Decreased CD4+Circulating T Lymphocytes in Patients with Gastrointestinal Chagas Disease

Relationship between Trypanosoma cruzi and human chagasic megaesophagus: blood and tissue parasitism.

“…However, the detection of T. cruzi not associated with inflammation may be explained by the presence of intact nests of parasites. 34,36 Such parasite nests were indicative of tissue invasion so recent that the local inflammatory process has not yet developed, or then are related to some degree of host immunosuppression, which has been shown in severe gastrointestinal forms 37 and suggested in cardiac 38 forms of Chagas disease. The cellular immune response is an important factor in the control of T. cruzi in all stages of the disease, and an immune imbalance could result in an increase in tissue and blood parasitism, 39 a fact that is consistent with observations in the present study among chagasic patients with megaesophagus.…”

“…This can be demonstrated by the elevated percentage of T lymphocytes (CD4 ϩ and CD8 ϩ ) expressing Class II molecules of major histocompatibility complex (MHC) human leukocyte antigen D-related (HLA-DR) in the peripheral blood of patients with the gastrointestinal form of Chagas' disease. 37 …”

Innate immunity and regulatory T-cells in human Chagas disease: what must be understood?

“…With the aim of contributing to this field of investigation, studies have been developed to characterise immunological biomarkers in patients presenting distinct clinical manifestations of the disease (Reis et al 1993, Dutra et al 1994, 1996, Lemos et al 1998, Gomes et al 2003, Sathler-Avelar et al 2003, Souza et al 2004, Vitelli-Avelar et al 2005, 2006, 2008. Additionally, other investigators have also focused on what impact etiological treatment with benznidazole (Bz) may have on the anti-T. cruzi immune response (Bahia-Oliveira et al 2000, Sathler-Avelar et al 2006, 2008, Vitelli-Avelar et al 2008.…”

Evolution and pathology in Chagas disease: a review

“…In the gastrointestinal form, however, a significant decrease in the absolute number of CD3 + lymphocytes and in CD19 + B lymphocytes as well as an inversion of the CD4/CD8 ratio was seen, whereas this ratio remained unchanged in the heart patients as compared to that of control (Lemos et al 1998). These T cells showed down-regulation of CD62L, which has been associated with effector memory phenotype.…”