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M S Lima

Publications and source records attributed to M S Lima.

32 records · Page 2Linked to original sources
PubMed1988

Immune responses during human schistosomiasis mansoni. XV. Anti-idiotypic T cells can recognize and respond to anti-SEA idiotypes directly.

We previously have shown that former patients and patients with active cases of schistosomiasis mansoni have T lymphocytes in their PBMC that proliferate when exposed to immunoaffinity-purified antibodies against Schistosoma mansoni soluble egg antigens (SEA). These T cell anti-idiotypic responses required the participation of adherent cells, but the role of these cells in the response to the Id has been unclear. We now show that chloroquine does not interfere with Id-elicited stimulation of cells from former patients but completely inhibits their response to the SEA. F(ab')2 fragments of anti-SEA Id are stimulatory, and excess normal human IgG does not alter anti-Id responses. Soluble Id F(ab) fragments are not stimulatory, but rather inhibit stimulation by the intact Id from which they were made. Either intact Id or their F(ab')2 fragments can stimulate non-adherent T cells in the absence of adherent cells if an exogenous source of purified or recombinant human IL-1 is supplied. Nonstimulatory F(ab) fragments can stimulate nonadherent cells if they are bound first to Sepharose 4B and presented in conjunction with IL-1. Thus, T cells from former schistosomiasis patients can react with polyclonal anti-SEA-related Id directly. Under these conditions T cell proliferation requires receptor cross-linking and a source of IL-1 but does not require either "processing" of Id or MHC co-presentation.

Antibodies, Anti-Idiotypic↗
PubMed1986

Immune responses during human Schistosomiasis mansoni. Evidence for antiidiotypic T lymphocyte responsiveness.

We present a method for the examination of antiidiotypic cell-mediated reactivity during chronic human infections. Pooled and individual sera from patients with schistosomiasis mansoni were purified on immunoaffinity columns of schistosomal egg antigens (SEA). The eluates contained anti-SEA antibodies, but not SEA. These antibody preparations, and their F(ab)2 fragments, stimulated dose-dependent proliferation of peripheral blood mononuclear cells (PBMN) and T lymphocytes from some, but not all active or former schistosomiasis mansoni patients, and could do so autologously. Stimulation required presentation by plastic-adherent cells. The eluates did not stimulate PBMN from persons who had never had schistosomiasis. Affinity-purified anti-SEA antibodies from former patients (cured for greater than 10 yr) did not stimulate PBMN from patients with active infections. Reabsorption on SEA columns removed stimulatory activity from the eluates. We propose that multiclonal, SEA-related idiotypes expressed by some anti-SEA antibodies stimulate proliferation of T lymphocytes that express antiidiotypic specificities.

Antibody Formation↗
PubMed1985

The hypotensive effect of intracarotid injections of adenosine triphosphate depends on its hydrolysis to adenosine.

The effects of intra-carotid injections of adenosine, adenosine triphosphate (ATP) and alpha-beta-methylene ATP were studied on arterial blood pressure of anaesthetized cats. Adenosine and ATP decreased arterial blood pressure, whilst the ATP stable analogue, alpha-beta-methylene ATP caused a dose-dependent increase in arterial blood pressure. These results suggest that the hypotensive action of ATP might depend on its previous hydrolysis into adenosine.

Adenosine↗
PubMed1985

Demonstration of leukocyte inhibitory factor in human Schistosomiasis mansoni and its evaluation from patients in an endemic setting.

