The Blockade of Interleukin-2 During the Acute Phase of Infection Reveals Its Dominant Regulatory Role.

infection causes Chagas' disease in humans. The infection activates the innate and adaptative immunity in an orchestrated immune response to control parasite growth, guaranteeing host survival. Despite an effective immune response to the parasite in the acute phase, the infection progresses to a chronic stage.

Administration of a nondepleting anti-CD25 monoclonal antibody reduces disease severity in mice infected with Trypanosoma cruzi.

The role of CD25+ regulatory T cells during the course of Trypanosoma cruzi infection has been previously analyzed, and the bulk of results have shown a limited role for this T cell subpopulation. In this study, we have used an IgM, nondepleting monoclonal antibody (mAb) aiming at blocking interleukin (IL)-2 activity on CD25+ T cells. The administration of this antibody 10 days before infection increased the resistance of outbred Swiss mice to the Colombian strain of T.

Enhancement of experimental cutaneous leishmaniasis by Leishmania molecules is dependent on interleukin-4, serine protease/esterase activity, and parasite and host genetic backgrounds.

Most inbred strains of mice, like the BALB/c strain, are susceptible to Leishmania amazonensis infections and resistant to Leishmania braziliensis infections. This parasite-related difference could result from the activity of an L. amazonensis-specific virulence factor.

The ACE inhibitors enalapril and captopril modulate cytokine responses in Balb/c and C57Bl/6 normal mice and increase CD4(+)CD103(+)CD25(negative) splenic T cell numbers.

Increasing evidence implies beneficial effects of angiotensin-converting enzyme (ACE) inhibitors beyond those of their original indications to control hypertension. One of the most attractive non-hemodynamic properties of ACE inhibitors is their ability to regulate cytokine production. The mechanism(s) underlying the role of ACE inhibitors on cytokine synthesis are not well understood but they have traditionally been attributed to the inhibition of angiotensin (Ang) II formation.

Requirement of L-selectin for gammadelta T lymphocyte activation and migration during allergic pleurisy: co-relation with eosinophil accumulation.

Intra-thoracic antigenic challenge (ovalbumin, 12.5 microg/cavity) led to increased numbers of gammadelta T lymphocytes in pleural cavities, blood and thoracic lymph nodes in sensitized mice within 48 h. Part of these cells expressed CD62L, which increased on gammadelta T cell surfaces obtained from lymph nodes after ovalbumin (OVA) challenge.