PubMed · 7888062
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R Kradin. 1995. Reply to Tauber.. https://doi.org/10.1016/0167-5699(95)80104-9
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We argued that immune system is an adaptive complex system. It is shown that it has emergent properties. Its network structure is of the small world network type. The network is of the threshold type, which helps in avoiding autoimmunity. It has the property that every antigen (e.g. virus or bacteria) is typically attacked by more than one effector. This stabilizes the equilibrium state. Modelling complex systems is discussed. Cellular automata (CA)-type models are successful, but there are much less analytic results about CA than about other less successful models e.g. partial differential equations (PDE). A compromise is proposed.
The co-signaling receptors specific for the different members of the B7 molecular family are cell surface glycoproteins that are essential to modulate and tune the TCR-mediated activation of T lymphocytes. The common characteristic is that their function appears to be dependent on the engagement of TCR by antigenic peptides presented in the MHC context by antigen-presenting cells. Interestingly, co-signaling molecules can be distinguished into costimulators and co-inhibitors, the prototype being represented by CD28 and CTLA-4, respectively. In the case of costimulators, the co-signals integrate the signal originated from the TCR resulting in optimal T cell activation (two-signal model). In the case of co-inhibitors, the co-signals would moderate and/or switch off the Ag-dependent T cell activation, thus acting as negative regulators of immune responses. The growing number of novel co-signaling molecules has recently highlighted the need to integrate the two-signal model with the emerging data on the different co-inhibitory interactions. Thus, a model has been proposed based on the idea that the TCR signal alone cannot take a full decision on the nature of the functional outcome following an antigen-specific stimulation and that this final event is governed by the co-signaling molecules.
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