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Recognition of pathogens by innate immune cells is mediated by pattern recognition receptors (PRR), which include scavenger receptors (SR). The class A SR, SR-A/CD204 and MARCO, are characterized by the presence of collagenous and SR cysteine-rich domains in their extracellular portions. Both receptors are expressed mainly on macrophages and dendritic cells. Thanks to their ability to bind to a wide range of polyanionic ligands, the class A SR may participate in numerous functions of these cells, such as endocytosis, and adhesion to extracellular matrix and to other cells. Among SR-A ligands are oxidized lipoproteins and β-amyloid fibrils, which link SR-A to the pathogenesis of arteriosclerosis and Alzheimer's disease. Despite the demonstration of class A SR involvement in so many processes, the lack of selective ligands precluded reaching definite conclusions concerning their signaling abilities. Using specific receptor ligation with antibodies, we showed that SR-A and MARCO trigger intracellular signaling, modulating pro-inflammatory and microbicidal activities of macrophages. Surprisingly, despite similarities in structure and ligand binding repertoires, SR-A and MARCO exert opposite effects on interleukin-12 (IL-12) production in macrophages. SR-A ligation also stimulated H₂O₂ and IL-10 production, but had no effect on the release of several other cytokines. These limited effects of specific SR-A ligation contrast with generalized enhancement of immune responses observed in SR-A-deficient mice. Recent studies have revealed that many of these effects of SR-A deficiency may be caused by compensatory changes in the expression of other receptors and/or disinhibition of signal transduction from receptors belonging to the Toll/IL-1R family, rather than by the loss of the receptor function of SR-A.

Splenic lymphocytes from T. gondii infected mice produced high levels of IFN-gamma in vitro. The production of IFN-gamma was increasing until 10-th day of infection, reaching a level 1600-fold higher to that found in control cultures, then it began to decrease. The level of IL-10 released by lymphocytes to the medium was also increasing up to the 10-th day of infection, afterwards its content dropped down to the level 18-fold higher than that at the beginning of experiments. There were no effects of immunization with antigens of killed parasites on the production of IFN-gamma by splenic cells in vitro.

T cells are involved in the pathogenesis of nephrotic syndrome (NS). The aim of the study was to determine whether the activity of T-helper-1 (Th1) and T-helper-2 (Th2) cells are predictive for steroid sensitivity in children with primary NS. These parameters were assessed at the onset of disease, before initiation of steroid therapy. Two groups of NS children were retrospectively formed according to steroid sensitivity(SS) or resistance(SR). Activity of Th1 and Th2 cells was defined by the production of IL-2, IFN-gamma and IL-4, IL-10 (ELISA), respectively, in the supernatants of the culture of CD4+ T cell cultures activated with autologous monocytes presenting tetanus toxoid (TT). Peripheral lymphocyte subsets were determined using double or triple colour flow cytometry. In SS children with NS we found the cytokine synthesis indicating the predominance of Th2 activity. We conclude that prior to treatment the Th1 and Th2 cell activity provides a useful tool to evaluate the probability of steroid sensitivity in patients with primary NS.

The authors studied the immunological response before and after beginning anti-tuberculous therapy, of a previously health, HIV negative, 22 year old black male, from the Republic of Cape Verde. The patient had multiple vertebral bony lesions associated to subcutaneous abscesses. As immunological markers of antigen recognition, we measured blastogenic and cytotoxic responses and gamma-IFN secretion towards 30 kD, 65 kD, filtrate proteins of M. tuberculosis, M. tuberculosis (H37Rv) and PPD cultures. To characterise the role of cytokines during infection, expression of mRNA for gamma-IFN, IL-4 and IL-10 was also analysed. A slight increase of lymphocyte proliferation and gamma-IFN production was seen in response to purified protein derivative (PPD) and short term culture filtrate proteins (ST-CFP), after one month of therapy. More significant, was the increase in M. tuberculosis and PPD-specific cytolytic T lymphocyte response after one one month of treatment. After 6 months of treatment, blastogenic and cytotoxic responses and gamma-IFN production were considerably higher toward the antigen panel. The CD4/CD8 ratio increased from 0.7 to 1.4 after treatment. We observed that ST-CFP and MT-CFP induced increasingly higher lymphoproliferation and gamma-IFN production, confirming their role in the protective immune responses to M. tuberculosis. The reduced immune responses in the peripheral blood of this patient probably reflect a high activity in the local sites of infection. This case of disseminated tuberculosis infection maybe related to nutritional or social factors or may represent an example of reduced in ate resistance against tuberculosis infection.

Interleukin-10 (IL-10) is produced predominantly by T-helper lymphocytes and macrophages. IL-10 inhibits lymphocyte-induced cytokine production (CSIF--cytokine synthesis inhibitory factor), cooperates in B lymphocytes activation as well as macrophages--monocytes deactivation (MDF--macrophage deactivating factor). Due to its immunosuppressive properties IL-10 may be used in therapy of some T-cell induced diseases.