Dynamics of memory T cell proliferation under conditions of heterologous immunity and bystander stimulation
Department of Pathology
Adoptive Transfer; Animals; Arenaviridae Infections; Bystander Effect; CD8-Positive T-Lymphocytes; Cell Cycle; Cell Division; Cell Line; Cricetinae; Epitopes, T-Lymphocyte; Fluoresceins; Fluorescent Dyes; *Immunologic Memory; Lymphocyte Activation; Lymphocyte Count; Lymphocytic Choriomeningitis; control; Lymphocytic choriomeningitis virus; Male; Mice; Mice, Inbred C57BL; Pichinde virus; Poly I-C; Succinimides; T-Lymphocyte Subsets
Life Sciences | Medicine and Health Sciences
By examining adoptively transferred CSFE-labeled lymphocytic choriomeningitis virus (LCMV)-immune donor T cells in Thy-1 congenic hosts inoculated with viruses or with the cytokine inducer poly(I:C), strikingly different responses of bona fide memory T cells were found in response to different stimuli. Poly(I:C) (cytokine) stimulation caused a limited synchronized division of memory CD8 T cells specific to each of five LCMV epitopes, with no increase and sometimes a loss in number, and no change in their epitope hierarchy. Homologous LCMV infection caused more than seven divisions of T cells specific for each epitope, with dramatic increases in number and minor changes in hierarchy. Infections with the heterologous viruses Pichinde and vaccinia (VV) caused more than seven divisions and increases in number of T cells specific to some putatively cross-reactive but not other epitopes and resulted in substantial changes in the hierarchy of the LCMV-specific T cells. Hence, there can be memory T cell division without proliferation (i.e., increase in cell number) in the absence of Ag and division with proliferation in the presence of Ag from homologous or heterologous viruses. Heterologous protective immunity between viruses is not necessarily reciprocal, given that LCMV protects against VV but VV does not protect against LCMV. VV elicited proliferation of LCMV-induced CD8 and CD4 T cells, whereas LCMV did not elicit proliferation of VV-induced T cells. Thus, depending on the pathogen and the sequence of infection, a heterologous agent may selectively stimulate the memory pool in patterns consistent with heterologous immunity.
DOI of Published Version
J Immunol. 2002 Jul 1;169(1):90-8.
Journal of immunology (Baltimore, Md. : 1950)
Kim S, Brehm MA, Welsh RM, Selin LK. (2002). Dynamics of memory T cell proliferation under conditions of heterologous immunity and bystander stimulation. Open Access Publications by UMMS Authors. https://doi.org/10.4049/jimmunol.169.1.90. Retrieved from https://escholarship.umassmed.edu/oapubs/1119