Occasionally one finds research articles published in the top journals, which rather than simplifying and clarifying the subject matters, make them more confusing. Frequently, even after reading and then re-reading them, one still cannot comprehend the "significance" of the finding.
I have one rule: if I cannot understand an immunology research paper with one read, I blame the editors. The author, of course, wants to publish his/her research in top journal, but it is a responsibility of the editors to be a gatekeepers and to make sure that the article is written in an easy to understand style.
I have another rule: the good data naturally make paper writing and reading easy.
The following paper from journal Science is such a disappointment. It starts strong with FucciRG mice model to track T cells acquiring a quiescent state after active cycling. The rest is confusing. The authors proposed that signal 1 (antigen), signal 2 (co-stimulation), and signal 3 (inflammatory milieu) play equal and quantitatively linear role in imprinting T cell division rate (they called it division destiny (DD), as if it would make it easier to understand).
First of all, if one takes, for example cytokine IL-2, it not just quantitatively affects the T cell division rate but it qualitatively changes T cell fate and memory potential too. The authors suggestion that IL-2's physiological role is to maintain T cell division at a later stage of activation, at the tissue site, away from priming site (such as spleen or lymph nodes) does not account for IL-2's role in T cell effector class differentiation (CTL, IFN-gamma or IL-2 producers) or memory imprinting. These latter concepts could equally well explain the authors' observation with IL-2 receptor alpha deficient T cells.
I personally would suggest to Science editors to avoid publishing research papers filled with unnecessary models (especially mathematical models) or with one-sided explanations.