Jm. Ramage et al., T cell responses to heat-shock protein 60: Differential responses by CD4(+) T cell subsets according to their expression of CD45 isotypes, J IMMUNOL, 162(2), 1999, pp. 704-710
We demonstrate that human T lymphocytes proliferate in vitro to highly puri
fied human heat-shock protein 60 (Hu.hsp60). The response to this self Ag w
as confined to the CD45RA(+)RO(-) T cell subset, with minimal responses by
adult CD45RA(-)RO(+) T cells. Experiments using keyhole limpet hemocyanin a
s a prototypic novel Ag, or tetanus toroid as a recall Ag, were consistent
with the notion that CD45RA(+)RO(-) and CD45RA(-)RO(+) T cell subsets can b
e designated as naive and memory cells, respectively; thus, responses to Hu
.hsp60 were confined to the putative naive subset, In contrast, both CD45RA
(+)RO(-) and CD45RA(-)RO(+) T tell populations proliferated to bacterial hs
p60 from Mycobacterium leprae, Escherichia coli, or Chlamydia trachomatis,
However, only CD45RA(-)RO(+) (memory) T cells responded to a mycobacterial
hsp60-derived peptide previously defined as a major bacteria-specific epito
pe, Experiments with cord blood T cells, which are CD45RA(+)RO(-) and can b
e considered truly naive, showed that the peptide could elicit responses fr
om naive T cells in vitro; cord blood cells also responded to Hu.hsp60, Sin
ce bacterial hsp60 Ags contain both conserved and nonconserved epitopes, we
speculate that in vivo challenge with bacterial hsp60 will activate T cell
s capable of seeing either type of epitope, but only those that see noncons
erved epitopes maintain the CD45RA(-)RO(+) memory phenotype. However, T cel
ls recognizing conserved epitopes, while not apparently being recruited to
the memory pool, may nevertheless play a role in immunoregulation, particul
arly in the context of inflammation, when expression of Hu.hsp60 is increas
ed.