Impaired cell-mediated immunity in certain patients with nonlymphoid cancer is indicated by depressed skin reactivity to common antigens (1, 2), delayed homograft rejection (3), decreased ability to become sensitized to dinitrofluorobenzene (4) or dinitrochlorobenzene (5, 6), and decreased in vitro lymphocyte responsiveness to the mitogen phytohemagglutinin (7,8). It is not known whether depressed cell-mediated immunity precedes or follows the development of cancer.Tumor-specific antigens and cell-mediated tumor immunity are noted in cases of human cancer. Blood lymphocytes from patients with some neoplasms inhibit tumor cell growth (9, 10) or undergo blast transformation when cultured with autochthonous tumor cells (11). In addition to the cell-mediated responses, the sera of these patients contain antibodies or antigen-antibody complexes (12) that specifically block lymphocyte-tumor cell interaction through a poorly understood phenomenon termed immunologic enhancement (13,14).In the present studies, patients with primary intracranial tumors were found to have depressed cell-mediated immunity. Unlike other patients with solid systemic tumors and impaired delayed hypersensitivity, our patients did not have clinical evidence of metastases, weight loss, or hematologic abnormalities. These patients, then, afforded an unusual opportunity to study host mechanisms responsible for defective cell-mediated immunity.Although delayed hypersensitivity and other cell-mediated responses were depressed, we found evidence of lymphocyte sensitization to tumor antigens. To clarify these apparently paradoxical findings, we evaluated mononuc]ear leukocyte function with the one-way mixed lymphocyte reaction. Cellular reactivity in the absence of patient plasma was normal. Such plasma, however,

T-lymphocyte subsets in marrow aspirates taken from normal donors were analyzed with the use of monoclonal antibodies and flow cytometry. Peripheral blood specimens from the same donors were analyzed concurrently and served as controls. Eighty-six percent of CD8-positive cells from marrow expressed the pan-T-cell markers CD2 and CD3, compared with 91% and 81%, respectively, of CD8-positive cells from peripheral blood. Virtually all CD8-positive marrow lymphocytes, however, were negative for CD11b as opposed to peripheral blood, where 18% exhibited positivity for this marker. Further, a higher percentage of marrow CD8-positive T-lymphocytes expressed HLA-DR (15.4%) than did those from peripheral blood (4%). Marrow CD4-positive subsets did not differ substantially from those of peripheral blood. These results support the concept of a selective homing of CD8-positive T-cells to the marrow and indicate that CD8-positive T-cells in the marrow are effector T-cells.

The molecular basis of immunoglobulin idiotypes (1) has been pursued in several well-defined antibody systems (2-7). The accumulated results have suggested that the hypervariable regions (complementarity-determining regions, CDR) 1 of the light and heavy polypeptide chains usually contribute to the formation of idiotypic determinants. In the extensively analyzed murine antidextran model, one private idiotype and one public idiotype (cross-reactive idiotypes, CRI) were assigned, respectively to the third and the second hypervariable regions of the heavy chain (6). In most other cases, idiotypic determinants have not been associated definitively with a specific amino acid sequence (2). The latter result is not surprising, considering that antiidiotype antibodies elicited by immunization with intact immunoglobulin often recognize determinants dependent upon a particular quaternary interaction of the light and heavy chains (2).Using carefully absorbed rabbit antisera, Kunkel and colleagues (8) first described the unusual existence of two major CRI (Wa and Po) among human monoclonal IgM anti-IgG autoantibodies (rheumatoid factors, RF) from unrelated individuals with cryogiobulinemia. The larger Wa group includes ~60% of monoional 9). Amino acid sequence analysis of the variable regions of two Wa-CRI positive IgM-RF (Sie and Wol) has revealed a marked homology between the kappa light chains, but not the heavy chains (10). However, the precise chemical nature of the Wa-CRI has remained unclear.To clarify these issues, we generated a murine monoclonal antibody (mAb 17-109) that recognized a CRI

A simple, straightforward, and rapid method for the detection of beta-2 transferrin in otorrhea and rhinorrhea that can be used in a routine clinical laboratory is described. The beta-2 transferrin was detected by agarose gel electrophoresis of the fluid on Beckman Paragon equipment, followed by pressure transfer to a nitrocellulose membrane and then incubation with enzyme-labeled antitransferrin antibody and substrate. The procedure was fast (3.5 h) and sensitive (detected as little as 1 microgram/ml) and required only 3 microliters of fluid. Beta-2 transferrin was detected in cerebrospinal fluid diluted up to eightfold. No special training or expertise was needed, and all equipment and procedures used are commonly available in a routine clinical laboratory.

No abstract