PubMed · 7191171
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A Hofstetter. 1980. [Bidocef (Cefadroxil)].. https://pubmed.ncbi.nlm.nih.gov/7191171/
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We have assessed regulatory Th cell and cytokine responses in mice after oral immunization with recombinant Salmonella (BRD 847) expressing fragment C of tetanus toxoid, since little information is available to explain how these vectors induce mucosal IgA responses. A single dose of BRD 847 elicited serum IgG2a and mucosal IgA anti-tetanus toxoid Ab responses. To assess Th1-and Th2-type responses, CD4+ T cells from Peyer's patches and spleen were restimulated in vitro, and cytokine-specific ELISPOT, ELISA, and reverse transcriptase-PCR assays were used to assess cytokine patterns. CD4+ T cells produced IFN-gamma and IL-2 as well as IL-10, but not IL-4 or IL-5. Although IL-6 was elevated, further purification of cells from in vitro cultures into CD4+ Mac-1- T cells and Mac-1+ CD4- cells revealed that only the latter cell population had consistently elevated IL-6 gene expression, whereas both sorted populations exhibited increased IFN-gamma and IL-10 gene expression. Thus, orally administered recombinant Salmonella expressing fragment C of tetanus toxoid elicited dominant Ag-specific Th1-type responses together with Th2-type cells producing IL-10 in both mucosal and systemic tissues. Macrophages producing IL-6 were also evident. Our results are consistent with the suggestion that Ag-specific Th1 cells and their derived cytokines, IFN-gamma and IL-2, and Th2-derived IL-10 together with IL-6 produced by macrophages provide important signals for the development of mucosal IgA and serum IgG subclass responses in the absence of preferential expression of Th2 cytokines IL-4 and IL-5.
OBJECTIVE: To determine 1) whether patients with coccidioidal meningitis who had achieved remission with oral azole therapy were cured and 2) when oral azole therapy could be discontinued in these patients. DESIGN: Data were gathered on patients with coccidioidal meningitis who had successfully responded to azole therapy in previous clinical trials. SETTING: Referral centers, including university, county, and veterans' hospitals and clinics. PATIENTS: 18 patients in whom azole therapy for meningitis had been discontinued, usually because of a presumption of cure. MAIN OUTCOME MEASURES: Clinical and cerebrospinal fluid relapse. RESULTS: 14 of 18 patients (78% [95% CI, 52% to 94%]) had relapse with disseminated disease after discontinuation of therapy, for a total of 1 nonmeningeal and 15 meningeal relapses to date. Relapse occurred both soon and late (range, 0.5 to 30 months) after therapy was discontinued. The characteristics of patients who did not have relapse, including the particular azole used, the duration of therapy, the reason therapy was discontinued, and the cerebrospinal fluid indices before discontinuation, were similar to the characteristics of patients who had relapse. Relapse had serious consequences in some patients; 3 patients died. CONCLUSION: Our data suggest 1) that disease is only suppressed in patients with meningitis who achieve remission while receiving azole therapy and 2) that discontinuing azole therapy is unsafe. The alternative is lifelong treatment with azoles; this appears to be acceptable, because toxicity is uncommon with triazole therapy, even long-term triazole therapy.
We have been investigating the mechanisms by which exogenous protein Ags activate CD8+ T cells. Previously, we have shown that OVA primed CTL precursors in vivo if administered as an emulsion with an adjuvant such as CFA. Such CTLs inhibit development of Ab responses when adoptively transferred into syngeneic mice. Thus, CD8+ CTL are immunosuppressive. These studies were initiated to determine whether CD8+ suppressor T cells were cytolytic T cells. Oral administration of protein Ags is a well-established method for inducing tolerance in humoral and delayed hypersensitivity responses which is associated with development of CD8+ suppressor T cells. OVA was chosen as a model Ag because it has been used extensively in oral tolerance studies, and target cells expressing the OVA gene are well characterized. Our data show that multiple, intragastric doses of native OVA inhibited priming of CD8+ CTL precursors and also inhibited CD4+ T cells and Ab responses. Oral OVA inhibited CTL priming in mice immunized with OVA-loaded EL4 cells, OVA-expressing transfectants, or OVA in CFA. The observed tolerance is specific to the orally administered Ag. Although oral OVA did not prime CTL precursors, it did activate spleen cells that transferred unresponsiveness to naive syngeneic mice. Suppression was mediated by CD4-CD8+ T cells. These CD8+ suppressor T cells were phenotypically distinguished from CTL by reactivity with a mAb that recognizes activated suppressor T cells.