It is known that mammals are capable of adjusting the T cell response to match the overall severity of an infection. These cytokines help cells to communicate with other cells and, therefore, to tailor the overall immune responses to deal with a particular pathogen. Cells called T cells plays a variety of roles in the immune response: some T cells directly destroy infected cells, some recruit other cells called phagocytes to the site of infection, and some release small proteins called cytokines. The cells of the immune system face the challenge of removing viruses and other pathogens without endangering healthy tissues. Our study reveals how time-integration of these regulatory loops within individual cell signaling generates scaled collective responses and can be leveraged for immune monitoring. Through experimental quantitation and computational modeling, we demonstrate that this scaling is enforced by an inhibitory cross-talk between antigen and IL-2 signaling, and a nonlinear acceleration of IL-2 secretion per cell. Surprisingly, we found that T cells scale their collective output of IL-2 to total antigen input over a large dynamic range, independently of population size. ![]() However, cytokine production may saturate as a function of antigen input, or be dominated by the precursor frequency of antigen-specific T cells. Such coordination of individual cell responses within multicellular populations is critical for accurate collective reactions to shared environmental cues. ![]() Variability within isogenic T cell populations yields heterogeneous ‘local’ signaling responses to shared antigenic stimuli, but responding clones may communicate ‘global’ antigen load through paracrine messengers, such as cytokines.
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