Abstract
If viral strains are sufficiently similar in their immunodominant epitopes, then populations of cross-reactive T cells may be boosted by exposure to one strain and provide protection against infection by another at a later date. This type of pre-existing immunity may be important in the adaptive immune response to influenza and to coronaviruses. Patterns of recognition of epitopes by T cell clonotypes (a set of cells sharing the same T cell receptor) are represented as edges on a bipartite network. We describe different methods of constructing bipartite networks that exhibit cross-reactivity, and the dynamics of the T cell repertoire in conditions of homeostasis, infection and re-infection. Cross-reactivity may arise simply by chance, or because immunodominant epitopes of different strains are structurally similar. We introduce a circular space of epitopes, so that T cell cross-reactivity is a quantitative measure of the overlap between clonotypes that recognize similar (that is, close in epitope space) epitopes.
Highlights
Of particular relevance in this instance is the potential role played by pre-existing immunity in the form of cross-reactive T cells or B cells generated during previous common coronavirus infections [11,20,21]
Since we were interested in the population dynamics of the T cell repertoire, we focused on parameters that describe behaviors that directly affect the populations of cells
While much has yet to be determined about the nature of T cell cross-reactivity, it is clear that cross-reactive CD8+ T cells play a role in the immune response to respiratory infections, those that an individual can experience repeatedly during a life time
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. T cell cross-reactivity and pre-existing immunity, and to propose our own mathematical models of cross-reactivity in an immune system faced with heterologous viral infections. We focus on cross-reactive CD8+ T cells in the context of influenza and coronavirus infections Both Andrew Sewell and Don Mason laid out the argument that T cells must be cross-reactive because the number of possible pMHCs that the immune system could encounter far exceeds the number of potential T cells in a given host [1,13]. Of particular relevance in this instance is the potential role played by pre-existing immunity in the form of cross-reactive T cells or B cells generated during previous common coronavirus infections [11,20,21]. In addition to reproducing observations and fitting models to real-life datasets, we can use mathematical models to propose and test new hypotheses, and test these against new biological data (see Figure 3)
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