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Department of Veterinary Microbiology and Pathology, Washington State University, Pullman, WA 99164;
Department of Animal Sciences, University of Illinois, Urbana-Champaign, IL 61801
Genogroup II ehrlichia, including the agent of human granulocytic
ehrlichiosis, Ehrlichia phagocytophila, and the bovine
pathogen Anaplasma marginale, express a markedly
immunodominant outer membrane protein designated major surface protein
2 (MSP2). MSP2 is encoded by a multigene family, resulting in the
expression of variant B cell epitopes. MSP2 variants are sequentially
expressed in the repeated cycles of rickettsemia that characterize
persistent A. marginale infection and control of each
rickettsemic cycle is associated with development of a variant-specific
IgG response. Importantly, these persistent rickettsemic cycles are
controlled at levels 100-1000 times lower than those responsible for
clinical disease during acute infection. Control of rickettsemia during
persistence could result from an anamnestic Th lymphocyte response to
conserved regions of MSP2 that enhances the primary Ab response against
newly emergent variants. Comparison of MSP2 variants reveals conserved
N and C termini flanking the central, surface-exposed hypervariable
region that represents the variant B lymphocyte epitopes. We
demonstrate MSP2-specific CD4+ T lymphocyte recognition of
epitopes common to several strains of A. marginale and
the related pathogen A. ovis. Furthermore, T lymphocyte
lines from three individuals identified six to nine overlapping
peptides representing a minimum of four to seven dominant or
subdominant epitopes in these conserved N and C termini. Immunodominant
peptides induced high levels of IFN-
, a cytokine associated with
protection against ehrlichia and needed for rapid generation of
variant-specific IgG2. The presented data support the potential
importance of a strong Th lymphocyte response to invariant MSP2
epitopes in controlling rickettsemia during persistent infection to
subclinical levels.
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