mechanisms is therefore possible. Although the two terms, inherited from the biology of the last century, present themselves as antithetical, the high degree of cooperation and interdependence between immunological mechanisms makes a clear-cut distinction between the two concepts increasingly difficult.

Innate immunity and adaptive immunity are two complementary aspects of the immune response, which consists of a complex system of interactions aimed either at the clearance of pathogens or at the elimination of transformed cells.

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