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Updated: Jun 23, 2026
Accessing Early Differentiation of Virus-Specific Follicular Helper CD4+ T Cell in Acute LCMV-Infected Mice
Published on: April 26, 2024
Mice deficient in stem cell antigen-1 (Sca1, Ly-6A/E) develop normal primary and memory CD4+ and CD8+ T-cell
Jason K Whitmire1, Boreth Eam, J Lindsay Whitton
1Department of Immunology and Microbial Science, The Scripps Research Institute, La Jolla, CA 92037, USA. whitmire@scripps.edu
Stem cell antigen-1 (Sca1, Ly-6A/E) is a well-established marker of murine hematopoietic stem cells, and also is expressed on memory T cells. It has been suggested that the functional maintenance of T-cell memory requires the expression of Sca1 on a specialized population of memory T cells termed "memory stem cells". Here, we evaluate the requirement for Sca1 in the primary T-cell response to virus infection, and in the establishment and maintenance of T-cell memory. We find that Sca1 expression increases on almost all CD4(+) and CD8(+) T cells during virus infection, and remains high on virus-specific memory cells. However, Sca1-deficient (Sca1KO) mice generate normal primary T-cell responses to infection; the kinetics, the immunodominance hierarchy, and the absolute numbers of CD4(+) and CD8(+) T cells are essentially indistinguishable from those observed in WT mice. Furthermore, by several criteria, primary and memory T cells in Sca1-deficient mice are phenotypically and functionally normal. These data indicate that Sca1, although perhaps a useful marker of virus-specific memory T cells, is not required for the regulation of T-cell quantity or quality, or for the development of a competent pool of memory cells.
Stem cell antigen-1 (Sca1, Ly-6A/E) is a well-established marker of murine hematopoietic stem cells, and also is expressed on memory T cells. It has been suggested that the functional maintenance of T-cell memory requires the expression of Sca1 on a specialized population of memory T cells termed "memory stem cells". Here, we evaluate the requirement for Sca1 in the primary T-cell response to virus infection, and in the establishment and maintenance of T-cell memory. We find that Sca1 expression increases on almost all CD4(+) and CD8(+) T cells during virus infection, and remains high on virus-specific memory cells. However, Sca1-deficient (Sca1KO) mice generate normal primary T-cell responses to infection; the kinetics, the immunodominance hierarchy, and the absolute numbers of CD4(+) and CD8(+) T cells are essentially indistinguishable from those observed in WT mice. Furthermore, by several criteria, primary and memory T cells in Sca1-deficient mice are phenotypically and functionally normal. These data indicate that Sca1, although perhaps a useful marker of virus-specific memory T cells, is not required for the regulation of T-cell quantity or quality, or for the development of a competent pool of memory cells.
