The cellular lineage of sinonasal T/NK (natural killer) cell lymphoma remains controversial. Lineage assignment is difficult because T cells and NK cells have a similar morphology and surface markers. Consequently, the assignment must depend heavily on the status of T-cell receptor (TCR) rearrangement. A monoclonal TCR rearrangement supports a T lineage; however, a corresponding monoclonality test for NK cells has not yet been established. Each NK cell bears a distinct set of killer cell immunoglobulin (Ig)-like receptors (KIRs) that are randomly distributed over three groups. In principle, restriction of the KIR repertoire signifies a monoclonal or possibly oligoclonal NK-cell proliferation, just as Ig light-chain restriction usually indicates a monoclonal B-cell neoplasm. Using a novel group-specific reverse transcriptase-polymerase chain reaction, we found a restricted KIR repertoire in most sinonasal lymphomas (9 of 10), but only rarely in T-cell lymphomas (2 of 10) or reactive conditions involving T/NK cells (1 of 10). KIR+ sinonasal lymphomas usually lacked a monoclonal TCR-gamma rearrangement pattern, expressed another NK cell receptor, NKG2a, and were usually CD56-positve, cyclin-dependent kinase-6 (CDK6)-positive, CD44-negative, a phenotype already reported to indicate a true NK cell lineage. We conclude that, although sinonasal lymphomas have heterogeneous genotypes and phenotypes, a restricted KIR repertoire without TCR-gamma rearrangement provides preliminary support for the monoclonality hypothesis and can be used for defining a true NK-cell lineage in a subset of sinonasal lymphomas.
To aid in the initial diagnosis of Kikuchi lymphadenitis and to assess whether the composition of the T cells might shed light on the pathogenesis, we used nested polymerase chain reaction tests followed by high-resolution gel electrophoresis to determine the pattern of T-cell antigen receptor rearrangement in 56 consecutive cases. Except for 1 unusual case with recurrent lymphadenopathy, none had a monoclonal beta or gamma rearrangement. Eight cases had a polyclonal pattern at both beta and gamma loci, 20 cases had a mixed polyclonal beta and oligoclonal gamma pattern, and 27 cases had an oligoclonal pattern at both loci. The high frequency of oligoclonality did not indicate an early-stage T-cell lymphoma in evolution, as confirmed by spontaneous resolution of the lymphadenopathy in all cases within 6 months. Rather, it is consistent with reports of oligoclonal T cells in a variety of immune reactions. We conclude that, in the vast majority of cases, absence of a monoclonal T-cell receptor rearrangement excludes the possibility of T-cell lymphoma, and the presence of an oligoclonal pattern implies a benign immune reaction.
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