Address for correspondence: J. Todd Abrams, Meniscus Limited, West Conshohocken, Pennsylvania 19428-2935. Voice: 610-832-8181; fax: 610-834-9934.
tabrams{at}meniscus.com
Séezary T cell-activating factor (SAF) was originally
defined as an inducer of functional interleukin-2 (IL-2) receptors
on normal and malignant T cells in patients suffering from Sézary
syndrome. In fact, a combination of SAF and IL-2 stimulated
the propagation of T cell lines from the peripheral blood mononuclear
cells (PBMC) of those patients, with approximately one third
of those cell lines containing the predominant malignant clone
as determined via cytogenetic and/or T cell receptor gene rearrangement
analysis. Although the primary source of SAF was mitogen-stimulated
PBMC of a patient with Sézary syndrome, we were unable
to isolate the gene encoding SAF from eukaryotic libraries.
However, we observed SAF activity in the cytoplasm of one of
the malignant cell lines in a complex containing RNA and DNA.
This observation led us to consider the possibility that SAF
is not of eukaryotic origin. Intracellular pathogens replicate
in the cytoplasm of host cells and contain proteins, DNA, and
RNA. Using a panel of antichlamydial antibodies with confirmation
from polymerase chain reaction primers, we found that most patients
with mycosis fungoides were positive for these determinants.
Immunoelectron microscopy and protein blotting further confirmed
antibody reactivity. We showed that
Chlamydia pneumoniae were
capable of infecting normal human keratinocytes in culture.
We also demonstrated that
C. pneumoniae antigen expression was
associated with active disease because these determinants were
not expressed after psoralen and ultraviolet A therapy. We hypothesize
that chronic infection by
C. pneumoniae leads to expansion of
C. pneumoniae-specific T cells, thereby potentiating the development
of cutaneous T cell lymphoma.