Leukocyte migration inhibitory Factor (LIF) is produced by the peripheral blood mononuclear cells (PBMN) of most patients with Schistosoma mansoni infection upon their exposure to soluble egg antigens (SEA). PBMN of some patients also respond to adult worm (SWAP) antigens by LIF production. LIF is stable at 37 degrees C for 60 min but is sensitive to heating at 56 degrees C for even 30 min. The serine protease inhibitor PMSF destroyed LIF activity at concentrations of 10(-2) to 10(-3) M. Concanavalin A stimulated production of detectable levels of LIF by 8 hr, while SEA and SWAP did so by 15 and 39 hr, respectively. PBMN of healthy normal controls did not produce LIF upon exposure to SEA or SWAP. PBMN of a few field controls (stool negative subjects from an endemic area) produced detectable LIF activity when exposed to SEA or SWAP. PBMN from most infected (stool positive) patients from an endemic area produced LIF when exposed to SEA and only occasionally did so to SWAP. Previous studies have shown that most often only the PBMN of former, cured patients, and not chronically infected patients, produce the lymphokine activity termed mitogenic factor (MF). The current data indicate that because LIF is primarily produced by actively infected patients, its production may be controlled by different immunoregulatory mechanisms. Furthermore, although most SEA-related responses are highly immunoregulated in active, chronically infected patients, SEA appears to be a better stimulus for patient PBMN production of LIF than SWAP.

Chronic Disease↗
PubMed1985

Immune responses during human Schistosomiasis mansoni. XI. Immunologic status of patients with acute infections and after treatment.

Sixteen patients, 8 to 30 yr of age, with acute (toxemic) phase schistosomiasis mansoni were studied immunologically within 2 to 3 mo of their exposure to Schistosoma mansoni cercariae, and were monitored after chemotherapy. Total leukocyte levels and peripheral blood eosinophilias were higher in these patients than in similar individuals with chronic schistosomiasis mansoni. In contrast to chronic patients, the eosinophilias of the acute cases were decreased rather than elevated upon treatment. Total lymphocyte population (T and B cell) percentages were not altered during acute infection. Lymphoid subset (T3+, T4+, and T8+) analysis revealed elevated levels of both T4+ and T8+ cells. In vitro blastogenic responses of peripheral blood mononuclear cells (PBMN) to heterogeneous schistosome-derived antigens (eggs, SEA; adult worms, AW; and cercariae, CERC) were evaluated. SEA responsiveness was considerably higher than that of patients with chronic S. mansoni infections. The ratios of SEA to AW responses in acute cases gave a mean of 2.0, as opposed to 0.5 for a comparable group of chronically infected patients. The sera of most acute patients already contained suppressive factors that specifically decreased schistosomal antigen-induced PBMN blastogenesis. Chemotherapy of acute cases lead to a diminution of PBMN responsiveness to SEA and CERC. Treatment of patients with chronic infections lead to the elevation of such responses. PBMN from patients with acute infections produced lymphokine leukocyte inhibition factor upon exposure of the cells to SEA but not AW. A similar pattern was true for production of the lymphokine activity mitogenic factor. Levels of antibody in sera of acutely infected patients against SEA, CERC, and AW were considerably higher than levels in sera of chronically infected patients matched for age and intensity of their infections. These high antibody titers persisted for at least 6 mo after treatment, and were unrelated to the intensity of infection. The immunologic status of these patients with acute schistosomiasis mansoni differed considerably from patients with chronic infections. These findings re-emphasize the immunoregulatory events that apparently develop upon continued exposure to schistosomes and their products during chronic infection.

Acute Disease↗
PubMedDate not supplied

Inflammatory cutaneous reaction induced by the lectin of Dioclea grandiflora (Mart.).

The lectin from Dioclea grandiflora (Mart.) that selectively binds glucose and mannose, when subcutaneously injected in mouse induces an inflammatory cutaneous reaction whose histological analysis reveals an hemorrhagic ulceration with exudative reaction accompanied by an influx of polymorphonuclear leukocytes and giant cells. The presence of lymphocytes and plasma cells in the lesion was insignificant. In order to characterize the in vivo action of inflammatory factors generated by this lesion, distinct lines of mice were used: high and low antibody responder mice; the genetically selected mice to the acute phase of inflammatory reaction; lines of mice deficient in C5, a protein of the complement system. It is shown that the lectin of D. grandiflora acts as an inflammatory agent probably promoting exocytosis and release of mediators.

Acute-Phase Reaction↗