# Emily R Stirk's research while affiliated with University of Leeds and other places

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## Publications (5)

We construct a birth and death process for the number of Tcells belonging to one clonotype. Cells are released from the thymus
into the peripheral lymphoid organs. We assume that after this time, no more Tcells of this clonotype are exported by the
thymus, so that further Tcells of this clonotype can only be generated by homeostatic proliferation,...

Diversity in the na iveTcell repertoire is maintained throughout the majority of an individual’s lifetime. The homeostatic
mechanisms involved include competition for survival stimuli furnished by antigen-presenting cells, dependent on weak recognition
of arrays of self-peptides by the Tcell antigen receptor. We study the dynamics of this process f...

Recognition of antigens by the adaptive immune system relies on a highly diverse T cell receptor repertoire. The mechanism that maintains this diversity is based on competition for survival stimuli; these stimuli depend upon weak recognition of self-antigens by the T cell antigen receptor. We study the dynamics of diversity maintenance as a stochas...

The limiting conditional probability distribution (LCD) has been much studied in the field of mathematical biology, particularly in the context of epidemiology and the persistence of epidemics. However, it has not yet been applied to the immune system. One of the characteristic features of the T cell repertoire is its diversity. This diversity decl...

The reliability of the immune response to pathogenic challenge depends critically on the size and diversity of the T cell repertoire. We study naïve T cell repertoire diversity maintenance by a stochastic model that incorporates the concept of competition between T cells for survival stimuli emanating from self-antigen presenting cells (APCs). In t...

## Citations

... We were interested in developing mathematical models to describe the dynamics of T cell responses to different pathogens, and T cell cross-reactivity and its roles in infection, T cell homeostasis and the establishment of T cell memory. We followed the mathematical methods and approaches developed by Stirk et al. [56][57][58][59][60] and introduced a bipartite network which encodes the pMHC (or antigen) recognition pattern for each T cell clonotype, characterized by its specific TCR (see Figure 6). We note that the bipartite network introduced by Stirk et al. considers only self-pMHC complexes. ...

... We were interested in developing mathematical models to describe the dynamics of T cell responses to different pathogens, and T cell cross-reactivity and its roles in infection, T cell homeostasis and the establishment of T cell memory. We followed the mathematical methods and approaches developed by Stirk et al. [56][57][58][59][60] and introduced a bipartite network which encodes the pMHC (or antigen) recognition pattern for each T cell clonotype, characterized by its specific TCR (see Figure 6). We note that the bipartite network introduced by Stirk et al. considers only self-pMHC complexes. ...

... We were interested in developing mathematical models to describe the dynamics of T cell responses to different pathogens, and T cell cross-reactivity and its roles in infection, T cell homeostasis and the establishment of T cell memory. We followed the mathematical methods and approaches developed by Stirk et al. [56][57][58][59][60] and introduced a bipartite network which encodes the pMHC (or antigen) recognition pattern for each T cell clonotype, characterized by its specific TCR (see Figure 6). We note that the bipartite network introduced by Stirk et al. considers only self-pMHC complexes. ...