In this study we present new differential characteristics of NK cells expressing CD56 surface antigen in low (CD56dim) or high (CD56bright) density. In contrast to CD56bright NK cells CD56dim cells express killer cell immunoglobulin (Ig)‐like receptors (KIR) such as CD158a, CD158b, and NKB1. However, c‐type lectin‐like receptors (KLR) CD94/NKG2 and CD161 are present on both subsets. The ability to form conjugates with susceptible targets is approximately twice as strongly pronounced in CD56dim vs. CD56bright NK cells. Last but not least, granules of CD56dim cells contain about tenfold more perforin and granzyme A enabling potentially more effective cytolysis compared to CD56bright NK cells. On the other hand, CD56bright NK cells are superior in producing the proinflammatory cytokines IFN‐γ (28.5% vs. 20.8%, p<0.05) and TNF‐α (28% vs. 15.8%, p<0.001). The differentNK cell populations retained their specific phenotype in vitro during culture in the presence of IL‐2 contradicting that they simply display different stages of maturity. Taken together our data support the view that CD56bright cells are specialized NK cells that regulate immunological response mechanisms rather by cytokine supply than by their cytotoxic potential. The poor cytolyticcapacity of CD56bright NK cells can be explained by weak ability in forming conjugates with target cells and low contents of perforin and granzyme A in their granules.

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By using three different assay methods, circulating immune complexes have been detected in 85% of sera from patients with malignant melanoma, and in 77% of sera from patients with breast cancer. These methods were a C1q-binding assay, a double-antibody conglutinin-binding ELISA, and a polyethylene glycol 6000 precipitation technique followed by quantitative determination of immunoglobulins in the redissolved precipitate. Detection rates of circulating immune complexes using any one of these methods separately ranged from 33% to 56%, indicating the presence of different types of circulating immune complexes in cancer patients' sera. The combined use of the three methods mentioned resulted in an increased diagnostic sensitivity and a doubling of the predictive value. However, tests for circulating immune complexes cannot be considered as useful parameters for early diagnosis of cancer, since the comparatively low incidence of malignancies in the population at large, together with the presence of circulating immune complexes in other, nonmalignant, diseases of considerable prevalence, appears to preclude effective application of any nonspecific method for early diagnosis of cancer in general.

The T gamma-lymphoproliferative syndrome is characterized by a proliferation of large granular lymphocytes (LGL). It is often associated with neutropenia, and in 30% of cases with rheumatoid arthritis (RA). Phenotypic analysis has demonstrated that in most cases of RA with T gamma-proliferative disease, the LGL represent T cells with a clonal rearrangement of the alpha/beta T cell receptor (TCR2). Here, three patients with gamma/delta TCR1+ LGL proliferation suffering from long-standing arthritis and neutropenia are described. The first patient with RA showed an expansion of a heterogeneous CD2+ CD16+ CD56- LGL population, of which 30% coexpressed TCR1 with V delta 1 rearrangement. The second patient with ankylosing spondylitis and RA was suffering from proliferation of TCR1+ (V gamma 9-, V delta 1-), CD2+ CD16- CD56- LGL with low coexpression of CD8. The third patient with RA was suffering from a proliferation of TCR1+ (V delta 1+, V gamma 9-) CD4- CD8- CD16- CD56- lymphocytes. On the basis of these unusual findings, the pathogenetic role of TCR1+ T cells in RA is discussed.