Fluctuating fitness shapes the clone size distribution of immune repertoires

TL;DR

This paper models how fluctuating fitness in immune cell clones leads to the universal power law distribution of clone sizes, providing insights into immune diversity and environmental influences.

Contribution

It introduces effective models of somatic evolution where clone fitness fluctuations explain the observed clone size distributions in immune repertoires.

Findings

Fitness fluctuations are key to power law clone size distributions.

The models quantify environmental fluctuation scales in immune tissues.

Tools are provided to identify growth signals in various tissues.

Abstract

The adaptive immune system relies on the diversity of receptors expressed on the surface of B and T-cells to protect the organism from a vast amount of pathogenic threats. The proliferation and degradation dynamics of different cell types (B cells, T cells, naive, memory) is governed by a variety of antigenic and environmental signals, yet the observed clone sizes follow a universal power law distribution. Guided by this reproducibility we propose effective models of somatic evolution where cell fate depends on an effective fitness. This fitness is determined by growth factors acting either on clones of cells with the same receptor responding to specific antigens, or directly on single cells with no regards for clones. We identify fluctuations in the fitness acting specifically on clones as the essential ingredient leading to the observed distributions. Combining our models with experiments we characterize the scale of fluctuations in antigenic environments and we provide tools to identify the relevant growth signals in different tissues and organisms. Our results generalize to any evolving population in a fluctuating environment.