Antigen Essay

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Due to the absence of self-antigen presentation in the thymus [36], or the low affinity of T cells for self-antigens [37], autoreactive T cells escape sometimes from thymic negative selection. To complete the efficacy of central tolerance, the immune system developed many tools to neutralize these cells and avoid autoimmune diseases. These mechanisms are either passive, concerning antigen ignorance, T-cell anergy or apoptosis induction and phenotypic skewing, or active when mediated by regulatory cells [38]. Antigen ignorance allows autoreactive T cells to persist as functional circulating T cells while never primed by any antigen [39]. Indeed, antigens can be masked by anatomical barriers like lens proteins, spermatozoids, or nervous…show more content…
Without CD28/ CD80-CD86 engagement, interactions between TCRs and alloantigens induce the anergy of T cells. CTLA-4 (CD152) has a large structural homology with CD28 and interacts with CD80- CD86 with better affinity than CD28 molecule and functions as a negative regulator of T-cell activation [56]. The expression of these two molecules regulates the balance between activation and inhibition of T cells and allows the control of an over-reaction of the immune system leading to inflammation or autoimmunity [57]. Similarly, the expression of Programmed Death-1 (PD-1) after antigenic stimulation and interaction with its ligand PDL-1 reduces IL-2 synthesis and induces T-cell anergy [58]. Another important co-stimulatory pathway is the CD40/CD40L co-stimulatory pathway. The CD40 molecule is a transmembrane protein that Tolerance in Organ Transplantation http://dx.doi.org/10.5772/62653 51 belongs to the TNF receptor family. It is expressed on vascular endothelial cells [59], activated DCs [60], monocytes/macrophages, platelets [61] and B lymphocytes [62]. The CD40L, also called CD154, exists in soluble form or at the cell membrane [63]. It is expressed on activated CD4+ T cells, basophiles, eosinophils [64], DCs from the blood [65], endothelial cells, macro‐ phages
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