Concluding Remarks

Activation of a T cell requires the existence of a peptide/MHC combination that fits to its TCR as a signal and the presence of this antigen on an activated, costimulatory APC. If it is true that recognition of self-peptides on HLA molecules is involved in

TCR CD28

TCR CD28

Toll-like receptor ligands

Figure 7 Induction of adaptive immune response. A resting antigen presenting cell (APC) does not express costimulatory molecules like B7. Upon contact with an infectious agent, substances thereof bind to their matching toll like receptors on the APC and induce cellular signalling, which initiates expression of B7. In parallel, antigen from the infectious agent is acquired by the APC and presented by the major histocompatibility complex (MHC) molecules on the cell surface. Thus, the activated APC provides both MHC-presented antigen and costimulation.

Toll-like receptor ligands

Figure 7 Induction of adaptive immune response. A resting antigen presenting cell (APC) does not express costimulatory molecules like B7. Upon contact with an infectious agent, substances thereof bind to their matching toll like receptors on the APC and induce cellular signalling, which initiates expression of B7. In parallel, antigen from the infectious agent is acquired by the APC and presented by the major histocompatibility complex (MHC) molecules on the cell surface. Thus, the activated APC provides both MHC-presented antigen and costimulation.

the etiology of autoimmunity, one has to assume that an autoreactive T cell that has slipped through central-negative selection happens to be activated on a mature DC, presenting either the very same self-peptide during an infection, or presentation of a cross-reactive peptide derived from the infectious agent, and both in the absence of sufficient regulatory T cells. In conclusion, we know of a number of potential checkpoints that are possibly, or even most likely, involved in the etiology of autoimmune diseases and dependent on the particular interaction of peptides, HLA molecules, and T-cell receptors. Detailed knowledge of these interactions should help us to understand and, as a result, counteract autoimmune diseases.

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