Decoding caspase signaling in host immunity to the protozoan Trypanosoma cruzi

Lopes, Marcela F.; Guillermo, Landi V. C.; Silva, Elisabeth M.

doi:10.1016/j.it.2007.06.004

Cited by 16 publications

(16 citation statements)

References 71 publications

(109 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Blockade of FasL interaction partially increases CD4 + T lymphocyte recovery, in vitro and in vivo [51]. Moreover, in vivo administration of anti-FasL blocked AICD and enhanced T CD8 proliferation in infected mice [71]. Blockade of activated T CD8 death increased IFN-γ secretion in initial stages and IL-4/IL-10 secretion in latter stages of infection [71].…”

Section: Splenomegaly Is a Constant Feature In T Cruzi Infectionmentioning

confidence: 99%

Differential Regional Immune Response in Chagas Disease

et al. 2009

View full text Add to dashboard Cite

Following infection, lymphocytes expand exponentially and differentiate into effector cells to control infection and coordinate the multiple effector arms of the immune response. Soon after this expansion, the majority of antigen-specific lymphocytes die, thus keeping homeostasis, and a small pool of memory cells develops, providing long-term immunity to subsequent reinfection. The extent of infection and rate of pathogen clearance are thought to determine both the magnitude of cell expansion and the homeostatic contraction to a stable number of memory cells. This straight correlation between the kinetics of T cell response and the dynamics of lymphoid tissue cell numbers is a constant feature in acute infections yielded by pathogens that are cleared during the course of response. However, the regional dynamics of the immune response mounted against pathogens that are able to establish a persistent infection remain poorly understood. Herein we discuss the differential lymphocyte dynamics in distinct central and peripheral lymphoid organs following acute infection by Trypanosoma cruzi, the causative agent of Chagas disease. While the thymus and mesenteric lymph nodes undergo a severe atrophy with massive lymphocyte depletion, the spleen and subcutaneous lymph nodes expand due to T and B cell activation/proliferation. These events are regulated by cytokines, as well as parasite-derived moieties. In this regard, identifying the molecular mechanisms underlying regional lymphocyte dynamics secondary to T. cruzi infection may hopefully contribute to the design of novel immune intervention strategies to control pathology in this infection.

show abstract

Section: Splenomegaly Is a Constant Feature In T Cruzi Infectionmentioning

confidence: 99%

Differential Regional Immune Response in Chagas Disease

et al. 2009

View full text Add to dashboard Cite

show abstract

“…However, T. cruzi has evolved a series of mechanisms to evade this response and persist in the host. Some of these mechanisms include the release of molecules that induce T-cell suppression, inhibition of secretion of pro-inflammatory cytokines, modulation of expression of HLA and CD40-L, induction of hostcell apoptosis (Brodskyn et al 2002;Zambrano-Villa et al 2002;Lopes et al 2007) and release of proteases, such as oligopeptidase B, and cysteine proteases like cruzipain (McKerrow et al 2006;Scharfstein et al 2008).…”

Section: Discussionmentioning

confidence: 99%

Proteolytic cleavage of chemokines by Trypanosoma cruzi's cruzipain inhibits chemokine functions by promoting the generation of antagonists

et al. 2010

View full text Add to dashboard Cite

“…In agreement with these data, it has been shown that the in vivo injection of anti-FasL and a general caspase inhibitor (zVAD-fmk) into acutely infected mice impairs T and B lymphocyte death and improves the host immune response to infection in both SCLN and SP (55, 57). Blockade of activated CD8 + T cell death increases IFN-γ secretion by splenocytes in the initial stages of infection, and IL-4 and IL-10 are induced at later stages (55, 58). …”

Section: Systemic Trypanosoma Cruzi Entry Induces a Differential Respmentioning

confidence: 99%

Trypanosoma cruzi Entrance through Systemic or Mucosal Infection Sites Differentially Modulates Regional Immune Response Following Acute Infection in Mice

et al. 2013

View full text Add to dashboard Cite

Acute Chagas disease is characterized by a systemic infection that leads to the strong activation of the adaptive immune response. Outbreaks of oral contamination by the infective protozoan Trypanosoma cruzi are frequent in Brazil and other Latin American countries, and an increased severity of clinical manifestations and mortality is observed in infected patients. These findings have elicited questions about the specific responses triggered after T. cruzi entry via mucosal sites, possibly modulating local immune mechanisms, and further impacting regional and systemic immunity. Here, we provide evidence for the existence of differential lymphoid organ responses in experimental models of acute T. cruzi infection.

show abstract

Decoding caspase signaling in host immunity to the protozoan Trypanosoma cruzi

Cited by 16 publications

References 71 publications

Differential Regional Immune Response in Chagas Disease

Differential Regional Immune Response in Chagas Disease

Proteolytic cleavage of chemokines by Trypanosoma cruzi's cruzipain inhibits chemokine functions by promoting the generation of antagonists

Trypanosoma cruzi Entrance through Systemic or Mucosal Infection Sites Differentially Modulates Regional Immune Response Following Acute Infection in Mice

Contact Info

Product

Resources

About