1. Department of Pathology, and,
2. Department of Microbiology, University of Alabama at Birmingham, 845 19th Street South, Birmingham, Alabama 35294, USA
3. Present address: Department of Cell Biology, University of Alabama at Birmingham, 845 19th Street South, Birmingham, Alabama 35294, USA.

Correspondence to: Casey T. Weaver¹ Correspondence and requests for materials should be addressed to C.W. (Email: cweaver@uab.edu).

Abstract

A hallmark of adaptive immunity is the generation of memory T cells that confer long-lived, antigen-specific protection against repeat challenges by pathogens^{1, 2, 3, 4, 5}. Understanding the mechanisms by which memory T cells arise is important for rational vaccination strategies and improved therapeutic interventions for chronic infections and autoimmune disorders. The large clonal expansion of CD8 T cells in response to some infections has made the development of CD8 T-cell memory more amenable to study, giving rise to a model of memory cell differentiation in which a fraction of fully competent effector T cells transition into long-lived memory T cells^{4, 6, 7}. Delineation of CD4 T-cell memory development has proved more difficult as a result of limitations on tracking the smaller populations of CD4 effector T cells generated during a pathogenic challenge^{8, 9, 10}, complicating efforts to determine whether CD4 memory T cells are direct descendants of effector T cells or whether they develop by alternative pathways^{3, 4}. Here, using two complementary cytokine reporter mouse models to identify interferon (IFN)--positive effector T cells and track their fate, we show that the lineage relationship between effector and memory CD4 T cells resembles that for CD8 T cells responding to the same pathogen. We find that, in parallel with effector CD8 T cells, IFN--positive effector CD4 T cells give rise to long-lived memory T cells capable of anamnestic responses to antigenic rechallenge.

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