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Adenosine deaminase is an enzyme of the purine metabolism whose function is to convert adenosine to inosine and deoxyadenosine to deoxyinosine. The ecto-ADA1 binding to the cell surface through CD26 contributes to the regulation of cytokines and stimulates the proliferation of T cells by activating CD45. The deficiency of this enzyme generates the severe combined immunodeficiency syndrome, characterized by the accumulation of deoxyadenosine and adenine metabolites, which have toxic effects on lymphocytes, affecting DNA synthesis and consequently, clonal expansion. Early diagnosis of this immunodeficiency is essential, as it significantly reduces morbidity and mortality associated with recurrent infections. Recent advances in molecular biology and genetics have led to the identification of genetic defects of many primary immunodeficiencies and the development of promising diagnostic tools and treatment.

In congenital infection by Trypanosoma cruzi, morbidity and mortality vary from asymptomatic cases to severe clinical forms of the disease. It has been found that there is no specific clinical profile in newborns infected by T. cruzi, since during intrauterine development diverse pathological changes take place, causing alterations in the serological and parasitological profiles. Some intrinsic factors of the host, such as: the placental barrier and the ability of both, mother and fetus, to develop a specific immune response to control parasite multiplication, could be involved in such differences. Another possibility includes the genetic polymorphism of T. cruzi, since it is considered that strains of greater virulence can cross the placenta more easily and are more pathogenic to the fetus and/or the neonate.

In experimental leishmaniasis, the role of antibodies is not entirely clear, as some authors consider that these proteins are not involved in protection against infection. However, histopathological studies in human and experimental leishmaniasis lesions, show plasma cell infiltrates positive for IgA and secretion of IgM, IgG and IgA could mediate the formation of immune complexes with parasite antigens or self components, favoring necrosis leading to the elimination of the parasite. In this study, we determined if the serum IgA in the murine model has specific reactivity against antigens of Leishmania (Leishmania) mexicana of diagnostic utility. To do this, we used mice either susceptible or resistant to cutaneous leishmaniasis, and demonstrated by indirect ELISA that serum IgA is elevated in susceptible mice compared with that produced by resistant mice. Although other studies in murine models show that the serum IgG from mice infected with L. (L) mexicana present cross reactivity with unrelated parasite antigens derived from Trypanosoma cruzi, the analysis of the specificity of IgA by antigens of L. (L) mexicana and T. cruzi, by Western Blot, showed that the IgA serum of mice infected with T. cruzi reacts too with antigens of L. (L) mexicana. These findings suggest that IgA may be useful for the clinical management and prognosis of the disease.

The objective of this study was to detect the cytokines IFN-gamma, IL-4 and IL-10 expressed by CD4+ T cells in tissues of fetal mice with acute chagasic infection. For this, we examined the fetuses of NMRI mice whose mothers were infected with 22x10(3) metacyclic trypomastigotes of the M/HOM/BRA/53/Y strain of T. cruzi and made pregnant during the acute phase of infection. For the detection and localization of inflammatory infiltrates, nest parasites, antigens of T. cruzi a nd cytokines w eused hematoxylin-eosin techniques, peroxidase-anti-peroxidase and immunofluorescence. The immunohistochemical study revealed the presence of inflammatory infiltrates and antigens with amastigote nests in fetal skeletal muscle. CD4 + T cells producing IFN-gamma, as well as deposits of IFN-gamma and IL-10, were detected in sections of placenta, heart and skeletal muscle of fetuses of mice infected, while CD4+/IL-10+ was found only in skeletal muscle; in addition, deposits of IL-4 were detected only in placentas of healthy mice. These results indicate that fetuses are capable of generating their own immune response to antigens transmitted by their mother, which induces the secretion of cytokines and that, acting in synergy with the maternal antibodies, confer them a state of protection against infection; and that the transmission of the parasite depends on factors specific to each mother, which may modify its ability to control such transmission at the placental or systemic levels.

