MHC class Ib-restricted CTL provide protection against primary and secondary Listeria monocytogenes infection

M. S. Seaman, C. R. Wang, J. Forman

Research output: Contribution to journalArticle

65 Citations (Scopus)

Abstract

Infection of B6 mice with the intracellular pathogen Listeria monocytogenes (LM) results in the activation of CD8+ T cells that respond to Ag presented by both MHC class Ia and class Ib molecules. Enzyme-linked immunospot analysis reveals that these CTL populations expand and contract at different times following a primary sublethal LM infection. Between days 4 and 6 postinfection, class Ib-restricted CTL exhibit a rapid proliferative response that is primarily H2-M3 restricted. The peak response of class Ia-restricted CD8+ T cells occurs a few days later, after the majority of bacteria have been cleared. Although class Ia-restricted CTL exhibit a vigorous recall response to secondary LM infection, we observe limited expansion of class Ib-restricted memory CTL, even in MHC class Ia-deficient mice (B6.K(b-/-)D(b-/-)). Despite this lack of enhanced expansion in vivo, class Ib-restricted memory CTL retain the ability to proliferate and expand when provided with Ag in vitro. Furthermore, we demonstrate that in vivo depletion of CD8+ T cells in LM-immune B6.K(b-/-)D(b-/-) mice severely impairs memory protection. Together, these data demonstrate that class Ib-restricted CTL play an important role in clearing a primary LM infection and generate a memory population capable of providing significant protection against subsequent infection.

Original languageEnglish (US)
Pages (from-to)5192-5201
Number of pages10
JournalJournal of Immunology
Volume165
Issue number9
DOIs
StatePublished - Nov 1 2000

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Listeriosis
Listeria monocytogenes
T-Lymphocytes
Aptitude
Contracts
Infection
Population
Bacteria
Enzymes

ASJC Scopus subject areas

  • Immunology

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MHC class Ib-restricted CTL provide protection against primary and secondary Listeria monocytogenes infection. / Seaman, M. S.; Wang, C. R.; Forman, J.

In: Journal of Immunology, Vol. 165, No. 9, 01.11.2000, p. 5192-5201.

Research output: Contribution to journalArticle

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