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Clinical and immunological changes after immunotherapy (ITS) for respiratory allergy were evaluated in 29 subjects during a one year follow up period. No adverse effects were noted with alum-absorbed allergen extracts. However, only patients receiving ITS for grass pollens demonstrated clinical improvement and blocking IgG increase as compared with those with multiple allergen sensitivity.

Despite the fact that the percentage of circulating CD3-positive cells is similar in cord and adult blood, the proliferative response induced by anti-CD3 monoclonal antibody (mAb) was impaired in the majority of human cord peripheral blood mononuclear cell (PBMC) samples we tested. The cell proliferative defect was associated with low interleukin 2 (IL 2) gene expression and scant IL 2 production. However, interleukin 2 receptor was fully expressed at both the mRNA and protein levels. Such a finding is consistent with the observation that exogenous recombinant IL 2 is able to boost the anti-CD3-mediated response of cord PBMC. Furthermore, when anti-CD3 and phorbol myristate acetate (PMA) were added together, they exerted a very marked synergistic effect on both the proliferation of, and IL 2 production by, cord PBMC. The addition of allogeneic antigen presenting cells plus soluble anti-CD3 or Sepharose-coupled anti-CD3 mAb to the cord T cell cultures had no significant effect on proliferation, whereas both elicited good mitogenesis of adult T cells. Moreover, addition of exogenous recombinant interleukin 1 to anti-CD3-stimulated T cells failed to trigger any proliferation in either adult or cord samples. Since the combination of PMA and calcium ionophore A23187 is effective in triggering optimal proliferation of cord T cells, the defect would seem to be associated with a failure in transmembrane transduction of the activation signals provided by the anti-CD3 stimulus for the cord T cell.

A study was carried out on cord blood T cell activation via the CD2-mediated pathway. Despite similar percentages of circulating CD3+ and CD2+ cells in adult and cord blood, the proliferation of cord PBMC to the anti-CD3 mAb and cord T cells to anti-CD2 mAb were defective. The T cell CD3-surface structure was normally able to control CD2-mediated activation, as its modulation by a non-mitogenic anti-CD3 mAb blocked cord PBMC proliferation induced by anti-CD2 mAb. CD2-stimulated cord T cells did not proliferate and did not produce a significant amount of IL-2 in culture, although they expressed the IL-2R. This observation was confirmed by the optimal proliferation of CD2-induced cord T cells when rIL-2 was added. Despite the alternative T cell activation pathway is monocyte-independent in adults, the defective cord T cell activation via the CD2 molecule could also be bypassed by the addition of PMA, small amounts of either autologous or allogeneic adult and cord AC or simply rIL-1 alone. Our findings provide evidence for an intrinsic functional defect in cord CD2-mediated T cell activation, which is linked to an impaired increase of free cytoplasmic calcium, as confirmed by the effectiveness of calcium ionophore A23187 in restoring a good CD2-induced cord T cell proliferation and by measurement of cellular calcium uptake after activation via the CD2 molecule. The characteristics of cord T cells revealed by this study recall the thymocyte functional pattern and may represent functional expression of the previously described phenotypic immaturity of cord T cells.

By a study of 87 oncologic hospitalized patients, affected by serious infectious complications and treated with high-dose antibiotic therapy including co-trimoxazole, the authors evaluate the allergic and immunologic reactions to the drug on clinical and serological basis and try to outline the pathogenic implicated mechanisms.

Alcoholic liver disease (ALD) patients had normal absolute lymphocyte counts, increased percentage of Leu3+/T4+ cells (p less than 0.001) and raised T4/T8 ratio (p less than 0.01). Double-colour immunofluorescence analysis using isotype-specific goat anti-mouse immunoglobulins, fluorescein or rhodamine-conjugated, demonstrated that the rise in inducer (Leu3+/T4+) T-cells was almost entirely represented by an expanded population of T4+TQ1- and 5/9+ true helper lymphocytes. T4+ cells also expressed IL2 receptors, as detected by the anti-Tac monoclonal antibody (range 1-18%). On the other hand, the percentage of Leu3+/T4+ cells which bind the K562 cell-line or co-express NK markers on their surface, such as Leu7 (HNK-1), was within the normal range in the majority of ALD patients. Functional studies on patients' cultured total or B-enriched lymphocytes in a pokeweed-mitogen-driven B-cell differentiation assay showed an enhanced plasma cell generation even in unstimulated cultures. Co-culture experiments with normal enriched-B lymphocytes demonstrated that both irradiated and non-irradiated patient T cells led to an increased plasma cell generation. These findings indicate that helper T cells and B cells are all simultaneously activated in vivo, and that the suppressor T lymphocyte function is normal in ALD.

Lymphocytes from 22 patients with chronic myeloid leukemia (CML), 13 treated with polychemotherapy, eight by monochemotherapy, and one untreated, were analyzed for the presence of classic T and B cell surface markers (E-rosette, EAC-rosette, surface immunoglobulins) and for their ability to respond to phytohemagglutinin (PHA). The absolute number and percentage of E-rosetting cells (T-cells), EAC-rosetting cells and cells staining for surface immunoglobulins (B cells) were all significantly lower than controls (P less than or equal to 0.025). The response to PHA was also significantly lower in patients than in controls at the smaller concentrations of the mitogen (3.75 micrograms/ml, 30 micrograms/ml) tested (P less than or equal to 0.01); at a higher PHA concentration (120 micrograms/ml) the decrease in PHA stimulation approached significance (P = 0.07). These lymphocyte abnormalities support the concept that CML lymphocytes may be derived from the leukemic clone.