Adenosine deaminase (ADA) is an enzyme of purine metabolism which has been the subject of much interest because the congenital defect of this enzyme causes severe combined immunodeficiency syndrome. One of the three isoforms of the enzyme (ecto-ADA) is capable of binding to the glycoprotein CD26 and adenosine receptors A1 and A2B. ADA-CD26 interaction produces a costimulatory signal in the events of T cell activation and secretion of IFN-gamma, TNF-alpha and IL-6. During this activation, the enzyme activity is regulated positively by IL-2 and IL-12 and negatively by IL-4, based on the mechanism of translocation. Diverse studies suggest that seric and plasmatic levels of ADA rise in some diseases caused by microorganisms infecting mainly the macrophages and in hypertensive disorders, which may represent a compensatory mechanism resulting from increased adenosine levels and the release of hormones and inflammatory mediators estimulated by hipoxia.

The objective of the present study was to detect the presence of Trypanosoma cruzi DNA in the placenta and fetal tissues of NMRI mice (Mus musculus) inoculated with 22 x 10(3) trypomastigotes metacyclic of the M/HOM/BRA/53/Y strain by intraperitoneal route. Mice were pregnant in the acute phase of the infection. The course of patent parasitemia by T. cruzi was evaluated before mating and during pregnancy. At day twenty of gestation, animals were sacrificed and the fetuses and their placentas were removed to evaluate T. cruzi infection. Samples of fetal placenta, heart and skeletal muscle were fixed in 10%, formalin, included in paraffin and stained with hematoxilin and eosin (HE). The histopathological study of sections of fetal tissues revealed inflammatory infiltrates with mononuclear and polymorphonuclear cells and without parasitism in these tissues. The amplification of T. cruzi DNA by Polymerase Chain Reaction (PCR) showed a positive reaction in 18% of placental tissue of pregnant infected mice. The samples of heart and skeletal muscle of the fetuses of mothers infected with T. cruzi did not show the presence T. cruzi DNA. The placenta and skeletal muscle of the fetuses analyzed by Peroxidase anti Peroxidase inmunostaining showed T. cruzi antigens in those tissues. Negative results by PCR in fetal tissues might be related with the virulence and tropism associated with the biological and genetic characteristic Of the T. cruzi strain used in the experimental infection of female mice.

Hepatitis B is an important cause of morbidity and mortality around the world. One-third of the world's population has been estimated to be infected with hepatitis B virus (HBV). A significant amount of evidence suggests that both humoral and cellular immune responses are important to eliminate the virus and that, cellular immunity is involved in the pathogenesis of the disease. Vaccination with HBsAg is considered as the main strategy for effective control of the infection and viral transmission. However, approximately 5-10% of immunized individuals fail to elicit detectable specific antibodies and remain at risk for hepatitis B infection. In this work we have reviewed the current status in the pathogenesis of the disease and the mechanisms described to explain nonresponsiveness to the vaccine as well. Since nonresponders to the vaccine are at risk for the infection, a common mechanism to explain the absence or inappropriate immune response to virus components is proposed. Within the suggested model an impaired activation of T lymphocytes against viral antigens, both in nonresponders to vaccination and chronically infected patients, is described. These observations could be consistent with potential differences in the MHC/Ag presentation; therefore contributing to our understanding of the altered T helper response as an underlying mechanism for the lack of protective immunity against VHB.

The hallmark of the immunodeficiency virus infection is a progressive detriment of the immune response which has been associated to a gradual loss of its responsible components, in particularly, CD4 positive T cells. Although this cell population is considered the main target of the virus, there is a recent deal of interest in studying other components that may not be targets of the virus, but are important elements to control infectious microorganisms and that have been demonstrated to be altered during HIV infection. Neutrophils (PMN) are innate immune components that play a fundamental role against HIV infection and these cells have been described as functionally altered during AIDS. It has been suggested that such a dysfunction could be attributed to an increased susceptibility of these cells to accelerated spontaneous apoptosis. However, the underlying mechanisms that induce programmed cell death of neutrophils remain unknown. In previous works we have explored some events involved during cell death of neutrophils from HIV infected patients. It is the purpose of this work to review the current knowledge of apoptosis signals in neutrophils and to discuss our own data about some mechanisms involved in spontaneous and Fas mediated apoptosis, which may contribute to understand neutrophils dysfunction during HIV infection.