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Clonal Salivary Gland Infiltrates Associated With Myoepithelial
Sialadenitis (Sjögren's Syndrome) Begin as Nonmalignant
Antigen-Selected Expansions
David W. Bahler and
Steven H. Swerdlow
From the Division of Hematopathology, Department of Pathology,
University of Pittsburgh School of Medicine, Pittsburgh, PA.
Myoepithelial sialadenitis (MESA) is the reactive salivary gland
lymphoid infiltrate that occurs in patients with Sjögren's syndrome. Although it is well established that mucosa-associated lymphoid tissue (MALT)-type lymphomas may develop from MESA, the issue
of whether monoclonal B-cell populations in early MESA-associated lesions represent MALT lymphomas or more benign types of expansions has
been very controversial. In addition, it is unknown whether antigen
stimulation plays a role in the development or growth of
MESA-associated clones. To investigate these issues, we have analyzed
the Ig VH genes used by MESA-associated clones in sequential biopsies
obtained from contralateral sites of seven different patients. In three
cases, single clones were identified in the follow-up biopsies that
were distinct from the single clones identified in the initial
specimens, whereas in three other cases, the same clone was identified
in both the initial and subsequent specimens. In the remaining case,
two clones were identified in the second biopsy specimen, one of which
was distinct from the initial clone. Of the 11 distinct clones
identified in the 14 specimens that were analyzed, 8 were derived from
a V1-69 VH gene segment, whereas the other 3 were derived from a V3-7
VH gene segment. In addition, the MESA clones also showed conserved
amino acids sequence motifs in their third complementarity-determining
regions (CDR3), some of which were encoded by N nucleotides. The marked
VH gene restriction along with the similar CDR3 sequences suggests that
MESA-associated clones even from different patients may bind the same
or similar antigens and are selected for clonal expansion on that
basis. The high rates of ongoing VH gene mutation observed in some of the cases futher suggest that the growth of early MESA clones is still
dependent on antigen stimulation. In addition, our finding that
different biopsies from the same patient may contain distinct clones
indicates that some MESA-associated clones have not yet evolved to
malignant lymphomas.
Blood, Vol. 91 No. 6 (March 15), 1998:
pp. 1864-1872
© 1998 by The American Society of Hematology.
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