Because T-cell dysfunctions have been reported in patients with primary Sjögren's syndrome (SS), peripheral blood mononuclear cell (PBMC) proliferation obtained with anti-CD3 and anti-CD2 monoclonal antibodies was evaluated in these patients. Anti-CD3-induced mitogenesis, which varied widely among the patients, was lower in subjects with evidence of anti-SSA and anti-SSB antibodies than in controls. Moreover, the anti-CD2-induced response was depressed in about half the patients and the nonresponders were mainly those with anti-SSA and anti-SSB antibodies. Phorbol myristate acetate, a protein kinase C activator, used alone or added to anti-CD3, induced greater proliferation in patients than in control PBMC. In contrast, exogenous recombinant interleukin 2 (rIL-2) did not significantly enhance the anti-CD2-induced response of patients' PBMC, as it did in normal PBMC. Peripheral blood and parotid T cells from a patient with well-defined primary SS and parotid enlargement also responded poorly to anti-CD2 stimulation. Exogenous rIL-2 restored T-cell proliferation only in the salivary gland cultures of this patient. The present findings suggest that there is a T-cell activation defect in subjects with primary SS, particularly in those with circulating anti-SSA and anti-SSB antibodies. In addition, the difference in the response to IL-2 of peripheral blood and parotid-infiltrating T cells would seem to indicate that T-cell subsets are differently distributed in the blood and inflammation site.

A 78-year old man is presented with a characteristic case history and physical and laboratory findings typical of angio-immunoblastic lymphadenopathy with dysproteinemia (AILD). The disease had an acute onset with constitutional symptoms, generalized lymphadenopathy and hepato-splenomegaly. The presence of a large pleural effusion was of particular interest. Histologically the distinctive feature was a pronounced proliferation of small blood vessels and immunoblasts in the lymph nodes. Management of patient with AILD is problematic. Since AILD is a non-neoplastic process, symptomatic treatment with small doses of steroids, if necessary, would seem to be the best therapeutic approach. However, in our patient, as well as in other cases reported in the literature, a rapid and long standing (18 months so far in our case) complete remission was obtained with a short cycle of chemiotherapy.

Double-labelling immunofluorescence analysis within the CD4+ cell subset was carried out in 27 bronchoalveolar lavage fluids and 11 peripheral blood samples of sarcoidosis patients with anti-TQ1, anti-2H4 and anti-4B4 monoclonal antibodies. Helper/inducer CD4+TQ1-/4B4+ cells were strongly increased in the lung and slightly, but significantly, decreased in the blood of sarcoidosis patients with respect to normal controls. No differences were found in the number of both lung and blood CD4+2H4+ cells between sarcoidosis patients and controls. The findings are further evidence for a compartmentalization of T cell subsets in sarcoidosis.

Phenotypic analysis of helper CD4+TQ1- cell population, the major helper T-cell subset for B-cell responses, was carried out in BAL fluid of sarcoidosis patients. Most of the BAL CD4+ cells lacked TQ1 membrane antigen. A correlation between the number of helper CD4+TQ1- cells and IgM and IgA levels was observed in 27 sarcoidosis patients' BAL. A role of CD4+TQ1- cells in modulating lung B-cell immunoglobulin secretion in sarcoidosis was confirmed by the fact that BAL IgG level and helper T-cell number correlated well in patients with low-intensity alveolitis. Results showed an inverse correlation between symptom duration and BAL IgM levels and CD4+TQ1- cell number. The number of helper cells was above normal in patients who had symptoms for less than 12 months and within normal range in those who had symptoms for more than that. The pathogenic and clinical relevance of these data is discussed.

The correlation between leukocyte migration-inhibition and delayed skin hypersensitivity was studied in the sera of 15 anergic untreated Hodgkin's disease patients before and after administration of thymostimulin. Skin tests, negative in all patients before treatment, turned positive in 9 after thymostimulin. Prior to treatment, 10 patients had normal and 5 enhanced migration; none was leukocyte migration-inhibition factor (LIF) positive (mean 1.14 +/- 0.30). Seven of the 9 patients (77.9%) whose skin tests became positive, 3 of whom had an initially enhanced migration, were LIF positive after thymostimulin. LIF closely paralleled skin hypersensitivity both before and after thymostimulin. It is suggested that thymostimulin evokes the differentiation of a lymphocyte subpopulation(s) responsible for both factors investigated.

A longitudinal study on human T lymphoid surface antigens was performed on blood samples from 6 infants during their first month of life. Although the results indicate a sudden increase in the percentage of OKT3+ and E-RF+ cell types a few hours after birth and a less rapid decrease of OKT6+ and OKT9+ circulating cells, high levels of OKT10+ cells persisted. This finding suggests that infant blood contains immature phenotypic T lymphocytes after birth.