Blood Cells - Tissue Functioning and Remodeling in the Circulatory and Ventilatory Systems - page 113

processes, as both induce thymocyte proliferation and similar up- or downregulation
of several developmental markers and transcription factors as well as rely on
epigenetic events.

3.10.1.2 Galectins

T-lymphocyte differentiation and maturation are governed by received cues as
well as the tissue site (thymus, gut, lung, skin, etc.). Maturation, activation, and
migration of T lymphocytes are influenced by galectins, members of the lectin
family. The activity of galectins depends on glycans and glycoproteic receptors
on the T-cell surface, different galectin types targeting different species of these
molecules [ 219 ]. 101

3.10.2 Antigen Presentation

The first step of T-cell activation is engagement of a T-cell receptor with a peptide-
MHC component complex on the surface of an antigen-presenting cell. 102 Adaptive
immunity relies on discrimination between self and non-self antigens. Secondary
lymphoid organs include the spleen, lymph nodes, tonsils in the pharynx, and
Peyer's patches in the intestine. The spleen does not receive lymphatic flow, but
filters blood [ 220 ]. Cells of Peyer's patches and tonsils sample antigens from the
mucosa. Lymph nodes process antigen from interstitial fluid that flows through
tissue-draining lymphatics.
In secondary lymphoid organs that are sites of immune surveillance organized
into specialized stromal niches, antigenic contents of blood, lymph, and mucosa
brought by migrating and resident antigen-presenting cells are checked by leuko-
cytes of the adaptive immune system. Migratory antigen-presenting cells that carry
antigens are directed to B- and T-cell zones when they enter into secondary
lymphoid organs. Antigens that are freely delivered by lymph are processed and
presented by resident antigen-presenting cells [ 220 ].

101 Both galectin-1 and -9 trigger death of different types of thymocytes and T cells using different
pathways.
102 In general, MHC class-1 molecules connect to endogenous peptides derived from cytosolic
proteins and interact with TCRs of CD8 + T lymphocytes, whereas MHC class-2 molecules tether
to exogenous antigens and bind TCRs of CD4 + T lymphocytes [ 220 ]. However, specialized subsets
of dendritic cells can present peptides derived from exogenous proteins associated with MHC
class-1 molecules. In addition, endogenous antigens can be loaded on MHC class-2 molecules for
autophagy.