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The authors studied immune response and exposure to 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin (dioxin) among veterans of Operation Ranch Hand, the US Air Force unit responsible for the aerial spraying of herbicides in Vietnam from 1962 to 1971. A comparison group of Air Force veterans who served in Southeast Asia but were not involved in spraying herbicides was included. The authors studied delayed-type hypersensitivity skin test responses to Candida albicans, mumps, Trichophyton, and a bacterial antigen made from lysed Staphylococcus aureus. Lymphocyte measurements included total lymphocyte counts; T-cell (CD3, CD4, CD5, and CD8), B-cell (CD20), and NK-cell (CD16 and CD56) subsets; and expression of the activation antigen CD25 on CD3 T cells. The authors quantitated the serum concentrations of immunoglobulin (lg)A, IgG, and IgM; examined sera for the presence of monoclonal immunoglobulins (M proteins); and looked for a broad range of autoantibodies (rheumatoid factor, antinuclear antibody, smooth muscle autoantibody, mitochondrial autoantibody, parietal cell autoantibody, and thyroid microsomal autoantibodies). They measured the level of dioxin in 1987 or 1992, extrapolated the result to the time of service in Vietnam, and assigned each veteran to one of four exposure categories: Comparison and three Ranch Hand groups (Background, Low, or High). Overall, the authors found no evidence of a consistent relation between dioxin exposure category and immune system alteration. Am J Epidemiol 1999; 149:1038–46. [ABSTRACT FROM PUBLISHER]

Peripheral blood mononuclear cells isolated from patients with systemic lupus erythematosus (SLE) developed lower levels of skin test antigen stimulated natural killer cell like cell-mediated cytolysis (NK-like CMC) than did similar cells from age and sex matched non-SLE volunteers. When the subjects were grouped according to disease activity the cells from the patients with mild disease activity developed lower levels of NK-like CMC than did those from the non-SLE control subjects. The cells isolated from SLE patients who had moderate to severely active disease developed little if any NK-like CMC after exposure to various skin test antigens. Greatly decreased skin test antigen stimulation of NK-like CMC in the cells from the SLE patients with more active disease did not appear to be due to therapy with corticosteroids or to a suppressor effect on this response by monocytes present in the peripheral blood mononuclear cell populations. [ABSTRACT FROM AUTHOR]

We performed a battery of tests on peripheral blood samples from 94 patients with lung cancer to determine the extent to which immunological depression was due lo abnormal lymphocyte function, as compared to changes in the number of lymphoid cells In the peripheral blood or in the efficiency of purification of cells in Ficoll- Hypaque gradients in preparation for testing. The percentage of lymphocytes in the gradient-derived cell suspension (%LG) was the most informative test. It decreased significantly with advancing stage of cancer and could predict survival of patients with uniform stage. The %LG correlated with survival better than any other test when multivariate analyses of all test combinations were performed. Low values of %LG reflected both the depressed lymphocyte counts and the altered buoyant density of the leucocytes of many patients with advanced cancer. A large proportion of the depression in other immune function tests was statistically attributed to changes in %LG. We concluded that this simple measurement provides valuable information about patients with lung cancer. [ABSTRACT FROM AUTHOR]

A battery of immunologic tests were performed on 42 patients with recurrent cancer of the head and neck whose median survival time was 6.8 months. Two tests correlated with survival: total white blood cell (WBC) count and the percentage of lymphoid cells (% LG) in the Ficoll-Hypaque gradient separated leukocyte fraction of blood. [ABSTRACT FROM AUTHOR]

Objective: Cerebral cavernous malformations (CCMs) affect more than one million Americans, predisposing them to a lifetime risk of hemorrhagic stroke and epilepsy. A potential role of the immune response in this disease has not been postulated previously but is compelling given the unique antigenic milieu of CCM lesions with sequestered thrombi and a leaky blood-brain barrier and the numerous examples of immune modulation of angiogenesis in other disease states. The objective of this article is to reveal novel observations about apparent immune responses in CCM lesions excised from human patients and to outline the potential pathobiological significance of these observations, specific hypotheses for future research, and potential clinical implications., Methods: We reviewed data from differential gene expression revealing several immunoglobulin and other related genes markedly upregulated within human CCM lesions. Other observations are presented revealing infiltration of antibody-producing B lymphocytes and plasma cells in CCM lesions. We also present recent data demonstrating fivefold enrichment of gamma globulin to albumin ratio in a human lesion compared with serum from the same patient and oligoclonality of IgG in four of five CCM lesions, but not in paired sera from the same patients or in control specimens., Results: We describe ongoing research aiming to characterize cellular and humoral components of the immune response in CCMs and initiating investigation into its clonality by isoelectric focusing on the predominant immunoglobulin isotypes isolated from the lesion, in comparison to the patient's serum, and by the distribution of lengths of complementary-determining region 3 of the immunoglobulin heavy chain genes in messenger ribonucleic acid isolated from lesions and from pooled plasma cells and B cells laser captured from CCMs in comparison to peripheral lymphocytes from the blood of the same patients., Conclusion: Immune response could play a role in or represent a potential marker of CCM lesion proliferation and hemorrhage or could otherwise contribute to lesion phenotype. The ongoing studies will generate preliminary data for future research aimed at comparing the immune response in quiescent versus clinically aggressive CCM lesions. An oligoclonal immune response shown in this research would stimulate future experiments to identify autoimmune or extrinsic antigenic triggers involved in CCM disease.